Reflex responses on blood pressure and renal nerve activity to local intra-arterial injection of capsaicin in anesthetized dogs

The present study was performed to examine effects of intra-arterial and intravenous injection of capsaicin on efferent renal sympathetic nerve activity (RNA) in pentobarbital anesthetized dogs. In animals with intact baroreceptors, intra-arterial injection of capsaicin (4 +/- 1 microgram) produced significant increases in mean blood pressure (MBP) and heart rate (HR) by +43 +/- 8 mmHg and +33 +/- 15 beats/min at 20 s after the injection, respectively. There followed a recovery toward the control so that 60 s after the intra-arterial injection changes in MBP and HR were +8 +/- 5 mmHg and +18 +/- 8 beats/min, respectively. RNA showed a biphasic response, comprising of an initial increase (+52 +/- 28% of the control at 20 s) followed by a decrease by -30 +/- 8% of the control 60 s after the injection. Following bilateral cervical vagotomy the initial increase in RNA did not differ significantly from the value of RNA in animals with intact baroreceptors. However, the later decrease in RNA reversed above the control so that 60 s after the injection change in RNA was +5 +/- 10% of the control. Complete baroreceptor denervation showed a similar response on RNA in the vagotomized animals (+49 +/- 9 and +14 +/- 10% of the control at 20 and 60 s after the injection, respectively). In contrast, intravenous injection of capsaicin (6 +/- 1 microgram/kg) resulted in significant decreases in MBP (-19 +/- 11 mmHg) and HR (-9 +/- 4 beats/min). RNA at 20 s after the injection showed a unidirectional decrease by -16 +/- 7% of the control in animals with intact baroreceptors. These responses reversed above the control after cervical vagotomy. Thus, these data indicate that activation of C-fiber afferents in skeletal muscles by intra-arterial injection of capsaicin results in renal sympathoexcitation, and that the later sympathoinhibition is mediated by combined activation of systemic baroreceptors.     

Enhanced blood pressure responses to loud noise in offspring of monkeys with high blood pressure

Sixteen unanesthetized immature Macaca fascicularis monkeys, 18-43 months of age, were tested for mean arterial blood pressure (MBP) and heart rate (HR) responses to 30 minutes of continuous broadband noise (95 dB). Eight animals (OH group) were offspring of monkeys with high blood pressure (parents' MBP = 115.5 +/- 1.0 (SEM) mmHg), and eight (OC group) were offspring of control animals with normal blood pressure (parents' MBP = 96.6 +/- 1.7 mmHg). Resting MBP during a 17-24 hour period prior to the experiment in the OH group was 100.6 +/- 1.9 mmHg, significantly higher (p less than 0.05) than the MBP of the OC group (94.3 +/- 2.2 mmHg.) Immediately prior to noise exposure, MBP in the OH group was stable for 30 minutes, at 104 +/- 3 mmHg. During noise exposure, MBP increased significantly to 108 +/- 4 mmHg. In the OC group, MBP during the 30 min baseline interval was 95 +/- 2 mmHg, and during noise exposure was not significantly changed at 94 +/- 3 mmHg. Heart rate decreased significantly during noise in the OC group and did not change in the OH group. The results indicate that the offspring of monkeys with high blood pressure had higher resting MBP than control animals and showed significant MBP increases in response to loud noise. Control animals showed no change in MBP and decreases in HR in response to noise.     

Baroreflex increases correlation and coherence of muscle sympathetic nerve activity (SNA) with renal and cardiac SNAs

