Electric muscle stimulation in the hind leg of the spontaneously hypertensive rat induces a long-lasting fall in blood pressure

The influence of prolonged low-frequency, low-intensity electric stimulation of the gastrocnemius muscle or of the biceps femoris muscle on blood pressure and heart rate was investigated in unanaesthetized, spontaneously hypertensive rats (SHR). In both groups, elevations of blood pressure and heart rate were elicited during the 60 min of muscle stimulation. After cessation of the stimulation, a depressor response developed within 60 min. Thirty to sixty minutes post-stimulation the fall in blood pressure was 19 ± 3 and 17 ± 4 mmHg, respectively (mean ± SE) compared with controls. In both groups, the depressor response lasted for over 5 h. In addition, the gastrocnemius-stimulated animals also developed a post-stimulatory bradycardia. In one group of SHR the sciatic nerve was anaesthetized with bupivacaine. The arousal response during stimulation was similar to that in the other groups, but after termination of stimulation blood pressure returned to the control level without any further drop. To investigate further the neurotransmitters involved, one group of gastrocnemius-stimulated SHR was given naloxone by infusion during the stimulation. A modest post-stimulatory blood pressure fall also occurred in this group, but it lasted only 90 min. Another SHR group was pre-treated with parachlorophenylalanine, a serotonin synthesis blocker, which completely abolished the post-stimulatory depressor response. These results indicate that prolonged muscle stimulation gives rise to a post-stimulatory long-lasting drop in blood pressure and that this response is mediated by somatic nerve afferents. Involvement of the endorphin and serotonin systems is also suggested.     

Long-lasting cardiovascular depression induced by acupuncture-like stimulation of the sciatic nerve in unanaesthetized rats. Effects of arousal and type of hypertension

Prolonged low frequency stimulation of the sciatic nerve in conscious spontaneously hypertensive rats (SHR), is reported to induce a naloxone-reversible long-lasting depressor response (Yao et al. 1982a). In the present study this depressor response was compared during daytime and night-time conditions to determine whether different degrees of arousal affect this response. In addition, the effect of sciatic nerve stimulation was examined in one-clip, two-kidney renal hypertensive rats (RHR); a type of secondary hypertension which lacks the central autonomic hyper-reactivity which characterizes the SHR variant of primary hypertension. A maximal fall in blood pressure of 20 mm Hg was observed 1 h after sciatic nerve stimulation in SHR examined in daytime. We also found a significant bradycardia that lasted for 2.5 h. Neither poststimulatory depression nor bradycardia were observed in RHR examined at daytime. A short-lasting, non-significant decrease in blood pressure and heart rate was found following sciatic stimulation in SHR examined at night.     

Electrical stimulation of the gastrocnemius muscle in the spontaneously hypertensive rat increases the pain threshold: role of different serotonergic receptors

In a previous study, prolonged low-frequency muscle stimulation in the hind leg of the fully conscious spontaneously hypertensive rat (SHR) was shown to induce a long-lasting reduction of blood pressure. It was also shown that opioid and serotonergic (5-HT) systems were involved. More recently, we have shown that the 5-HT₁ receptors are involved in the post-stimulatory decrease in blood pressure. In the present study, the influence of this type of muscle stimulation on the pain threshold was investigated. Pain perception was measured as the squeak threshold to noxious electric pulses. After cessation of the stimulation, an analgesic response was elicited within 60 min and peak analgesia developed after 120 min, being 139 ±10% (P < 0.01) of the prestimulatory control value. The increased pain threshold lasted for another 2 h. One group of SHR was pretreated with PCPA, a serotonin synthesis blocker, which completely abolished the post-stimulatory analgesia. To analyse further the involvement of different serotonin systems, drugs with selective affinity for 5-HT receptors were used. In one group a prestimulatory dose of metitepine maleate (a 5-HT_1&2 receptor antagonist) abolished the post-stimulatory elevation of the pain threshold. The prolonged analgesic response was still present after prestimulatory treatment with ritanserin or ICS 205–930 (5-HT₂ and 5-HT₃ blocking agents respectively). In another group of experiments, the serotonin receptor antagonists were administered post-stimulation to animals with fully elicited analgesia. None of the antagonists used could reverse the elevation of pain threshold towards prestimulatory levels. Thus, intact 5-HT systems were necessary to elicit the analgesia to muscle stimulation and the response was mediated by the 5-HT₁ receptor. However, the results indicate that serotonin is not required to maintain the analgesia once it has been elicited.     

