Excitation of afferent cardiac sympathetic nerve fibres during myocardial ischaemia

1. Occlusion of the main left coronary artery of lightly anaesthetized cats provoked a pseudaffective reaction. The afferent pathway was in the cardiac sympathetic nerves.2. The compound action potential evoked in the inferior or middle cardiac nerves by stimulation of the thoracic sympathetic trunk contained two elevations, a small Adelta wave and a much larger sC wave. Occasionally a B wave was present.3. During coronary occlusion, the Adelta elevation was reduced by 35-55%, indicating afferent activity in these fibres. Multifibre preparations also showed increased afferent discharge during occlusion.4. It seems probable that the afferent activity in these fibres was mainly responsible for signalling the pseudaffective response elicited by coronary occlusion.5. Myocardial ischaemia produced by coronary occlusion was probably the stimulus for the increased activity.     

The innervation of sheep mesenteric veins

1. An isolated preparation of sheep mesenteric vein is described from which contractions of the longitudinal smooth muscle of the adventitia have been recorded in response to stimulation of intramural and periarterial nerves.2. The preparation did not respond to single stimuli but the relation between amplitude of response and frequency of stimulation was characteristic of that described for other smooth muscles innervated by sympathetic nerves.3. Responses were blocked by tetrodotoxin, guanethidine, and by a number of alpha-receptor blocking drugs. Responses to peri-arterial stimulation were unaffected by hexamethonium. It was concluded that the longitudinal smooth muscle is supplied with post-ganglionic noradrenergic motor nerves and the presence of such fibres in the adventitia was confirmed by fluorescence microscopy.4. Acetylcholine also caused contractions. Although a direct excitatory action on the smooth muscle could not be excluded, results suggest that acetylcholine may release noradrenaline from the axons of the sympathetic ground plexus.     

Respiratory responses to electrical stimulation of the cervical sympathetic nerves in decerebrate, unanaesthetized cats

1. The effects of respiration of electrical stimulation of the peripheral cut end of the cervical sympathetic nerve were studied in seventeen decerebrate, unanaesthetized cats.2. The tidal volume increased and the end-tidal CO(2) fell within 2-3 breaths after the onset of stimulation in fourteen cats.3. In three experiments tidal volume and respiratory rate fell during stimulation and increased above the control when the stimulus was interrupted.4. All respiratory responses to sympathetic stimulation were abolished after cutting the carotid sinus nerves and are attributed to activation of chemo- and baroreceptor afferents.5. With the carotid sinus nerves intact, respiratory responses could be eliminated completely only by cutting the post-ganglionic sympathetics that pass directly to the carotid body and the post-ganglionic sympathetics that join the glossopharyngeal nerves to course with the sinus nerves to the carotid bifurcation.6. Pentobarbitone (10 mg/kg) or chloralose (40 mg/kg) given intravenously depressed spontaneous ventilation and responses to sympathetic nerve stimulation.7. Stimulation changed blood pressure slightly in fourteen experiments; in ten it fell and in four it increased 10 mm Hg or less. After pentobarbitone or chloralose, stimulation elicited a pronounced pressor response.8. The results of the study indicate that activation of sympathetic pathways to the carotid body constitutes an effective stimulus to ventilation.     

Electrical and mechanical response of arteries to stimulation of sympathetic nerves

1. When common carotid arteries of sheep were studied in vitro by the sucrose-gap method, application of acetylcholine or nicotine caused small irregular spikes of depolarization. The discharge was prevented by hexamethonium, Hydergine, phentolamine, or chronic denervation, indicating that it represented electrical activity of groups of smooth muscle cells induced by the stimulation of sympathetic nerve fibres.2. The size of spikes produced by acetylcholine or nicotine, together with counts of the total number of smooth muscle cells in cross-sections of the arterial strips, indicated that the larger groups of smooth muscle cells activated by one sympathetic nerve fibre contained approximately 1300 cells.3. Sections of arteries treated with hot formaldehyde vapour contained numerous fluorescent fibres which were intensified by previous injection of noradrenaline into the animal and were scanty or absent after chronic sympathetic denervation. They are therefore believed to be post-ganglionic sympathetic nerve fibres.4. Most of these fibres ran circularly in the outer (1/2)-(3/4) of the media. A few ran longitudinally in the adventitia. There were none in the inner (1/4)-(1/2) of the media.5. Electrical stimulation of the cervical sympathetic nerve of anaesthetized sheep caused large contractions of the common carotid artery of the same side, reducing its external diameter by 30-39%.     

