Reflex adrenergic control of endocrine pancreas evoked by unloading of carotid baroreceptors in cats

The effects of unloading of the carotid baroreceptors on arterial plasma glucose concentration as well as on portal plasma immunoreactive glucagon (IRG) and insulin (IRI) concentrations were studied in an-estethized, vagotomized cats either by sectioning the sinus nerves or by lowering the pressure in the isolated carotid sinuses. Complete elimination of the carotid baroreceptor discharge by cutting the sinus nerves caused an increase in the arterial plasma glucose concentration by 100% and an increase in the portal IRG level by about 200%, whereas the portal IRI concentration decreased to 50% of its basal value. These baroreceptor-induced changes of the plasma IRG and IRI levels seemed to be graded in relation to the drop in carotid blood pressure and they were clearly detectable when the pressure was lowered from 120 to 90 mmHg in the isolated carotid sinus preparation. The described reflex hyperglycemia, hyperglucago-nemia and hypoinsulinemia were mediated to the pancreas and liver mainly by the sympatho-adrenal system, since cutting the splanchnic nerves above the adrenal glands abolished the hyperglycemic and hypoinsulinemic responses and markedly depressed the magnitude of the hyperglucagonemic response. In adrenalectomized cats, complete unloading of the baroreceptors evoked both hyperglucagonemia and hypoinsulinemia although the magnitude of the hormonal responses was diminished. In animals where the pancreas and liver were sympathectomized but the adrenal glands left intact, cutting the sinus nerves evoked a doubling of the IRG level and a slight increase in plasma glucose, but no significant change of the IRI level. I.v. infusion of adrenaline (1 γg/kg × min) or noradrenaline (5 γg/kg × min) caused pronounced increases in IRG and plasma glucose and a clear-cut reduction of IRI. We conclude that the function of the endocrine pancreas in the cat can be influenced by variations in the blood pressure by means of a reflex control which originates from arterial baroreceptors. This reflex adjustment of the endocrine pancreas is mediated chiefly by two links of the sympatho-adrenal system, namely by catecholamine-release from the adrenal medulla and, more importantly. by a direct adrenergic nerve fibre influence on the α- and β-cells.     

Reflex adrenergic control of endocrine pancreas evoked by unloading of carotid baroreceptors in cats.

The effects of unloading of the carotid baroreceptors on arterial plasma glucose concentration as well as on portal plasma immunoreactive glucagon (IRG) and insulin (IRI) concentrations were studied in anestethized, vagotomized cats either by sectioning the sinus nerves or by lowering the pressure in the isolated carotid sinuses. Complete elimination of the carotid baroreceptor discharge by cutting the sinus nerves caused an increase in the arterial plasma glucose concentration by 100% and an increase in the portal IRG level by about 200%, whereas the portal IRI concentration decreased to 50% of its basal value. These baroreceptor-induced changes of the plasma IRG and IRI levels seemed to be graded in relation to the drop in carotid blood pressure and they were clearly detectable when the pressure was lowered from 120 to 90 mmHg in the isolated carotid sinus preparation. The described reflex hyperglycemia, hyperglucagonemia and hypoinsulinemia were mediated to the pancreas and liver mainly by the sympatho-adrenal system, since cutting the splanchnic nerves above the adrenal glands abolished the hyperglycemia and hypoinsulinemic responses and markedly depressed the magnitude of the hyperglucagonemic response. In adrenalectomized cats, complete unloading of the baroreceptors evoked both hyperglucagonemia and hypoinsulinemia although the magnitude of the hormonal responses was diminished. In animals where the pancreas and liver were sympathectomized but the adrenal glands left intact, cutting the sinus nerves evoked a doubling of the IRG level and a slight increase in plasma glucose, but no significant change of the IRI level. I.v. infusion of adrenaline (1 microgram/kg X min) or noradrenaline (5 microgram/kg X min) caused pronounced increases in IRG and plasma glucose and a clear-cut reduction of IRI. We conclude that the function of the endocrine pancreas in the cat can be influenced by variations in the blood pressure by means of a reflex control which originates from arterial baroreceptors. This reflex adjustment of the endocrine pancreas is mediated chiefly by two links of the sympatho-adrenal system, namely by catecholamine-release from the adrenal medulla and, more importantly, by a direct adrenergic nerve fibre influence on the alpha- and beta- cells.     