Long-lasting cardiovascular depressor response to somatic stimulation in spontaneously hypertensive rats.

It has been known that a short-lasting stimulation of the somatic afferent nerves elicits either a depressor or a pressor response depending on the stimulus parameters (Johansson 1962). In the present study cardiovascular responses were observed during and after a long-lasting sciatic nerve stimulation in conscious spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar Kyoto rats (WKR).     

Electric muscle stimulation in the spontaneously hypertensive rat induces a post-stimulatory reduction in activity: role of different opioid receptors

We have previously shown that prolonged low-frequency muscle stimulation, inducing contractions of the gastrocnemius muscle, in conscious spontaneously hypertensive rats leads to an opioid-mediated post-stimulatory reduction in blood pressure and analgesia. In the present study we investigated whether muscle stimulation would also induce a post-stimulatory reduction in behavioural activity in the spontaneously hypertensive rats. Selective opioid receptor antagonists were used to analyse the involvement of endogenous opioids. Muscle stimulation, lasting 60 min, induced a post-stimulatory sedation that outlasted the stimulation for hours. Sniffing, locomotor activity and total behavioural activity were significantly reduced. The post-stimulatory reduction in activity was reversed back to control levels by a high dose of naloxone (15 mg kg-1 i.v.). The selective mu-receptor antagonist beta-funaltrexamine, given intracerebroventricularly before stimulation, did not influence the development of the post-stimulatory drop in activity. The delta-receptor antagonist ICI 154,129 had no effect at all on the already developed sedation, whereas MR 2266 BS, a kappa-receptor antagonist (3 mg kg-1 i.v.), completely reversed the drop in activity. These results show that muscle stimulation gives rise to an opioid-mediated post-stimulatory reduction in activity in spontaneously hypertensive rats. The results also indicate the involvement of the opioid kappa-receptor in the behavioural response.     

Systemic arterial baroreceptors in ducks and the consequences of their denervation on some cardiovascular responses to diving

1. In the duck systemic arterial baroreceptors which cause bradycardia in response to induced hypertension are located in the walls of the ascending aorta, innervated by the depressor nerves.2. The location of the baroreceptors was confirmed both histologically and by recording activity from the depressor nerve. Stimulation of the central cut end of a depressor nerve caused transient bradycardia and a fall in blood pressure which was maintained throughout the period of stimulation.3. Cardiovascular adjustments to submergence of 2 min duration were monitored in intact, sham-operated and denervated ducks. The sham-operated and denervated ducks were used in the experiments some 20-50 days post-operation. The denervations were checked at post-mortem.4. In the first series of experiments on young ducks mean arterial pressure during a 2 min dive fell by 30% in intact, 17.5% in sham-operated, and 48% in denervated ducks. In all ducks heart rate was reduced by 84-85%.5. In a second series of experiments on older ducks sciatic artery blood flow was also recorded and mean arterial blood pressure fell by 9.2% in intact and by 53% in denervated animals, although there were no significant differences in heart rate during the 2 min dives. In normal animals sciatic vascular resistance increased after 2 min submergence by 7.86 +/- 1.7 times, whereas in denervated ducks it increased by only 2.32 +/- 0.5 times.6. The role of systemic arterial baroreceptors in generation of the cardiovascular responses to submergence in ducks is discussed in terms of the input supplied by the baroreceptors to the central nervous system.     