Despite accumulating data of muscle sympathetic nerve activity (SNA) measured by human microneurography, whether neural discharges of muscle SNA correlates and coheres with those of other SNAs controlling visceral organs remains unclear. Further, how the baroreflex control of SNA affects the relations between these SNAs remains unknown. In urethane and alpha-chloralose anesthetized, vagotomized, and aortic-denervated rabbits, we recorded muscle SNA from the tibial nerve using microneurography and simultaneously recorded renal and cardiac SNAs. After isolating the carotid sinuses, we produced a baroreflex closed-loop condition by matching the isolated intracarotid sinus pressure (CSP) with systemic arterial pressure (CLOSE). We also fixed CSP at operating pressure (FIX) or altered CSP widely (WIDE: operating pressure +/- 40 mmHg). Under these conditions, we calculated time-domain and frequency-domain measures of the correlation between muscle SNA and renal or cardiac SNAs. At CLOSE, muscle SNA resampled at 1 Hz correlated with both renal (r(2) = 0.71 +/- 0.04, delay = 0.10 +/- 0.004 s) and cardiac SNAs (r(2) = 0.58 +/- 0.03, delay = 0.13 +/- 0.004 s) at optimal delays. Moreover,muscle SNA at CLOSE strongly cohered with renal and cardiac SNAs(coherence >0.8) at the autospectral peak frequencies, and weakly (0.4-0.5) at the remaining frequencies. Increasing the magnitude of CSP change from FIX to CLOSE and further to WIDE resulted in corresponding increases in correlation and coherence functions at nonpeak frequencies, and the coherence functions at peak frequencies remained high (>0.8). In conclusion, muscle SNA correlates and coheres approximately with renal and cardiac SNAs under closed-loop baroreflex conditions. The arterial baroreflex is capable of potently homogenizing neural discharges of these SNAs by modulating SNA at the nonpeak frequencies of SNA autospectra.     

Naloxone and haemorrhagic hypotension in rats. Evidence against sympathetic nervous system as the primary mediator of improved cardiovascular haemodynamics

Release of endogenous opiate-like substances seem to occur in different forms of stress. Earlier studies have shown that the opiate antagonist, naloxone, has a positive effect on cardiac performance and blood pressure in animals with haemorrhagic shock. In the present study, we have examined the involvement of the sympathetic nervous system in this response. Two groups of anaesthetized normotensive Wistar-Kyoto rats were studied. Both groups were bled rapidly (about 5 min) down to an arterial pressure of 50 mmHg and were kept at that level for 30 min. At the end of the 30-min bleeding period, naloxone 1, 2, or 5 mg kg-1 was injected i.v. in a small volume of saline. In the first group of rats (n = 6), the aortic pressure was kept constant at 50 mmHg by further bleedings after naloxone. In the other group (n = 7), the arterial pressure was allowed to rise after naloxone. As reported earlier, haemorrhagic hypotension caused a pronounced inhibition of renal sympathetic nerve activity. Naloxone injected after 30 min of hypotension caused an immediate rise in blood pressure, followed 1-2 min later by a rise in sympathetic nerve activity (SNA). In animals in which pressure was held constant by further bleeding after naloxone, only small and insignificant changes in SNA were observed. The conclusions are the following: injection of naloxone increases blood pressure in rats exposed to severe haemorrhage (Faden & Holiday 1979). The rise in aortic pressure is followed 1-2 min later by a rise in SNA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Resetting of the arterial baroreflex increases orthostatic sympathetic activation and prevents postural hypotension in rabbits

Since humans are under ceaseless orthostatic stress, the mechanism to maintain arterial pressure (AP) under orthostatic stress against gravitational fluid shift is of great importance. We hypothesized that (1) orthostatic stress resets the arterial baroreflex control of sympathetic nerve activity (SNA) to a higher SNA, and (2) resetting of the arterial baroreflex contributes to preventing postural hypotension. Renal SNA and AP were recorded in eight anaesthetized, vagotomized and aortic-denervated rabbits. Isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg (60 s for each CSP level) while the animal was placed supine and at 60 deg upright tilt. Upright tilt shifted the CSP–SNA relationship (the baroreflex neural arc) to a higher SNA, shifted the SNA–AP relationship (the baroreflex peripheral arc) to a lower AP, and consequently moved the operating point to marked high SNA while maintaining AP. A simulation study suggests that resetting in the neural arc would double the orthostatic activation of SNA and increase the operating AP in upright tilt by 10 mmHg, compared with the absence of resetting. In addition, upright tilt did not change the CSP–AP relationship (the baroreflex total arc). A simulation study suggests that although a downward shift of the peripheral arc could shift the total arc downward, resetting in the neural arc would compensate this fall and prevent the total arc from shifting downward to a lower AP. In conclusion, upright tilt increases SNA by resetting the baroreflex neural arc. This resetting may compensate for the reduced pressor responses to SNA in the peripheral cardiovascular system and contribute to preventing postural hypotension.     