Baroreflex control of jejunal blood flow and fluid transport in cats; effects of yohimbine,an α.-adrenergic antagonist

The aim of the study was to test the hypothesis that baroreceptor unloading increases jejunal fluid absorption rate via an α₂-adrenergic effect on electrogenic active transport. In 13 chloralose-anaesthetized cats, the carotid sinus baroreceptors were isolated and perfused with arterial blood, and we studied the effects of a graded decrease in carotid sinus pressure on intestinal vascular resistance, net fluid absorption rate and the potential difference between the intestinal lumen and the peritoneal cavity (PD). Experiments were performed in seven control animals and in six animals pretreated with yohimbine, an α₂-adrenergic antagonist, at a dose of 0.1 mg kg^-I i.v. Yohimbine per se had no significant effects on systemic arterial pressure, intestinal vascular resistance, net fluid absorption rate or PD. In the control animals, baroreceptor unloading induced an increase in systemic arterial pressure, intestinal vascular resistance and net fluid absorption rate, and a decrease in the PD. Yohimbine pretreatment did not significantly affect the systemic blood pressure response to baroreceptor unloading, but abolished the effect on intestinal vascular resistance and PD. After yohimbine treatment, decreases in carotid sinus pressure still enhanced net fluid absorption rate, but this response was observed in a higher range of carotid sinus pressures than in control animals. We conclude that (1) a major component of the increase in jejunal absorption rate during baroreceptor unloading is due to a non-electrogenic mechanism, which may be either active or passive; (2) this component of the response is not blocked by yohimbine at a dose sufficient for an effect on presynaptic α₂-receptors; (3) the absorptive response to baroreceptor unloading is not a phenomenon secondary to the concomitant jejunal vasoconstriction.     

Hyperglycemic and Hyperosmolar Responses to Graded Hemorrhage

Changes of the arterial plasma osmolality and of the glucose concentration were followed during a 30 min period of graded hemorrhagic hypotension (80, 50, and 30 mmHg) in the cat. Bleeding evoked a significant plasma hyperosmolality at all three hypotension levels and the responses were quantitatively related to the degree of hypotension. An approximate steady state increase in the arterial plasma osmolality was reached about 20 min after the start of the bleeding and it then averaged 8, 20, and 25 mOsm/kg H₂O at 80, 50, and 30 mmHg, respectively. Bleeding also evoked an increase in the plasma glucose concentration, which almost entirely accounted for the observed hyperosmolality, especially at 80 and 50 mmHg. In late stages of hypotension at 30 mmHg, elevated plasma lactate and potassium concentrations contributed to the overall hyperosmolality. — Previous hemorrhagic hypotension experiments at 50 mmHg (Järhult 1975 b) have shown that hyperosmolality serves as an important regulator of the plasma and extracellular fluid volumes during bleeding. The present results indicate that such an osmolar compensatory mechanism is operating over wide ranges of hemorrhagic hypotension.     

Involvement of renal alpha- and beta-adrenoceptors in release of renin by carotid baroreflex.