Role of different serotonergic receptors in the long-lasting blood pressure depression following muscle stimulation in the spontaneously hypertensive rat

In a previous study prolonged low-frequency muscle stimulation in the hind leg of the spontaneously hypertensive rat (SHR) was shown to induce a reduction in blood pressure (about 15 mmHg) that lasted for many hours. We showed in that study that endorphin and serotonin systems were involved. In the present study drugs with selective affinity for the serotonin (5-HT) receptors were used to analyse further the involvement of different serotonin systems. In one group of SHR, a prestimulatory dose of metitepine maleate (a 5-HT1 and 5-HT2 receptor antagonist) completely abolished the post-stimulatory depressor response. The long-lasting depressor response was still present, although less pronounced, after a bolus dose of the 5-HT2 blocking agent ritanserin (R 55667) at the start of stimulation. The 5-HT3 receptor antagonist ICS 205-930 did not influence the response at all, nor did the selective 5-HT1a receptor agonist 8-OH-DPAT enhance the depressor response. These results indicate that the reduction in blood pressure after muscle stimulation is mainly mediated by the 5-HT1 receptor.     

Effects of thermal stimulation, applied to the hindpaw via a hot water bath, upon ovarian blood flow in anesthetized nonpregnant rats

The effects of thermal stimulation, applied to the hindpaw via a hot bath set to either 40 degrees C (non-noxious) or 49 degrees C (noxious), upon ovarian blood flow were examined in nonpregnant anesthetized rats. Ovarian blood flow was measured using a laser Doppler flowmeter. Blood pressure was markedly increased following 49 degrees C stimulation. Ovarian blood flow, however, showed no obvious change during stimulation, although a small increase was observed after stimulation. Ovarian blood flow and blood pressure responses to 49 degrees C stimulation were abolished after hindlimb somatic nerves proximal to the stimuli were cut. Heat stimulation (49 degrees C) resulted in remarkable increases in both ovarian blood flow and blood pressure in rats in which the sympathetic nerves supplying the ovary were cut but the hindlimb somatic nerves remained intact. The efferent activity of the ovarian plexus nerve was increased during stimulation at 49 degrees C. Stimulation at 40 degrees C had no effect upon ovarian blood flow, blood pressure or ovarian plexus nerve activity. Electrical stimulation of the distal part of the severed ovarian plexus nerve resulted in a decrease in both the diameter of ovarian arterioles, observed using a digital video microscope, and ovarian blood flow.The present results demonstrate that noxious heat, but not non-noxious warm, stimulation of the hindpaw skin in anesthetized rats influences ovarian blood flow in a manner that is attributed to reflex responses in ovarian sympathetic nerve activity and blood pressure.     

Differentiation of sympathetic activity at the spinal level in Response to central cold stimulation

Summary Thermally induced adjustments of skin blood flow in chronically spinalized dogs may occur without alterations of arterial pressure and heart rate. In lightly anesthetized rabbits with chronic spinal transection at the level of C₆/C₇, the question was investigated, whether the isolated spinal cord can produce differentiated changes of regional sympathetic activity as a response to central cold stimulation.Selective cooling of the thoraco-lumbar spinal cord in chronically spinalized rabbits induced an increase in vasoconstrictor tone of the ear skin vessels as indicated by a drop of ear skin temperature at constant core and ambient air temperatures. Simultaneously, a decrease of activity in a splanchnic nerve branch was observed. Arterial pressure and heart rate remained unaffected on the average. 24 h after spinal transection, this response seemed to be less pronounced than 3 or more days after the operation. The presented results show that the pattern of regional vasomotor responses induced by central cold stimulation is, on principle, identical in intact and chronically spinalized rabbits. Therefore, the vasomotor pattern described in spinalized animals seems to represent a thermoregulatory response mediated by a vicarious spinal control system.     

Reflex Inhibition of Sympathetic Nerve Activity by Phenoxybenzamine

The effects on baroreceptor and sympathetic nerve activity of the a-adrenergic blocking agent phenoxybemamirie have been investigated in 13 anesthetized rabbits. Nerve activities were recorded at various blood pressure levels, obtained by stepwise changes of blood volume. With phenoxybenzamine, aortic nerve activity at 80 and 90 mm Hg exceeded control values by 66 and 62 %. At the same pressures, renal nerve activity was reduced by 30 and 55 %. Although blood pressure started to fall shortly after injecting the drug, about 20 min elapsed before development of maximum effects on the nerves. When studied during stepwise changes of blood pressure after a similar period of hypotension—but without the drug-sympathetic nerve activity had increased. Phenoxybenzamine had accordingly effected a suppression of sympathetic activity, suggesting that the hypotensive response to phenoxybenzamine is aided by increased reflex inhibition of sympathetic nerve activity.     