Contrasting reflex influences of cardiac afferent nerves during coronary occlusion

Afferent neurons contained within cardiac sympathetic nerves may have important influences on the circulation when activated during myocardial ischemia. Although such activation is known to reflexly excite upper thoracic sympathetic efferent neurons, effects on other components of sympathetic outflow are unknown. Therefore, cardiac sympathetic afferent nerves were stimulated by occlusion of coronary arteries to investigate their reflex influences on renal sympathetic nerve activity and systemic arterial blood pressure. Responses were observed in anesthetized cats in which sympathetic and/or vagal cardiac afferent nerves remained intact and arterial baroreceptors remained intact or had been denervated. Stimulating sympathetic afferent neurons caused excitation of renal nerve activity, which was accompanied by variable changes in arterial pressure. Stimulation of vagal afferents by coronary occlusion consistently produced inhibition of renal nerve activity and marked depressor responses. When both components of cardiac innervation remained intact, increases or decreases in renal nerve activity and blood pressure were elicited by coronary artery occlusion in the presence or absence of arterial baroreceptors. These results illustrate that cardiac sympathetic afferent nerves can contribute significantly to cardiovascular control during myocardial ischemia.     

Cerebrovascular responses to haemorrhagic hypotension in anaesthetized cats. Effects of alpha-adrenoceptor antagonists

Haemorrhagic hypotension induces the phenomenon of cerebrovascular autoregulation and, concomitantly, involves an activation of the sympathetic nervous system. As brain vessels in cats have an atypical adrenoceptor distribution we studied the effects of an alpha-adrenoceptor antagonist on the autoregulatory response to haemorrhage. Cortical blood flow was studied by the H2 technique in chloralose-anaesthetized cats subjected to a period of graded haemorrhage over 3 h. Three groups of cats were studied: control, i.e. those receiving saline (n = 10); yohimbine-treated (200 micrograms . kg-1 . h-1, n = 7); and prazosin-treated (50 micrograms . kg-1 . h-1, n = 6). In the control group, cortical blood flow remained relatively constant when mean arterial pressure was decreased from 102 +/- 1 mmHg (mean +/- SE) to approximately 50 +/- 1 mmHg; thereafter, blood flow decreased with decreasing perfusion pressure. In the arterial pressure range 64-55 mmHg, cortical blood flow was significantly higher in the yohimbine group (109 +/- 12 ml . 100 g-1 . min-1) compared to the control group (69 +/- 6 ml . min-1) and remained higher in the yohimbine-treated cats at more extreme levels of hypotension. Blood flow did not fall significantly in the yohimbine-treated cats until mean arterial pressures of 31 +/- 1 mmHg were attained. In the prazosin-treated cats, flow began to decrease at arterial pressures even greater than those observed in the control group. Thus, there is a sympathetic vasoconstriction of brain arteries that is primarily mediated by alpha 2-adrenoceptors in the feline cerebrovascular bed.     

Spinal sympathetic reflexes initiated by coronary receptors

1. The main left coronary artery of vagotomized spinal cats was perfused at different flows and pressures. The changes in pressure were limited to the coronary bed.2. Increased coronary flow which increased coronary arterial pressure provoked a reflex increase in sympathetic discharge in the white ramus of the third thoracic spinal nerve and the inferior cardiac nerve. Reflex reductions in activity were not observed.3. Occlusion of the coronary sinus and myocardial ischaemia, due to cessation of pump inflow, evoked similar reflex increases of sympathetic activity. The effect of myocardial ischaemia was apparent before systemic arterial blood pressure fell or left ventricular end-diastolic pressure rose.4. Increased coronary arterial pressure, myocardial ischaemia and coronary sinus occlusion could activate the same preganglionic neurone.5. The afferent limb of the excitatory coronary-sympathetic reflex was in the cardiac sympathetic nerves, mainly on the left. Afferent nerve fibres running in these nerves and in the third left thoracic sympathetic ramus communicans were excited by increased coronary arterial pressure, myocardial ischaemia, and occlusion of the coronary sinus. Inhibition was not observed. Many of the receptors were further localized by direct probing over the coronary vessels and adjacent myocardium.6. Some receptors were excited by increased coronary arterial pressure alone, others by coronary sinus occlusion, and still others by myocardial ischaemia. In addition, some receptors were excited by all three stimuli.     