In anesthetized vagotomized dogs with renal arterial pressure constant, carotid sinus hypotension (BCO) caused a reflex rise in systemic arterial pressure, a fall in renal blood flow, and a similar increase in renin release from both kidneys. Unilateral alpha-adrenoceptor blockade with phenoxybenzamine resulted in an increase in basal renal blood flow, a depression of basal renin release, and an abolition of the responses to BCO in the treated kidney. The untreated kidney responsed to BCO as before. Nonblocked and alpha-blocked kidneys released similar amounts of renin when renal blood flow was mechanically reduced by aortic constriction. Administration of propranolol to the nonblocked kidney prevented the release of renin but not the hemodynamic changes resulting from BCO. The experiments demonstrated that under certain conditions carotid sinus hypotension produced alpha-adrenoceptor-mediated changes in the kidney sufficient to cause increased renin release. A step in the renin release mechanism subsequent to the alpha-adrenoceptor-mediated changes in sensitive to propranolol.     

The effects of changes in the carotid sinus baroreceptor activity on splanchnic blood flow in anesthetized man

In 9 patients being subjected to abdominal surgery, electromagnetic blood flow measurements were obtained from the hepatic, mesenteric and iliac beds while the carotid sinus baroreceptors were stimulated by carotid sinus massage. Carotid sinus stimulation produced an average maximum decrease in mean arterial pressure of 21%. Hepatic and mesenteric blood flows decreased by 15% and calculated vascular resistances were not significantly changed in these vascular beds. Iliac blood flow, on the other hand, showed a slight increase and iliac vascular resistance was decreased by 29%. It is concluded that the splanchnic vascular bed is of less importance in the carotid sinus baroreflex control of systemic arterial pressure in anesthetized man.     

Circulatory effects of carotid sinus stimulation and changes in blood volume distribution in hypertensive man

In 8 patients with moderate hypertension and 8 normotensive subjects an attempt was made to study the circulatory effects of high and low pressure baroreceptor stimulation. Intrathoracic low pressure receptors were stimulated by changes in blood volume distribution using lower body negative pressure (LBNP) and lower body positive pressure (LBPP). The carotid sinus was stimulated by sinusoidal neck suction. Blood pressure, central venous pressure, heart rate, cardiac output and forearm blood flow were recorded. During LBNP and LBPP changes in central blood volume, reflected in changes in central venous pressure, induced significantly greater changes in cardiac output and forearm blood flow in the hypertensive subjects. In both normotensive and hypertensive subjects mean arterial blood pressure was essentially unchanged during LBNP and a slight increase was found during LBPP. Heart rate and blood pressure response to stimulation of the carotid sinus decreased with increasing resting mean arterial pressure. The results suggest impairment of reflex adjustments, via arterial baroreceptors, possibly in particular to dynamic stimuli, rather than via intrathoracic “low pressure” baroreceptors in subjects with moderate hypertension.     

Interaction between the baroreceptor and Bezold-Jarisch reflexes

The interaction between the carotid baroreflex and Bezold-Jarisch (BJ) reflex (intravenously administered veratridine) was studied in anesthetized rabbits after aortic nerve section. The carotid sinuses were vascularly isolated to regulate the intrasinus pressure (ISP). The extent of BJ reflex bradycardia and hypotension was progressively diminished as the ISP was elevated stepwise. When the carotid baroreflex was not operative by holding the ISP constant at control, the BJ reflex changes in heart rate (HR) and systemic arterial pressure (SAP) were not significantly different from those induced at the normal condition. Thus the calculated baroreflex static loop gain was greatly decreased during the BJ reflex. However, sinus denervation, analogous to keeping ISP below 50 mmHg, significantly enhanced the BJ reflex effects. A steady-state infusion of veratridine remarkably reduced the slope of the baroreflex function ISP-SAP and ISP-HR curves. The results indicate that the BJ reflex effects are affected by the prevailing arterial baroreceptor input, varying inversely with the ISP level. An attenuation in the baroreflex sinsitivity, in terms of the loop gain or slope of the transfer function curve, was observed during the BJ reflex. The presence of tonic cardiovascular inhibitions exerted by the arterial baroreceptors tends to reduce the BJ reflex bradycardia and hypotension, but the baroreceptors do not function adequately in buffering the cardiovascular inhibition produced by the cardiogenic reflex.     

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.     