The brief and the prolonged facilitatory effects of unmyelinated afferent input on the rat spinal cord are independently influenced by peripheral nerve section

Single C-fibre strength stimuli applied to the sciatic nerve in the decerebrate spinal rat evoke three separate bursts of activity in posterior biceps/semitendinosus flexor alpha motorneurones which are associated with the arrival in the spinal cord of volleys in the A-beta, A-delta and C-afferent fibres. Repetitive stimulation of the sciatic nerve at 1 Hz for 20 s generates a progressive wind-up of response and an after-discharge lasting up to 10 s. Twelve to fourteen days after section of the sciatic nerve, stimuli applied central to the section evoke a larger than normal response in the posterior biceps/semitendinosus flexor motorneurones and repetitive stimulation (1 Hz, 20 s) produces an after-discharge which is four times longer than that produced by stimulation of the intact nerve. In addition to the direct excitatory effects of sciatic nerve stimulation on the flexor motorneurones which lasts for seconds, conditioning stimuli to the sciatic nerve at C-fibre strength (1 Hz, 20 s) produce a facilitation of the flexor reflex evoked by a standard pressure stimulus to the ipsilateral and contralateral toes which lasts for 70 min. However, although the direct excitatory effects of stimulating a sectioned sciatic nerve on the posterior biceps/semitendinosus flexor motorneurones are exaggerated, the facilitation of the cutaneous flexion reflex evoked by stimulating sectioned sciatic nerves (1 Hz, 20 s) only lasts for 17 min. These results show that the mechanism which produces the rapid effects of sciatic nerve stimulation on the flexor reflex circuit can be separated from the mechanism which produces the prolonged facilitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of central and peripheral inputs on single pineal cell activity in the rat

The influences exerted by central and peripheral afferents to the pineal gland have been studied in rats anesthetized with urethane (1.2 g/kg, i.p.). Spontaneous action potentials arising from the pinealocytes were recorded by means of glass micropipettes filled with 3 M NaCl containing a dye. The electrical stimulation of suprachiasmatic nucleus, superior cervical ganglia, sciatic nerve and retina evoked discharge changes in a significant number of pineal cells. However, a relatively higher proportion of pinealocytes failed to respond to these afferents. Three types of responses could be observed. Inhibitions were the predominant response patterns to suprachiasmatic nucleus, superior cervical ganglia and sciatic nerve, while excitations were mainly elicited following photic stimulation, whereas the remaining evoked activity was biphasic responses, which were observed in a small number of cells after stimulation of suprachiasmatic nucleus, superior cervical ganglia and retina. These data confirm some previous neural inputs to the pineal and demonstrate the existence of a modulatory effect of the suprachiasmatic nucleus on pinealocyte discharges as well as somatosensory afferents to the gland by way of the sciatic nerve.     

Renal nerve activity and exaggerated natriuresis in conscious spontaneously hypertensive rats

Exaggerated natriuresis upon volume loading occurs in both human and animal hypertension and is mainly due to suppressed tubular reabsorption. To explore whether altered renal sympathetic activity contributes to this response, conscious male spontaneously hypertensive rats (SHR) were exposed to isotonic saline loading in comparison with normotensive male Wistar Kyoto rats (WKR). After a 60 min control hydropenic period, during which mean arterial pressure, heart rate, renal sympathetic nerve activity and urinary sodium excretion were followed, a 60 min period of intravenous volume expansion with isotonic saline (0.2 ml/minx 100 g b. w.) was started followed by a 60 min hydropenic recovery period. Already during the control period sodium excretion was significantly higher in SHR. During the volume load and subsequent recovery period a clearly exaggerated natriuresis occurred in SHR compared with WKR. Further, volume loading reduced renal sympathetic nerve activity in all animals, but significantly more in SHR. Moreover, volume loading reduced mean arterial pressure and heart rate in both groups. It is suggested that the accentuated reflex inhibition of renal sympathetic activity in SHR upon volume loading emanates from cardiac mechanoreceptors and partly explains the exaggerated natriuresis in SHR. This augmented ‘volume’ reflex response is probably due to reduced systemic venous compliance in SHR with a consequently increased central filling and cardiac receptor activation.     