Sympathetic inhibition after surgical reversal of renovascular hypertension in rats. Role of vagal nerves

The present study was undertaken to study the changes in efferent renal sympathetic nerve activity (RSNA) and heart rate (HR) during the acute fall in blood pressure after surgical reversal of two-kidney, one-clip renovascular hypertension in rats, and to explore if cardiopulmonary vagal afferents can influence sympathetic outflow in this situation. In 14 rats with a MAP of 199 +/- 6 mmHg the renal artery clip was surgically removed and after 90 min MAP had decreased to 109 +/- 7 mmHg. The HR had then decreased by 26 +/- 15 beats min-1 (P less than 0.05) and RSNA did not increase as expected, but was somewhat reduced (84 +/- 8% of control). In contrast, lowering pressure with nitroprusside to the same extent produced large and significant increases in HR and RSNA in seven other renal hypertensive rats. Acute bilateral vagotomy was performed in seven of the declipped rats, which induced an immediate increase in MAP (+35 +/- 10 mmHg, P less than 0.05), HR +28 +/- 10 beats min-1, P less than 0.05) and RSNA (+51 +/- 19%, P less than 0.05). A few minutes afterwards the vagotomy pressure again started to fall and was, after another 90 min 107 +/- 10 mmHg together with slight reductions in HR and RSNA. Another group of six rats were initially exposed to bilateral vagotomy. In these vagotomized rats declipping also induced hypotension (204 +/- 10 to 95 +/- 7 mmHg, P less than 0.001), together with tendencies of decreases in HR (425 +/- 17 to 397 +/- 17 beats min-1) and in RSNA (-4 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Baroreflex participation of cardiovascular response to E. coli endotoxin

The purpose of this experiment was to evaluate the effects of the arterial baroreceptor buffering capacity on cardiovascular parameters during hypotension caused by E. coli endotoxin in anesthetized dogs. In the control group, mean blood pressure and cardiac output fell significantly from 104 +/- 10 mmHg to 63 +/- 7 mmHg and 1.17 +/- 0.16 l/min to 0.67 +/- 0.08 l/min, respectively, 60 min after intravenous injection of endotoxin (1 mg/kg). Central venous pressure also decreased significantly after the injection. Total peripheral resistance and portal vein pressure increased significantly immediately after the injection, and then returned toward baseline levels. The time course of changes in these five cardiovascular parameters after the injection of endotoxin was the same as that in dogs with sino-aortic denervation. Following the injection of endotoxin, stroke volume and left ventricular dP/dt fell significantly in both control and denervated dogs; however, these decreases in the denervated group were significantly greater. These findings suggest that the arterial baroreceptors may play a role in the poor compensatory response to hypotension induced by endotoxin, at least, in the cases of mean blood pressure, cardiac output, total peripheral resistance, central venous pressure, and portal vein pressure.     

Heart rate changes evoked by hypoxia in the anaesthetized, artificially ventilated cat.

Reflex changes in heart rate evoked by hypoxia were investigated in cats anesthetized with chloralose and ventilated by positive pressure during administration of vecuronium or gallamine. In five cats receiving vecuronium and with aortic pressure stabilized, systemic hypoxia (arterial O2 pressure (Pa, O2) 34.9 mmHg) reduced heart rate by 55.8 +/- 7.5 beats min-1 (mean +/- S.E.M.). After administration of atropine, hypoxia (Pa, O2 32.1 mmHg) increased heart rate by 28.2 +/- 3.4 beats min-1. After subsequent bilateral ablation of carotid sinus and vagus nerves, hypoxia (Pa, O2 31.9 mmHg) increased heart rate by 7.1 +/- 1.8 beats min-1. The cardiac accelerator response to hypoxia was further examined in groups of cats treated with gallamine and atropine. In four vagotomized cats, local perfusion of both carotid sinuses with hypoxic blood (Pa, O2 37.7 mmHg) increased heart rate by 15.5 +/- 2.3 beats min-1. In the same cats, systemic hypoxia (Pa, O2 38.3 mmHg) increased heart rate by 16.4 +/- 2.3 beats min-1. The heart rate increment in cats which had undergone either bilateral adrenalectomy or cardiac sympathectomy was similar to the increment in unoperated cats. The increment was significantly less in cats which had both adrenal glands and cardiac sympathetic nerves ablated. It is concluded that stimulation of the carotid bodies in the cat excites both parasympathetic and sympathetic cardiac nerves simultaneously.     

