The influence of aortic baroreceptors on venous tone in the perfused hind limb of the dog.

1. The aortic arch and both carotid sinuses were vascularly isolated and perfused. A hind limb was vascularly isolated and blood was pumped at constant flows into the femoral artery and the central end of a superficial metatarsal vein. 2. Large increases in aortic arch pressure resulted in decreases in arterial blood pressure, heart rate and femoral arterial perfusion pressure. The average response of the vein was a decrease of 11% in the pressure gradient between the perfused vein and the femoral vein. Similar responses were obtained when carotid sinus pressure was increased. 3. Crushing or cooling the lumbar sympathetic trunk caused responsed similar to those induced by increasing baroreceptor perfusion pressure. Stimulation at 1 HZ resulted in venous responses four times as great as the average reflex response, whereas frequencies of 2-5 Hz were required to produce changes in arterial resistance as great as those induced reflexly. 4. These experiments indicate, that although the large superficial veins of the dog's hind limb participate in the baroreceptor reflexes, the activities in the nerves supplying arterioles and veins must have been different.     

Responses of abdominal vascular capacitance in the anaesthetized dog to changes in carotid sinus pressure.

1. The abdominal circulation of anaesthetized dogs was vascularly isolated without opening the abdomen, by cutting or tying all structures immediately above the diaphragm and tying the proximal ends of the hind limbs. The region was perfused at constant flow through the aorta and drained at constant pressure from the inferior vena cava. 2. Vascular resistance responses were expressed as the changes in perfusion pressure and capacitance responses were determined by integrating changes in vena caval outflow. 3. Decreasing the pressure in the isolated carotid sinuses over the whole baroreceptor sensitivity range increased mean perfusion pressure from 91 to 149 mmHg (a 67% increase in resistance) and decreased mean capacitance by 111 ml. (5 ml. kg-1). 4. The range of carotid sinus pressures over which capacitance responses occurred was at a significantly higher level than the corresponding range for resistance responses. 5. Comparison of the reflex responses with the responses to direct stimulation of efferent sympathetic nerves shows that quantitatively similar responses of resistance and capacitance to those induced by a large step decrease in carotid pressure could be produced by stimulating maximally the efferent sympathetic nerves at 5 Hz. These results also suggest that at all levels of carotid sinus pressure there is no difference in the impulse traffic to resistance and capacitance vessels.     

The effect of baroreceptors on the latency of evoked responses in sympathetic nerves during the cardiac cycle

1. A rapid increase in pressure in a vascularly isolated perfused carotid sinus has been shown to inhibit a reflex response in efferent sympathetic nerves of the dog evoked by electrical stimulation of the radial nerve.2. In intact preparations with the carotid baroreceptors innervated, the mean latency and the variance of the latency of reflex sympathetic nerve responses was reduced when the stimuli evoking the responses were applied at one point of both cardiac and respiratory cycles. When the baroreceptors were denervated there were no significant differences in the responses to random and synchronized stimuli.3. In intact preparations the latency of evoked responses in sympathetic nerves was found to vary progressively during a cardiac cycle; the maximum increase in latency was observed with the responses that occurred at that phase of the cardiac cycle when the baroreceptors exert maximal inhibition on spontaneous sympathetic activity. After denervation of the carotid sinuses a much smaller change during the cardiac cycle was still present, possibly due to effects produced by baroreceptors of the aortic arch and elsewhere.4. It was concluded that changes in baroreceptor activity, due to beat to beat fluctuations of the systemic arterial pressure are a major factor causing variations in the latency of responses in sympathetic nerves evoked by stimuli applied to a cutaneous nerve.     

Passive vasodilatation of the hind limb after sympathetic preganglionic stimulation

1. The post-vasoconstriction dilatation (PVCD) observed after release of carotid clamping has been attributed to baroreceptor stimulation. However, PVCD has been observed in baroreceptor deafferented animals following cessation of stimulation of the diencephalon or of chemoreceptor fibres.2. The effects of preganglionic (ventral roots) and post-ganglionic (sciatic nerve) stimulation upon the vascular resistance of the hind limb of anaesthetized cats and dogs was investigated. The limb was vascularly isolated and perfused at constant flow with the animal's own arterial blood. The animals were atropinized and neuromuscular block was obtained with gallamine triethiodide.3. PVCD was observed upon cessation of stimulation of intact preganglionic fibres or of their peripheral stump.4. PVCD was dependent upon the existence of neurogenic vasomotor tone in the vessels, but independent from baroreceptor influences.5. PVCD was never observed after cessation of stimulation of the post-ganglionic fibres.6. Similar results were obtained after removal of the skin of the perfused limb.7. The possibility that the post-vasoconstriction dilatation observed in these experiments is due to the existence of a preganglionic inhibitory system is discussed.     