Cardiac sympathetic adrenergic pathways in which synaptic transmission is blocked by atropine sulphate

1. Stimulation of the thoracic sympathetic nerve trunk caused a rise in arterial blood pressure and heart rate which was reduced but not abolished during the infusion of hexamethonium chloride, pentolinium tartrate, mecamylamine or tetraethylammonium chloride.

2. Preganglionic stimulation no longer elicited a synchronous sC elevation in the post-ganglionic nerves. The persistent blood pressure and heart rate response was associated with an asynchronous discharge in these nerves.

3. Both the persistent response and the asynchronous discharge were abolished by the intravenous injection of atropine sulphate in doses of 30 μg/kg.

4. Atropine had no effect on spike amplitude or shape, conduction velocity or frequency response in either the pre- or post-ganglionic nerve trunks. Nor did it affect the rise in blood pressure and heart rate evoked by stimulation of the post-ganglionic cardiac sympathetic nerves.

5. It is concluded that atropine partially blocked synaptic transmission in cardiac sympathetic adrenergic pathways.

     

Effects of sympathetic stimulation on C-fibre responses in rabbit

Unmyelinated C-fibre responses to electrical stimulation were recorded in common peroneal, sural and tibial nerves of rabbits. Three distinct C elevations, here called C1, C2 and C3, were recorded. C2 is probably of somatic origin because it was depressed due to collision by peripheral stimulation of cutaneous receptors. The conduction velocity of C3 corresponded to that of sympathetic post-ganglionic fibres. During sympathetic trunk stimulation the A-fibre responses were not significantly changed while C responses, especially C2, were reduced in amplitude and slightly delayed. The C-fibre responses were also influenced by intra-arterial infusion of noradrenaline. In most cases, the latency of the response was increased. The effect of sympathetic stimulation was completely blocked by hexamethonium, and partly blocked by phentolamine, an adrenergic alpha-receptor blocking agent which also blocked the effect of noradrenaline. The findings suggest that there are adrenergic receptors distributed along unmyelinated somatic afferent fibres. Sympathetic activity may release noradrenaline in the peripheral nerve, resulting in changed conductive properties in unmyelinated fibres transmitting sensory information.     

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.     

The activity of post-ganglionic sympathetic nerves to the uterus of the rabbit

1. The spontaneous activity recorded from the central ends of the uterine nerves of the rabbit is described. The discharges resembled those reported from other post-ganglionic sympathetic nerves; the individual units appeared to discharge remarkably regularly at frequencies between 4/sec and 1 per 3 sec.2. The resting discharge in late pregnant rabbits was usually more intense than in non-pregnant rabbits; otherwise no clear relation existed between variations in the discharges and in the sexual state.3. The discharge was reduced by stimulation of the central end of the depressor nerve and increased by asphyxia.4. Stimulation of either the preganglionic or the post-ganglionic nerve by a single shock evoked a long after-discharge in the post-ganglionic nerve. It is shown that this after-discharge is a property of some of the post-ganglionic neurones supplying the rabbit's uterus which does not depend on the integrity of the preganglionic nerves or of the spinal cord, or on transmission through the ganglia, and that it is not a general property of the sympathetic post-ganglionic neurones of the rabbit.5. Repetitive stimulation of the preganglionic nerve at low frequencies augmented the after-discharge in some cases and depressed it in others; stimulation at high frequencies invariably depressed the after-discharge. Repetitive stimulation of the post-ganglionic nerve at low or high frequencies depressed the after-discharge.6. If the normal preganglionic activity was interrupted abruptly by an anode block, the post-ganglionic discharge also stopped abruptly.7. A ganglion-stimulating action of hexamethonium is described.8. Adrenaline inhibited the post-ganglionic neurones with no sign of excitation. This effect was antagonized by Rogitine without affecting the resting discharge, the action of the depressor nerve or the after-discharge in any way.     