Effects of sex and ovarian hormones on the initial renal sympathetic nerve activity response to myocardial infarction

The physiological mechanisms contributing to sex differences following myocardial infarction (MI) are poorly understood. Given the strong relationship between sympathetic nerve activity (SNA) and outcome, we hypothesized there may be a sex difference in SNA responses to MI. In anaesthetized, open-chest male, female and ovariectomized (OVX) female Wistar rats, mean arterial pressure, heart rate and renal SNA were recorded in response to ligation of the left coronary artery. In males, renal SNA increased by 30 ± 6% in the first minute of coronary occlusion (P < 0.05) and remained elevated at 18 ± 7% above baseline (P < 0.05) at 2 h following MI. In response to MI, ovary-intact females displayed no change in renal SNA, whereas OVX females displayed a significant increase, similar to that seen in the males (increases of 43 ± 11% at 1 min and 21 ± 7% at 2 h post-MI, P < 0.05 versus intact females). Arterial baroreflex control of renal SNA had a smaller range in females (ovary intact and OVX) than males; no changes in arterial baroreflex responses were observed 1 h post-MI in males or females. Denervating the arterial baroreceptors abolished the renal SNA response to MI in the males, whereas in ovary-intact females and OVX females the response was unaltered. These findings suggest that ovarian hormones are able to blunt the initial sympathetic activation post-MI in females and that the importance of the arterial baroreflex in mediating initial sympathetic activation post-MI is different between the sexes.     

Reflex Plasma Hyperglycemia and Hyperosmolality Evoked by Unloading of the Carotid Baroreceptors

Hemorrhage is usually accompanied by a considerable increase in the plasma osmolality and glucose concentration due to an augmented release of glucose from the liver. In the present cat experiments an attempt was made to investigate the possible role of different vascular receptors in mediating this hyperglycemic (hyperosmolar) response. Bilateral vagotomy or stimulation of the carotid chemoreceptors by perfusion of the carotid sinus with venous blood at normal pressure only slightly increased the arterial plasma glucose concentration. On the other hand, when the sinus nerves were cut in the vagotomized animal, thereby simulating complete unloading of the carotid baroreceptors, the arterial plasma glucose concentration rose by about 8 mM/L and the arterial plasma osmolality by about 10 mOsm/kg H₂O. Perfusion of the carotid baroreceptors with arterial blood at different levels of hypotension showed that the baroreceptor-induced hyperglycemia was graded in relation to the pressure level. Regional hypotension of the liver, pancreas, intestine, kidneys or brain did not significantly affect plasma glucose concentration or osmolality. We conclude that the reflex release of glucose from the liver during hemorrhage mainly is initiated from the unloading of arterial baroreceptors.     

Effects of sympathetic nerves on cerebral blood flow in awake dogs.

Although cerebral blood vessels are densely innervated by sympathetic nerve fibers, the functional significance of the nerves is controversial. Because previous studies have been primarily performed in anesthetized animals, it is possible that failure to observe prominent neural control of the cerebral circulation was secondary to anesthetic-induced depression of the sympathetic nervous system. Therefore, we studied sympathetic control of the cerebral circulation in 11 awake chronically instrumented dogs. Total and regional cerebral blood flow was measured with 15-micrometer microspheres at control blood pressure and during three levels of progressive hemorrhagic hypotension. Sympathetic nerves had only a small effect (11% decrease; P less than 0.05) on flow to the cerebrum during moderate hypotension (mean arterial pressure 49 +/- 2 mmHg). Also, during severe hypotension, there was a bilateral redistribution of brain blood flow that tended to preserve flow to the medulla. Although these studies suggest that sympathetic nerves have a definite constrictor effect on cerebral vessels, the data support the concept that the functional importance of sympathetic nerves to cerebral vessels is limited.     