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 transients caused by abrupt alterations of carotid baroreceptor activity in humans

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.     

The baroreceptor reflex and the cardiovascular changes associated with sustained muscular contraction in the cat

Summary In decerebrate unanaesthetised cats the cardiovascular effects of raising the pressure in a blind sac preparation of a carotid sinus on one side were examined at rest and during sustained contractions of hind-limb muscles. During a tetanic contraction the absolute value of the blood pressure and heart-rate components of the baroreceptor reflex response were not significantly changed from those at rest. The curve relating heart-rate and mean blood pressure, during carotid sinus distension, was similar at rest and when the muscles of the hind-limb were contracting tetanically, although each value of heart-rate was greater, suggesting a resetting of the baroreceptor reflex. By contrast, in the same experiments, suppression of the baroreceptor reflex changes in heart-rate and blood pressure could be demonstrated during the increases of blood pressure and heart-rate elicited by electrical stimulation of limb nerve. It was concluded that the increases in blood pressure and heart-rate elicited by the afferent discharge from muscles during sustained contraction are buffered to some extent by the baroreceptors, though their inhibitory effect is incomplete under these conditions.     

The role of the carotid body chemoreceptors and carotid sinus baroreceptors in the control of cerebral blood vessels

1. Cerebral blood flow was measured in 17 baboons, anaesthetized with pentobarbitone, paralysed with gallamine and mechanically ventilated and in which the right sinus and both aortic nerves had been cut and the left carotid sinus vascularly isolated. Later in each experiment, the head was artificially perfused with femoral arterial blood via the innominate artery.2. Stimulation of the carotid body chemoreceptors with venous blood invariably caused a rise in regional cerebral blood flow whether the head was naturally or artificially perfused. This response was almost completely abolished if the VIIth cranial nerves were cut intracranially.3. Regional cerebral blood flow varied inversely with carotid sinus pressure.4. After the remaining (left) sinus nerve had been cut, the cerebral vascular response to hypoxia was negligible and the response to hypercapnia was markedly reduced. Blood flow then varied with perfusion pressure.5. These results provide further evidence that cerebral blood vessels are reflexly controlled and that the peripheral arterial receptors are involved. Their action is most conspicuous in the vascular response to hypoxia and together with intrinsic factors in the cerebral vascular bed, they determine the size of the vascular response to changes in CO(2) and pressure.     

Types of nervous activity which may be recorded from the carotid sinus nerve in the sheep foetus

1. In the sinus nerve of mature foetal sheep (120-147 days gestational age) three types of nerve activity have been demonstrated: (a) baroreceptor afferent, in which the nerve activity was synchronous with the pulse pressure wave and which followed pressure changes in the carotid sinus including those caused by compressing the umbilical cord. The discharge of nine out of twelve baroreceptor afferents increased with sympathetic stimulation, (b) a subtype of (a) in which there was irregular activity from pressure receptors which most probably represented baroreceptors discharging at or about threshold, and (c) in the older foetuses (130-147 days), there was activity which was unaffected by changes in carotid sinus pressure, P(a, O2) or NaCN but which increased in discharge rate with compression of the umbilical cord or with stimulation of the cervical sympathetic; this activity then increased with injection of NaCN and was thus identified as chemoreceptor in origin. In addition, a pathway originating in the cervical sympathetic and which passed through the superior cervical ganglion was demonstrated by evoking a compound action potential on stimulation of the preganglionic cervical sympathetic nerve.2. Recordings from pre- or post-ganglionic cervical sympathetic nerves showed that spontaneous activity was present and increased when the umbilical cord was compressed.3. These results suggest that the carotid body chemoreceptors in the foetus are relatively insensitive to chemical changes and that, in their activation at birth, the sympathetic could be involved. Possible neural pathways and the mechanism of activation are discussed.     