Elevations in plasma ADH levels during PEEP ventilation in the dog: mechanisms involved

In an attempt to define more precisely the various mechanisms involved in antidiuretic hormone (ADH) release during positive end-expiratory pressure ventilation (PEEP), experiments were performed on seven groups of dogs. PEEP-10 and PEEP-15 cmH2O caused significant elevations of plasma ADH from basal values of 24.9 +/- 5.2 pg/ml (mean +/- SE) to 64.6 +/- 14.2 and 106.0 +/- 20.6, respectively (P < 0.02, P < 0.005). The ADH levels returned to basal values after cessation of PEEP. This rise in ADH levels was prevented by an infusion of dextran prior to PEEP. The fall in blood pressure and cardiac output that occurred during PEEP was also prevented by the dextran infusion. Changes in ADH levels were unrelated to lung volume, left transmural pressure, and serum osmolality. Bilateral vagotomy and carotid sinus denervation was followed by an attenuated rise in ADH levels in terms of the percent rise above base line, but it did not significantly alter the absolute rise in ADH during PEEP. ADH levels were, however, reduced significantly by decreasing intracranial pressure by the removal of cerebrospinal fluid during PEEP. Propranolol administration prior to PEEP completely blocked plasma renin activity. Although the peak ADH levels were unaffected by propranolol, the rise was delayed. The results obtained indicate that a number of physiological factors may affect plasma ADH levels during PEEP. These include the carotid body and aortic arch baroreceptors as wells as sensors of intracranial pressure.     

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat

The present study was designed to determine effect of the preganglionic splanchnic nerve activity (SNA) on the brief hypotension accompanied with the occlusion of left circumflex coronary artery (CxCAO) in chloralose anesthetized cats. Following CxCAO in animals with neuraxis intact, no significant alterations of SNA occurred despite the significant fall in mean blood pressure (MBP). A significant fall in MBP also occurred in vagotomized animals with arterial baroreceptors intact, but SNA was significantly augmented from 12.9 +/- 2.7 impulses/sec before CxCAO to 24.4 +/- 4.3 impulses/sec 60 sec after the occlusion. In vagotomized animals, in which their carotid sinuses were isolated and perfused with the constant pressure at a level equal to systemic blood pressure (112 +/- 6 mmHg) and with higher pressure (167 +/- 7 mmHg), SNA was not altered significantly during the hypotension due to CxCAO. When the carotid sinuses were perfused with lower pressure (53 +/- 8 mmHg), a significant increase in SNA occurred simultaneously with the decrease in MBP after CxCAO. The peak decreases in blood pressure during the coronary occlusion were significantly greater in the vagotomized group (-46 +/- 5 mmHg) and in the Low-CSP group (-50 +/- 5 mmHg) than in other groups. Onset of this excitatory efferent sympathetic response to the hypotension due to the coronary occlusion in the vagotomized and Low-CSP groups was delayed significantly despite a significant fall in arterial blood pressure. These results show that vagal afferents from the heart may play a role of inhibiting the sympathetic augmentation mediated by arterial baroreceptors during cardiogenic hypotension. An excessive activation of cardiac receptors with sympathetic afferents may be induced by the profound fall in blood pressure, resulting in further impairment of cardiac function due to progressive myocardial ischemia under the condition of high sympathetic tone activated by baroreceptor reflex.     

Characteristics of brachiocephalic and carotid sinus baroreceptors with non-medullated afferents in rabbit