Comparison of sarcomere alterations after muscle contraction and tension loading in the rat soleus muscle

Muscle contraction induced by 30 min of continuous nerve stimulation at 50 Hz resulted in sarcomere changes of the soleus muscle in the rat in our previous study. To further investigate the cause of sarcomere alterations, the sciatic nerve was electrically stimulated intermittently for 30 min. Nerve stimulation was also conducted after cutting the tendons of the soleus, gastrocnemius and plantaris muscles in order to prevent imposing tension on these muscles as a result to their own contractions. In addition, the muscles were pulled by weights via their tendons to load high tension for 30 min without nerve stimulation. Sarcomere alterations immediately after treatments were quantified by electron microscopy. The percentages of aberrant sarcomere areas of the soleus muscle were 25.7 ± 16.4% (mean ± SD) in the group of intermittent nerve stimulation with intact tendons and 21.1 ± 35.4% in the group of tenotomy and continuous nerve stimulation, which were roughly equal to or more severe than the group of continuous nerve stimulation with intact tendons (18.8 ± 15.8%) in our previous study. Sarcomere alterations consisted mainly of hypercontraction in these groups. Almost all sarcomere changes in the tension-loaded (pulled) soleus muscles were scarce myofilaments (1.7 ± 1.0% by 600 g; 4.5 ± 2.9% by 1200 g), and hypercontraction was not observed. These findings indicate that neither high tension nor a decrease of muscle blood flow during continuous contraction seems to be the primary cause of sarcomere alterations in the present study. There are probably other causes that produce aberrant sarcomeres.     

Cutaneous Mechanical Stimulation Regulates Ovarian Blood Flow via Activation of Spinal and Supraspinal Reflex Pathways in Anesthetized Rats

The reflex effects of noxious mechanical stimulation of a hindpaw or abdominal skin on ovarian blood flow, and the reflex pathways involved in those responses were examined in anesthetized rats. Blood flow in the left ovary was measured using a laser Doppler flowmeter, and the activity of the left ovarian sympathetic nerve and mean arterial pressure (MAP) of the common carotid artery were recorded. Stimulation of the left or right hindpaw for 30 s produced marked increases in ovarian sympathetic nerve activity and MAP. Ovarian blood flow slightly decreased during the stimulation and then slightly increased after the stimulation. After the left ovarian sympathetic nerves were severed, the same stimulus produced a remarkable monophasic increase in ovarian blood flow that was explained by passive vasodilation due to a marked increase in MAP. After spinal transection at the third thoracic (T3) level, the responses of MAP, ovarian sympathetic nerve activity, and ovarian blood flow to hindpaw stimulation were nearly abolished. Stimulation of the abdomen at the right or left side for 30 s produced slight increases in ovarian sympathetic nerve activity and MAP. Ovarian blood flow slightly decreased during the stimulation and then slightly increased after the stimulation. After the ovarian sympathetic nerves were severed, the response of the ovarian blood flow changed to a monophasic increase due to an increase in MAP. After spinal transection, stimulation of the left abdomen produced a moderate increase in MAP, a remarkable increase in ovarian sympathetic nerve activity and a slight decrease in ovarian blood flow during the stimulation. In contrast, stimulation of the right abdomen produced a smaller response in ovarian sympathetic nerve activity during the stimulation while it increased the MAP to a similar degree. Ovarian blood flow slightly increased after the end of stimulation, which was explained as passive vasodilation due to the increase in MAP. In conclusion, stimulation of somatic afferents affects ovarian blood flow by inducing changes in ovarian sympathetic nerve activities and blood pressure. When stimulation was applied to a hindpaw whose segment of afferent input is far from the segment of the ovarian sympathetic nerves, it took a supraspinal reflex pathway. However, when stimulation was applied to the abdomen whose spinal segment of the afferent is close to the segment of the ovarian sympathetic nerve output, there are spinal segmental reflex pathways. The present results demonstrate that spinal reflexes depend on the laterality of the stimulus, while supraspinal reflexes do not depend on the laterality of the stimulus.     