Baroreflex “resetting” by arterial hypoxia in the renal and cardiac sympathetic nerves of the rabbit

1. Renal and cardiac sympathetic baroreflex functions were studied in sodium pentobarbitone anaesthetized rabbits given succinylcholine, during constant artificial ventilation with air and with hypoxic gas mixtures. Mean arterial pressure (MAP) was raised and lowered between values of 40 and 140 mm Hg by means of aortic and vena caval periovascular balloons and integrated sympathetic nerve activity (SNA) was recordered. 2. The relationship between MAP and SNA was sigmoid, with upper and lower plateau levels. The curves were defined by calculating median blood pressure, SNA Range and reflex gain. In both renal and cardiac sympathetics section of the carotid sinus and aortic nerves completely abolished the MAP-related changes in SNA. 3. The renal baroreflex curves were reset from control levels during hypoxia. Median blood pressure increased, as did SNA Range and gain. These effects were due to central interactions between arterial baroreceptor, arterial chemoreceptor and vagal afferent activity. 4. The cardiac sympathetic baroreflex curves were shifted in the opposite direction from control with reduction in median blood pressure, SNA Range and reflex gain. These changes were due to chemoreceptor-arterial baroreceptor interactions. 5. Arterial hypoxia thus evokes a differentiated pattern of baroreflex resetting in the renal and cardiac sympathetic montoneuron pools with differing changes in neural response range and sensitivity to arterial pressure changes.     

Neural control of nutritional and nonnutritional circuits in the dog hindpaw

The neural control of blood flow and volume distribution between parallel nutritional and nonnutritional circuits has been investigated in the vascularly and neurally isolated dog hindpaw. Twelve paws were perfused by controlled pressure and ten paws were perfused by controlled flow via the cranial tibial artery. Venous outflow was measured and collected from the lateral saphenous vein. The superficial and deep fibular nerves and the tibial nerve were cut and individually stimulated, resulting in rates which at least doubled the blood flow resistance. Vascular volume changes were measured by injections of 51Cr-labeled red cells and 131I-labeled albumin. Tissue volume changes were measured by plethysmography. Capillary diffusion capacity was calculated from 86Rb extractions, and capillary filtration coefficients were determined. Superficial fibular nerve and deep fibular nerve stimulations apparently resulted in nonnutritional circuit constriction with resulting blood flow redistribution to nutritional circuits, possibly located in tissues other than the skin, e.g., adipose tissue. Tibial nerve stimulation caused no redistribution of blood flow between the two circuits presumably due to a uniform constriction of arteries and small vessel segments.     

Baroreflex modulation of sympathetic activity and sympathetic neurotransmitters in humans

We raised and lowered arterial pressures with stepwise intravenous infusions of phenylephrine and nitroprusside in ten healthy young men and measured changes of R-R intervals, post-ganglionic peroneal nerve muscle sympathetic activity, and antecubital vein plasma noradrenaline and neuropeptide Y concentrations. Respiratory peak-valley R-R interval changes declined with arterial pressure reductions, but did not rise with pressure elevations. Sympathetic activity was modulated by respiration over the entire range of pressures and, at each pressure, was more prominent in expiration than inspiration. Levels of muscle sympathetic nerve activity were low during supine rest, were suppressed almost completely during small increases of pressure, and were increased proportionally during pressure reductions. Over a range of average diastolic pressures from 69 to 89 mmHg, antecubital vein plasma noradrenaline levels were related linearly (r = 0.86, P = 0.0001) to muscle sympathetic nerve activity. Neuropeptide Y levels increased proportionally with muscle sympathetic nerve activity during pressure reductions, but did not decline during pressure elevations. Our results suggest that in man, muscle sympathetic outflow is modulated finely by small changes of baroreceptor input, and that during pharmacologically induced changes of arterial pressure, changes of antecubital vein plasma noradrenaline concentrations provide excellent estimates of changes of sympathetic nerve traffic to skeletal muscle.     

Lack of interaction between adenosine-induced vasodilatation and carotid baroreflex-induced changes in sympathetic activity in dog hindlimb artery

In anaesthetized dogs, a hindlimb was vascularly isolated and perfused at a constant flow rate of 7.7 +/- 1.9 ml min-1 100 g-1 (mean +/- S.E.M.; n = 5) through the femoral artery. The carotid sinuses were isolated and perfused at high (greater than 145 mmHg) or low (less than 75 mmHg) pressure to enable reflex sympathetic tone on the hindlimb vessels to be controlled. Both vagi were sectioned in the neck and mean aortic blood pressure was held constant by connection of the aorta to a reservoir. The responses to infusion of three doses of adenosine at high and low carotid sinus pressures were not significantly different: infusion of 0.60 +/- 0.16 microM-adenosine reduced femoral arterial perfusion pressure (FAPP) by 11.6 +/- 3.2% (n = 6) at high carotid sinus pressure and by 12.6 +/- 5.1% (n = 4) at low carotid sinus pressure, while 4.71 +/- 0.49 microM-adenosine reduced FAPP by 20.8 +/- 4.8% (n = 6) at high carotid sinus pressure and by 20.7 +/- 4.8% (n = 6) at low carotid sinus pressure; 50.1 +/- 7.3 microM-adenosine reduced FAPP by 36.7 +/- 5.5% (n = 6) at high carotid sinus pressure and by 27.7 +/- 7.8% (n = 5) at low carotid sinus pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Carotid Sinus Nerve—Structure,Function, and Clinical Implications