The characteristics of brachiocephalic and carotid sinus baroreceptors with non-medullated afferents have been studied in rabbits. The conduction velocities of 18 non-medullated fibers arising from the brachiocephalic baroreceptors were 0.4-0.8 m/s (0.59 +/- 0.03 m/s, mean +/- SE) and their thresholds were 74-104 mmHg (84 +/- 2 mmHg). 29 non-medullated carotid sinus baroreceptor afferents had thresholds ranging from 60 to 125 mmHg (92 +/- 3 mmHg). Their conduction velocities were 0.5-1.1 m/s (0.65 +/- 0.05 m/s). Blood pressure-baroreceptor response curves of both the brachiocephalic and the carotid sinus baroreceptors were constructed. As the aortic arch non-medullated baroreceptor afferents, the brachiocephalic and the carotid sinus baroreceptors with non-medullated afferents exhibited thresholds about 30 mmHg higher than the medullated ones, considerably lower firing rates, comparatively rapid adaptation and remarkable irregular discharge pattern. It is suggested that the non-medullated baroreceptor afferents are of little importance for the cardiovascular regulation under normal conditions but are likely to play an important role during a sudden rise in arterial pressure.     

A comparison of the stimulus-response curves of aortic and carotid sinus baroreceptors in decerebrated cats

Recordings of total nerve activity suggested differences in the sensitivities and working ranges between aortic and carotid sinus baroreceptors. This result however, conflicts with single fibre studies from isolated receptor zones. Thus it appeared of some interest to compare the function curves of aortic and carotid sinus baroreceptors in the intact animal.This was achieved by comparing the response characteristics of two groups of aortic and carotid sinus baroreceptors in decerebrated cats. One smaller group consisted of 11 receptor pairs, each member of the pair being studied simultaneneously in the same cat, and a larger group consisting of 98 aortic and 49 carotid sinus baroreceptors studied independently of each other.The response of each receptor to wide pressure variations was recorded by inflating and deflating an intraaortic catheter tip balloon. Function curves were derived by plotting receptor discharge in terms of spikes per second against mean aortic pressure. No significant differences were found either in the slope of the function curves or their mean pressures at minimum activity, the latter appearing to be set by the working blood pressure level.Thus it was concluded that aortic and carotid sinus baroreceptors differ neither in their sensitivities nor in their working ranges when in their physiological environment.The support of the Deutsche Forschungsgemeinschaft through the Sonderforschungsbereich 30, Kardiologie Düsseldorf is gratefully acknowledged     

Comparison of the reflex vasomotor responses to separate and combined stimulation of the carotid sinus and aortic arch baroreceptors by pulsatile and non-pulsatile pressures in the dog

1. In the anaesthetized dog the carotid sinuses and aortic arch were isolated from the circulation and separately perfused with blood by a method which enabled the mean pressure, pulse pressure and pulse frequency to be varied independently in each vasosensory area. The systemic circulation was perfused at constant blood flow by means of a pump and the systemic venous blood was oxygenated by an extracorporeal isolated pump-perfused donor lung preparation.2. When the vasosensory areas were perfused at non-pulsatile pressures within the normal physiological range of mean pressures, the reflex reduction in systemic vascular resistance produced by a given rise in mean carotid sinus pressure was significantly greater than that resulting from the same rise of aortic arch pressure.3. On the other hand, when the vasosensory areas were perfused at normal pulsatile pressures and within the normal physiological range of mean pressures, there was no difference in the size of the reflex vascular responses elicited by the same rise in mean pressure in the carotid sinuses and in the aortic arch.4. Whereas the vasomotor responses elicited reflexly by changes in mean carotid sinus pressure are modified by alterations in pulse pressure, those evoked by the aortic arch baroreceptors through changes of mean pressure are only weakly affected by modifications in pulse pressure. Evidence for this was obtained from single stepwise changes of mean pressure in each vasosensory area during pulsatile and non-pulsatile perfusion, and from curves relating the mean pressure in the carotid sinuses or aortic arch and systemic arterial perfusion pressure.5. The vasomotor response elicited by combined stimulation of the carotid sinus and aortic arch baroreceptors was greater than either response resulting from their separate stimulation.6. When the mean perfusion pressures in the two vasosensory areas are changed together, the curve relating mean pressure to systemic arterial pressure during pulsatile perfusion of the areas is considerably flatter than that for non-pulsatile perfusion.7. Increasing the pulse pressure in the carotid sinuses or aortic arch caused a decrease in systemic vascular resistance, the response elicited from the carotid sinuses being the larger.8. Altering the phase angle between the pulse pressure waves in the carotid sinuses and aortic arch had no effect on systemic vascular resistance.9. In both vasosensory areas, increasing the pulse frequency caused a reduction in systemic vascular resistance.     