Reflex responses from the main pulmonary artery and bifurcation in anaesthetised dogs

This study was undertaken to determine the reflex cardiovascular and respiratory responses to discrete stimulation of pulmonary arterial baroreceptors using a preparation in which secondary modulation of responses from other reflexes was prevented. Dogs were anaesthetised with -chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The main pulmonary arterial trunk, bifurcation and extrapulmonary arteries as far as the first lobar arteries on each side were vascularly isolated and perfused through the left pulmonary artery and drained via the right artery through a Starling resistance which controlled pulmonary arterial pressure. Pressures distending systemic baroreceptors and reflexogenic regions in the heart were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic systemic circulation, both of which were perfused at constant flows. Respiratory responses were assessed from recordings of efferent phrenic nerve activity. Increases in pulmonary arterial pressure consistently evoked increases in both perfusion pressures and in phrenic nerve activity. Both vascular and respiratory responses were obtained when pulmonary arterial pressure was increased to above about 30 mmHg. Responses increased at higher levels of pulmonary arterial pressures. In 13 dogs increases in pulmonary arterial pressure to 45 mmHg increased systemic perfusion pressure by 24 +/- 7 mmHg (mean +/- S.E.M.) from 162 +/- 11 mmHg. Setting carotid sinus pressure at different levels did not influence the vascular response to changes in pulmonary arterial pressure. The presence of a negative intrathoracic pressure of -20 mmHg resulted in larger vascular responses being obtained at lower levels of pulmonary arterial pressure. This indicates that the reflex may be more effective in the intact closed-chest animal. These results demonstrate that stimulation of pulmonary arterial baroreceptors evokes a pressor reflex and augments respiratory drive. This reflex is likely to be elicited in circumstances where pulmonary arterial pressure increases and the negative excursions of intrathoracic pressure become greater. They are likely, therefore, to be involved in the cardio-respiratory response to exercise as well as in pathological states such as pulmonary hypertension or restrictive or obstructive lung disease.     

Noise-enhanced heart rate and sympathetic nerve responses to oscillatory lower body negative pressure in humans

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as "stochastic resonance." It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately -10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.     

Coronary reactive hyperaemia and arterial pressure in anaesthetized goats

To study the effects of arterial pressure on coronary reactive hyperaemia, left circumflex coronary artery flow was measured, and reactive hyperaemia was determined after 5, 10 or 20 s of occlusion of this artery in anaesthetized goats during normotension, hypertension and hypotension. During hypertension induced by aortic constriction (mean arterial pressure, MAP = 140 +/- 6 mmHg) coronary vascular resistance (CVR), reactive hyperaemia (ratio of peak in hyperaemic flow to control flow and ratio of repayment to debt) and the decrease in CVR during the peak in hyperaemic flow were comparable to those during normotension. During hypertension induced by noradrenaline (MAP = 144 +/- 6 mmHg) CVR was 16% lower (P < 0.05), reactive hyperaemia was reduced by 14-25% (P < 0.05) and the decrease in CVR during the peak in hyperaemic flow was lower than the values of these parameters during normotension. During hypotension induced by constriction of the caudal vena cava (MAP = 40 +/- 4 mmHg) CVR was 22% lower (P < 0.05), reactive hyperaemia was reduced by 25-65% (P < 0.05) and the decrease in CVR during the peak in hyperaemic flow was less compared to the values of these parameters during normotension. During hypotension induced by isoprenaline (MAP = 45 +/- 4 mmHg) CVR was 59% lower, reactive hyperaemia was reduced by 55-100% (P < 0.01) and the decrease in CVR during the peak in hyperaemic flow was less compared to the values of these parameters during normotension. Arterial pressure is a main determinant of coronary reactive hyperaemia after brief periods of ischaemia, and the relationship between arterial pressure and reactive hyperaemia may depend in part on changes in CVR after variations in arterial pressure. These changes in CVR may be related to the action on coronary vessels of myocardial factors and vascular myogenic mechanisms.     