Interest has been renewed in the anatomy and physiology of the carotid sinus nerve (CSN) and its targets (carotid sinus and carotid body, CB), due to recent proposals of surgical procedures for a series of common pathologies, such as carotid sinus syndrome, hypertension, heart failure, and insulin resistance. The CSN originates from the glossopharyngeal nerve soon after its appearance from the jugular foramen. It shows frequent communications with the sympathetic trunk (usually at the level of the superior cervical ganglion) and the vagal nerve (main trunk, pharyngeal branches, or superior laryngeal nerve). It courses on the anterior aspect of the internal carotid artery to reach the carotid sinus, CB, and/or intercarotid plexus. In the carotid sinus, type I (dynamic) carotid baroreceptors have larger myelinated A-fibers; type II (tonic) baroreceptors show smaller A- and unmyelinated C-fibers. In the CB, afferent fibers are mainly stimulated by acetylcholine and ATP, released by type I cells. The neurons are located in the petrosal ganglion, and centripetal fibers project on to the solitary tract nucleus: chemosensory inputs to the commissural subnucleus, and baroreceptor inputs to the commissural, medial, dorsomedial, and dorsolateral subnuclei. The baroreceptor component of the CSN elicits sympatho-inhibition and the chemoreceptor component stimulates sympatho-activation. Thus, in refractory hypertension and heart failure (characterized by increased sympathetic activity), baroreceptor electrical stimulation, and CB removal have been proposed. Instead, denervation of the carotid sinus has been proposed for the “carotid sinus syndrome.” Anat Rec, 302:575–587, 2019. © 2018 Wiley Periodicals, Inc.     

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.     

腓肠神经营养动脉皮瓣的应用解剖学研究

目的研究腓肠神经营养动脉的数量、发出位置、血管的直径,小隐静脉与腓肠神经的关系,为确定腓肠神经营养血管皮瓣提供解剖学基础。方法采用红色明胶经股动脉灌注的尸体20具(40侧),在手术显微镜下对腓肠神经营养动脉和小隐静脉进行解剖观察测量。结果腓肠神经营养动脉2～4支,各营养动脉形成血管网相互吻合,其中三支发出较为恒定。腓肠神经的上、中、下三段营养分别由上述三支动脉提供。在小腿下1/3段,小隐静脉与腓肠神经之间距离为1～5mm。腓肠神经旁组织含有与神经伴行的营养血管,其分支与皮下血管网相吻合,供应相应区域的皮瓣。结论手术时带少量神经旁筋膜组织可保证蒂部神经营养血管不被破坏。此皮瓣不损害重要血管和神经,供区比较隐蔽,可用于修复下肢远端皮肤及软组织缺损。     

The vasomotor component of the carotid sinus baroreceptor reflex in the cat during stimulation of the hypothalamic defence area

1. The effect of moderate intensities of stimulation of the hypothalamic defence area on the baroreceptor reflex has been investigated in the cat by comparing the responses of arterial blood pressure and perfusion pressure of the isolated hind-limb muscle bed perfused at constant volume inflow, when the isolated carotid sinus was subjected to a series of non-pulsatile pressures with and without simultaneous hypothalamic stimulation.2. In the absence of hypothalamic stimulation the characteristic sigmoid curves relating sinus pressure to blood pressure or muscle perfusion pressure were obtained.3. With simultaneous stimulation of the hypothalamus a similar sigmoid relationship was found. There was no evidence of any reduction in the over-all power or maximum sensitivity of the baroreceptor reflex.4. However, in those cats which had been atropinized to abolish the cholinergically mediated muscle vasodilatation, the curves obtained during hypothalamic stimulation were displaced in such a manner as to suggest that, while baroreceptor modulation of vasoconstrictor tone continued during defence area stimulation, the blood pressure regulating mechanism had been ;reset' so that, within the physiological range of sinus pressures, any given level of sinus pressure was associated with a greater vasoconstrictor tone.5. In non-atropinized cats there was little displacement of the curves relating sinus pressure to blood pressure, while the curves relating sinus pressure to muscle perfusion pressure were displaced in the opposite direction so that over-all muscle vascular resistance was less than normal at each level of sinus pressure.     