改构体aFGF对颈动脉窦损伤的保护作用

目的　探讨损伤大白鼠颈动脉窦压力感受器神经末梢后 ,改构体aFGF的保护作用。方法　将Wistar大鼠随机分成对照组、改构体aFGF1组、改构体aFGF2 组、改构体aFGF3 每组各 10只。改构体组分别经静脉注射 0 14 μg/ml、0 4 3μg/ml、1 30 μg/ml的改构体aFGF(1ml/ 10 0g) ,而对照组注射同剂量的生理盐水。 2 0min后 ,用蘸有 80 %乙醇的棉球轻轻擦拭右颈动脉窦区 ,损伤颈动脉窦压力感受器神经末梢 ,并放置 5min。观察记录各组损伤前后夹闭颈总动脉血压即 :收缩压 (SP)、舒张压(DP)、平均动脉压 (MP)和心率 (HR)的变化。结果　 (1)损伤右颈动脉窦前 ,夹闭右颈总动脉 ,实验组和对照组血压均升高 ,夹闭前后相比差异均有统计学意义 (P <0 0 1) ;(2 )损伤右颈动脉窦后 ,夹闭右颈总动脉 ,改构体aFGF1组、对照组血压不变 ,夹闭前后相比差异无统计学意义 (P >0 0 5 ) ;改构体aFGF2 组、改构体aFGF3 组血压升高 ,夹闭前后相比差异有统计学意义 (P <0 0 5 ) ,夹闭前后两组的血压差分别与对照组的差值相比有统计学意义 (P <0 0 5 )。在本实验中 ,HR均无明显变化。结论　改构体aFGF对颈动脉窦损伤有保护作用 ,并显示一定的量效关系     

Role of the Symphato-Adrenal System in Hemorrhagic Hyperglycemia

Arterial and venous plasma glucose concentration was determined at intervals in cats subjected to hemorrhagic hypotension at 50 mm Hg. The rapid rise of arterial plasma glucose after hemorrhage could be. attributed to an increased release of glucose from the liver. This hyperglycemia could not be eliminated by bilateral adrenalectomy or by sectioning of the hepatic sympathetic nerves, although the response was somewhat depressed by the latter procedure. On the other hand the hyperglycemia was virtually abolished after adrenalectomy when combined with bilateral sectioning of the major and minor splanchnic nerves. The level of plasma glucagon during hemorrhage increased in cats with an intact sympatho-adrenal system, but was unchanged in animals with combined splanchnic sympathectomy and adrenalectomy. It is concluded that, during hemorrhage, the sympatho-adrenal system influences the glucose output from the liver by three different reflex mechanisms: (a) release of catecholamines from the adrenal glands; (b) direct sympathetic nerve influence on the liver; and (c) release of glucagon from the pancreas.     

Role of the symphato-adrenal system in hemorrhagic hyperglycemia.

Arterial and venous plasma glucose concentration was determined at intervals in cats subjected to hemorrhagic hypotension at 50 mm Hg. The rapid rise of arterial plasma glucose after hemorrhage could be attributed to an increase release of glucose from the liver. This hyperglycemia could not be eliminated by bilateral adrenalectomy or by sectioning of the hepatic sympathetic nerves, although the response was somewhat depressed by the latter procedure. On the other hand the hyperglycemia was virtully abolished after adrenalectomy when combined with bilateral sectioning of the major and minor splanchnic nerves. The level of plasma glucagon during hemorrgage increased in cats with an intact sympatho-adrenal system, but was unchanged in animals with combined splanchnic sympathectomy and adrenalectomy. It is concluded that, during hemorrhage, the sumpatho-adrenal system influences the glucose output from the liver by three different reflex mechanisms: (a) release of catecholamines from the adrenal glands; (b) direct sympathetic nerve influence on the liver; and (c) release of glucagon from the pancreas.     