Reflex Nature of the Cardiorespiratory Response to Primary Thoracic Blast Injury in the Anaesthetised Rat

Blast injuries represent a problem for civilian and military populations. Primary thoracic blast injury causes a triad of bradycardia, hypotension and apnoea. The objective of this study was to investigate the reflex nature of this response and its modulation by vagotomy or administration of atropine. The study was conducted on terminally anaesthetised (alphadolone/alphaxalone, 18-24 mg x kg x h(-1), I.V.) male Wistar rats randomly allocated to the groups indicated below. Blast injuries were produced with compressed air while sham blast involved the sound of a blast only. Primary blast injury to the thorax resulted in a bradycardia (measured as an increase in the interval between beats, or heart period (HP) to 489 +/- 37 ms from 133 +/- 3 ms with a latency of onset of 4.3 +/- 0.3 s, mean +/- S.E.M.), hypotension (fall in mean arterial blood pressure (MBP) from 128.1 +/- 3.7 mmHg to 34.8 +/- 4.1 mmHg, latency of onset 2.0 +/- 0.1 s) and apnoea lasting 28.3 +/- 2.3 s. Sham blast had no effect. The bradycardia and apnoea following thoracic blast were abolished by cervical vagotomy while the hypotension was attenuated. Atropine (0.3 mg x kg(-1), I.V.) caused a significant reduction in the bradycardia (HP increasing from 124 +/- 3 ms to 142 +/- 4 ms) but did not modulate either the hypotension or apnoea. It is concluded that a reflex involving the vagus nerve mediates the bradycardia, apnoea and a component of the hypotension associated with thoracic blast. The pattern of this response is similar to effects that follow stimulation of the pulmonary afferent C-fibres.     

Bezold-Jarisch reflex blunts arterial baroreflex via the shift of neural arc toward lower sympathetic nerve activity

Although the Bezold-Jarisch (BJ) reflex is potentially evoked during acute myocardial ischemia or infarction, its effects on the static characteristics of the arterial baroreflex remain to be analyzed in terms of an equilibrium diagram between the neural and peripheral arcs. The neural arc represents the static input-output relationship between baroreceptor pressure input and efferent sympathetic nerve activity (SNA), whereas the peripheral arc represents that between SNA and arterial pressure (AP). In 8 anesthetized rabbits, we increased carotid sinus pressure stepwise from 40 to 160 mmHg in increments of 20 mmHg at one-minute intervals while measuring renal SNA and AP under control conditions and during the activation of the BJ reflex by intravenous administration of phenylbiguanide (PBG, 100 microg.kg(-1).min(-1)). The neural arc approximated a sigmoid curve whereas the peripheral arc approximated a straight line. PBG decreased AP at the operating point from -91.3 +/- 2.4 to -71.7 +/- 3.1 mmHg (P < 0.01), and attenuated the total loop gain at the operating point from -1.31 +/- 0.44 to -0.51 +/- 0.14 (P < 0.05). The equilibrium diagram indicated that PBG caused a parallel shift of the neural arc toward lower SNA such that the maximum SNA was reduced to approximately 60% of control. PBG decreased neural and peripheral arc gains at the operating point to approximately 43% and 77%, respectively. In conclusion, the BJ reflex blunts arterial baroreflex via the shift of the neural arc toward lower SNA.     

Renin release and pressor response to renal arterial hypotension: effect of dietary sodium.

Changes in plasma renin activity (PRA) and mean arterial pressure (MAP) produced by renal arterial hypotension were studied in conscious, adrenalectomized dogs maintained on low-, normal-, or high-Na diet during constant steroid replacement therapy. In animals maintained on a low-Na diet, reduction of renal perfusion pressure to 50 mmHg for 45 min increased MAP 40 +/- 3 (SE) mmHg, while PRA rose rapidly by 36.5 +/- 6 ng ml-1 h-1. Similar renal hypotension in dogs maintained on a normal-Na diet increased MAP only 21 +/- 3 mmHg while PRA rose 5.5 +/- 0.9 ng ml-1 h-1; dogs on high-Na intake had a 6 +/- 1 mmHg pressure rise without a significant change in PRA. The rise in MAP correlated well with the log deltaPRA. Calculated open-loop gain was -1.2, -0.7, and -0.1 in dogs on low-, normal-, and high-Na diets, respectively. Nonpeptide angiotensin I converting enzyme inhibitor (CEI) reversed the elevated MAP observed during reduction of renal perfusion pressure in dogs on low- and normal-Na diets, but had little effect in dogs on high-Na intake. These observations suggest that the renin-angiotensin system becomes quantitatively more important in the regulation of blood pressure as Na intake is reduced.