Responses of adrenal sympathetic nerve activity and catecholamine secretion to cutaneous stimulation in anesthetized rats

Reflex effects of cutaneous mechanical stimulation on adrenal sympathetic efferent nerve activity and secretion rates of the adrenal medullary hormones (epinephrine and norepinephrine) were studied in anesthetized rats. Noxious pinching stimulation of the lower chest or hindpaw skin for 3 min produced proportional reflex increases in both the nerve activity and secretion rates of epinephrine and norepinephrine from the adrenal medulla in animals with an intact central nervous system. However, lower chest stimulation elicited a longer lasting response than hindpaw stimulation, 7-17 min vs 1 min after cessation of the stimulation, respectively. After spinal transection at the C1-2 level, only lower chest stimulation was capable of producing a reflex response, lasting 1 min after cessation of the stimulation. Contrary to the responses elicited by pinching, non-noxious brushing stimulation of the lower chest or hindlimb skin for 3 min in animals with an intact central nervous system produced proportional reflex decreases in nerve activity and epinephrine and norepinephrine secretion rates during the stimulation period only. Some slight increases in both nerve activity and secretion rates, lasting several minutes, followed cessation of the stimulation. However, in spinalized animals, non-noxious lower chest or hindlimb stimulation produced opposite effects, increasing both the nerve activity and secretion rates of epinephrine and norepinephrine. In spinalized animals lower chest brushing stimulation elicited a much stronger response than hindlimb brushing stimulation. It was concluded that; (1) the secretion of adrenal medullary hormones can be controlled reflexly by mechanical cutaneous stimulation through the central nervous system via adrenal sympathetic efferent nerves; (2) the excitatory effect of the cutaneo-adrenal medullary reflexes was independent of noxious or non-noxious stimulation at the spinal level, whereas in rats with an intact central nervous system the effect was either excitatory or inhibitory in response to noxious or non-noxious stimulation, respectively; (3) there is a marked segmental organization of this reflex at the spinal level which is modified into a generalized response through supraspinal central structures.     

Calcium dependency of the post-stimulatory potentiation of the neurogenic response in small mesenteric arteries from the rat

We have previously shown that the contraction of small mesenteric arteries in response to nerve stimulation is enhanced by preceding high-frequency stimulation. We have now investigated the calcium dependency of this post-stimulatory potentiation. Small arteries (inner diameter 150-250 microns) from normotensive rats were dissected free from surrounding tissue, and segments were mounted in a myograph where the wall tension was measured at well-defined circumferences. Nerve stimulation was performed by field stimulation. A single stimulation of the nerve caused a contraction of 2.6 +/- 0.25% of maximal adrenergic response. After a high-frequency nerve stimulation with 16 Hz and 480 pulses the response to a single nerve stimulation was enhanced 6.6 +/- 1.3 times. The potentiation decayed with a time constant of 93.7 +/- 20.0 s. The amplitude of the post-stimulatory potentiation was dependent on the extracellular calcium concentration during the conditioning stimulation. In a solution containing 2.5 mM calcium the single twitch was enhanced 6.6 times while after exposure to reduced calcium (0.5 mM) it was only enhanced twice. The contraction caused by a short burst of high-frequency nerve stimulation (20 Hz and 10 pulses) was potentiated four times by a conditioning stimulation (16 Hz and 480 pulses), and this potentiation seemed to be independent of the extracellular calcium concentration during the conditioning stimulation. Thus the magnitude of the post-stimulatory potentiation of single nerve stimulations is linearly related to the extracellular calcium concentration during the conditioning nerve stimulation. For the potentiation of the response to burst stimulation no relation was found between the potentiation and extracellular calcium.     