Arterial baroreceptors have minimal physiological effects on adrenal medullary secretion

The influence of arterial baroreceptors on secretion of catecholamines from the adrenal medulla was evaluated by several methods. Conscious mongrel dogs with surgically denervated hearts were hemorrhaged until an estimated 16% of their blood volume had been removed. On a separate day they were anesthetized and their blood pressure was lowered with intravenous nitroglycerin. Neither of these maneuvers produced appreciable increases in heart rate in these dogs. In contrast, in a group of sham-operated control dogs, hemorrhage induced a mean increase in heart rate of 20 beats/min (P less than 0.05), and nitroglycerin-induced hypotension induced an increase of 50 beats/min (P less than 0.05). In a separate group of conscious dogs with aortic arch denervation but intact cardiac nerves, occlusion of the common carotid arteries for 5 min increased blood pressure and heart rate significantly but elicited only small, insignificant increases in plasma epinephrine and norepinephrine; the peak concentration of epinephrine achieved was considerably less than the amount necessary to cause appreciable effects on blood pressure and heart rate as determined in another experiment by infusing varying amounts of epinephrine into conscious, cardiac-denervated dogs. We conclude that the arterial baroreceptor reflex, within the range of activity likely to occur during most physiological and pathophysiological adjustments in the conscious dog, exerts only minimal effects on the secretion of catecholamines from the adrenal medulla.     

Denervation of Carotid Baro- and Chemoreceptors in Humans

Experimental denervation in animals has shown that carotid baro- and chemoreceptors play an eminent role in maintaining blood pressure and blood gas homeostasis. Denervation of carotid sinus baro- and chemoreceptors in humans may occur as a complication of invasive interventions on the neck or after experimental surgical treatment in asthma. In this topical review, the short- and long-term effects of carotid baro- and chemoreceptor denervation on the control of circulation and ventilation in humans are discussed. Carotid baroreceptor denervation in humans causes a persistent decrease in vagal and sympathetic baroreflex sensitivity and an increase in blood pressure variability; however, carotid denervation does not lead to chronic hypertension. Therefore, although carotid baroreceptors contribute to short-term blood pressure control, other receptors are able to maintain normal chronic blood pressure levels in the absence of carotid baroreceptors. Conversely, carotid chemoreceptor denervation leads to permanent abolition of normocapnic ventilatory responses to hypoxia and reduced ventilatory responses to hypercapnia.     

Cardiovascular responses to changes in carotid sinus transmural pressure in man.

To study the relative importance of cardiac and peripheral effector mechanisms in the carotid sinus baro-reflex in man cardiovascular responses to equal changes of the carotid sinus transmural pressure (Ptm) in either direction of the normal were recorded and compared in eight physically well-trained young male volunteers. In both the supine and the 70 degrees head-up position, a decrease in Ptm produced a more potent reflex response of the systemic arterial pressure than did a similar increase in Ptm. Whereas the arterial pressure response to increased Ptm was due solely to a reduction in vascular resistance, a significant increase in cardiac output contributed to the more potent pressor response to a decrease in Ptm and thus to the predominantly antihypotensive properties that characterize the carotid sinus baroreceptor control system in man. However, since combined beta-adrenergic and parasympathetic blockade abolished the effect of reduced Ptm on cardiac output without greatly impairing the blood pressure response, it is concluded that adjustments in cardiac output are not of critical importance in the buffering function of the carotid sinus baroreceptors. Autonomic cardiac blockade exaggerated the fall in cardiac output on head-up tilt, the arterial pressure remaining unaffected due to a compensatory increase in systemic vascular resistance.