Mechanisms of cutaneous vasoconstriction during upright posture

The cutaneous circulation is thought to participate in the neurocirculatory adjustments during orthostatic stress, but the underlying mechanisms mediating such reflex cutaneous vasoconstriction are poorly understood. The aim of this study was to assess the relative importance of baroreceptor (cardiopulmonary and arterial) and positional (vestibular, exercise, veno-arteriolar and myogenic) reflexes in triggering cutaneous vasoconstriction during upright posture. First, hypotensive lower body negative pressure (LBNP) was compared with actual postural changes to assess the relative contributions of baroreceptor reflexes and positional reflexes. Then changes in body position were compared with changes in limb position in the absence or presence of proximal (axillary) or distal (local cutaneous) nerve blocks, to assess the relative contributions of vestibular, exercise, veno-arteriolar and myogenic reflexes. Skin sympathetic nerve activity was determined by microneurography, and skin blood flow was determined by laser Doppler velocimetry. LBNP of –50 mmHg (cardiopulmonary + arterial baroreceptors) had no effect on skin sympathetic nerve activity or skin vascular resistance. In contrast, an upright posture with the arms dependent (baroreceptor+vestibular+exercise+veno-arteriolar reflexes) caused a two- to threefold increase in skin vascular resistance. In the supine position, passive movement of the arm into a dependent position to activate veno-arteriolar reflexes alone evoked an increase in skin vascular resistance which approximated the response to normal upright posture. Blocking central sympathetic nerve impulses by application of an axillary blockade did not influence the cutaneous vasoconstrictor response to an upright posture or changes in limb position. In contrast, application of a distal nerve block by local cutaneous surface anaesthesia completely blocked vasoconstrictor responses evoked by these manoeuvres. In conclusion, these experiments in human subjects identify a primary role for veno-arteriolar reflexes in triggering vasoconstriction in the cutaneous circulation during upright posture.     

Evidence for the involvement in the baroreceptor reflex of a descending inhibitory pathway

1. The onset and time course of baroreceptor inhibition of pre- and post-ganglionic sympathetic reflex activity has been examined in the anaesthetized cat.2. The shortest time to the onset of inhibition of an intercostal evoked reflex response in cardiac and renal nerve was less than 90 msec following a rise in pressure in a carotid sinus blind sac, and around 55 msec following stimulation of the ipsilateral sinus nerve. The cardiac nerve response was completely inhibited before the renal nerve response.3. Because of the long delays in the somato-sympathetic reflex pathway it is argued that these minimum times will be much less than the real central delay of baroreceptor inhibition. These were estimated by adding on the central times for the somato-sympathetic reflexes to give latencies of 94-143 msec for the inhibition.4. A spinal sympathetic reflex was inhibited by 30-75% following a rise in pressure in a carotid sinus blind sac or sinus nerve stimulation. The minimum time for this inhibition was around 100 msec.5. The baroreceptor inhibition of the spinal sympathetic reflex was abolished following section of a restricted region in the dorsolateral part of the lateral funiculus of the cervical spinal cord.6. Both pre- and post-ganglionic reflexes could be inhibited when stimulating within three regions of the medulla oblongata. The latency to inhibition elicited from the ventromedial reticular formation was short, some 5-30 msec, whereas that elicited from a ventrolateral region or the mid line raphe nucleus was long, some 90-160 msec.7. The possibility is discussed that the baroreceptor inhibition of both the pre- and post-ganglionic reflexes examined in this study is occurring at the spinal level via a pathway from either the raphe nuclei or ventrolateral medulla.     

Time Course and Extent of Carotid Sinus Baroreceptor Threshold Resetting in Rats with Renovascular Hypertension

To study the extent and time course of arterial baroreceptor threshold resetting to increases in blood pressure, renal hypertension was induced in young normotensive male Wistar rats by unilateral renal artery constriction. At different intervals after operation the extent of baroreceptor threshold resetting in the carotid sinus was examined. Experiments were performed 7, 14 and 25 days after renal artery clipping to enable baroreceptor resetting to be correlated with the rate and extent of cardiovascular changes in rats which had renovascular hypertension of identical durations (Lundgren et al. 1974). Baroreceptor thresholds in the carotid sinuses were established by progressive clamping of both carotid arteries after partial vascular isolation of the sinuses. The results show that after one week of hypertension baroreceptor resetting is only just apparent but by two weeks resetting is gross and seems to be largely completed. This parallels the adaptive changes in the hindquarters of renal hypertensive rats and it is concluded that baroreceptor resetting is a secondary phenomenon related to the structural changes induced in the vessels by the elevated blood pressure.