Stimulation of lumbar sympathetic trunk produces vasoconstriction of the vasa nervorum in the sciatic nerve via alpha-adrenergic receptors in rats.

The effects of repetitive electrical stimulation of a lumbar sympathetic trunk (LST) for 30 s at various frequencies and supramaximum intensity on the nerve blood flow in a sciatic nerve were studied by laser Doppler flowmetry in anesthetized Fischer-344 male rats. The response was biphasic; i.e. an initial increase and then a decrease. The maximum mean increase after 2 Hz stimulation was 22 +/- 8%, while the maximum mean decrease after 20-50 Hz stimulation was 79 +/- 3%, of the prestimulus control level. The initial increase, which was greater at lower frequencies and existed even after local sympathetic denervation, was passive, and was caused by the systemic pressor response to LST stimulation. The decrease, which was nearly abolished by an i.v. alpha-adrenergic blocker, phentolamine (10 mg/kg), resulted from vasoconstriction in the vasa nervorum, mainly via activation of alpha-adrenergic receptors.     

Pressure-Independent Inhibition of Sympathetic Activity by Noradrenaline: Role of Baroreceptor C Fibres*

The effect of i.v. infusion of noradrenaline on activity in the renal sympathetic nerve was studied in rabbits anesthetized with chloralose and urethane. Noradrenaline (3–8 μg/kg·min) initially increased mean arterial pressure 20–40 mmHg and consequently reduced renal nerve activity. However, studies over a wide range of pressures—obtained by changing the blood volume, revealed that noradrenaline after a few minutes had induced a pressure-independent reduction of sympathetic discharge. The effect disappeared with baroreceptor denervation. An unchanged relationship between arterial pressure and integrated activity in the whole left aortic nerve (which is largely a measure of activity in A fibres) suggested that the sympathetic depression was due to excitation of aortic nerve C fibres. This conclusion was supported by studies of sympathetic responses to selective stimulation of aortic nerve A and C fibres at equal pressures before and during infusion of noradrenaline. Compared to the reflex activity from A fibres, C fibre stimulation was invariably less effective in suppressing renal nerve activity during the infusion. Our studies indicate that noradrenaline may effect a negative feedback control of sympathetic discharge through activation of baroreceptor C fibres.     

Spatiotemporal characteristics of cerebral blood volume changes in rat somatosensory cortex evoked by sciatic nerve stimulation and obtained by optical imaging

The spatiotemporal characteristics of changes in cerebral blood volume associated with neuronal activity were investigated in the hindlimb somatosensory cortex of alpha-chloralose-urethane anesthetized rats (n=10) with optical imaging at 570 nm through a thinned skull. Activation of the cortex was carried out by electrical stimulation of the contralateral sciatic nerve with 5-Hz, 0.3-V pulses (0.5 ms) for 2 s. The stimulation evoked a monophasic decrease in optical reflectance at the cortical parenchyma and arterial sites soon after the onset of stimulation, whereas no similar response was observed at vein compartments. The optical signal changes reached 10% of the peak response 0.70 +/- 0.32 s after the start of stimulation, and no significant time lag in this 10% start latency time was observed between the response at the cortical parenchyma and artery compartments. The decrease in optical reflectance reached a peak (0.25 +/- 0.047%) 2.66 +/- 0.61 s after stimulus onset at parenchymal sites, which is 0.40 +/- 0.20 s earlier (P<0.05) than that at arterial sites (0.50 +/- 0.068% 3.06 +/- 0.70 s). Varying the locations within the cortical parenchyma and arterial compartments did not significantly affect the temporal characteristics of the evoked signal. These results suggest that stimulation of the sciatic nerve evokes an increase in local blood volume in both capillaries (cortical parenchyma) and arterioles soon after the onset of a stimulus, but the blood volume increase evoked in capillaries could not be entirely accounted for by the dilation of arterioles.