The inhibitory innervation of the taenia of the guinea-pig caecum

1. The inhibitory innervation of the taenia of the guinea-pig caecum has been studied, after blocking the responses to stimulation of excitatory cholinergic nerves with atropine.

2. Stimulation of the perivascular nerves supplying the taenia caused relaxations. These nerves had properties which were typical of sympathetic post-ganglionic adrenergic nerves. The relaxations caused by stimulation were maximal at frequencies of stimulation above 30 pulses/sec and they were abolished by bretylium, guanethidine and 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP).

3. The taenia is also innervated by intramural inhibitory nerves with their cell bodies in Auerbach's plexus. These nerves can be excited by electrical stimulation of the taenia or by the application of ganglion-stimulating drugs.

4. The intramural inhibitory nerves have different properties from sympathetic adrenergic nerves. Relaxations in response to stimulation were maximal with frequencies of stimulation of about 5 pulses/sec and they were not blocked by bretylium, guanethidine or DMPP.

5. Preganglionic cholinergic fibres in the caecal wall make synaptic connexions with the intramural inhibitory neurones.

6. The role of the intramural inhibitory neurones in intestinal activity and their possible connexions with the central nervous system have been discussed.

     

Reflex respiratory and cardiovascular effects of stimulation of receptors in the nose of the dog

1. In forty-one out of forty-seven dogs under chloralose-urethane or Nembutal anaesthesia, mechanical stimulation of the nasal mucous membrane caused a reduction or inhibition of respiration, bradycardia, variable changes of arterial blood pressure, and a small rise in venous pressure.2. Simultaneous measurements of arterial and venous pressures, and also of blood flow in various arteries by means of an electromagnetic flowmeter indicate that the calculated vascular resistance increases in the intact limb, muscle, and skin, and the vascular beds of the vertebral, superior mesenteric, renal and splenic arteries. No changes in vascular resistance occur in the common carotid circulation.3. Evidence is presented that the increase in vascular resistance is due to vasoconstriction, and occurs in the absence of changes in pulmonary ventilation.4. Stimulation of the nasal mucous membrane causes a reduction in volume of the spleen.5. The respiratory and cardiovascular responses are reflex in nature, being abolished by the application of a local anaesthetic to the nose or by combined division of the maxillary and ethmoidal branches of the trigeminal nerves. The cardiac response is mediated largely by the vagus nerves, and the vascular responses by sympathetic adrenergic fibres.6. Cessation of the stimulus to the nose not infrequently results in the following temporary after-effects: hyperventilation, tachycardia, hypertension, and vasodilatation in the intact limb and in muscle.     

Effects of Drugs and Nerve Stimulation on the Spleen and Arteries of Two Species of Dogfish,Scyliorhinus canicula and Squalus acanthias

The effects of drugs and nerve stimulation on the spleen of 2 species of dogfish have been examined by experiments with perfused spleens and isolated spleen and artery strips. Adrenaline, noradrenaline and phenylephrine, acting via alpha adrenoceptors, constrict the perfused spleen of both species, thereby releasing erythrocytes, and contract the isolated spleen and artery strips. Phentolamine competitively antagonizes the excitatory effects of adrenergic agonists. The responses of the spleen to acetylcholine are very irregular, and a rapid desensitization makes evaluation of the mode of action of this drug difficult. In the artery strips acetylcholine produces a dose-dependent contraction. Fluorescent histochemistry reveals well developed adrenergic innervation of the arteries, and a few adrenergic terminals in the spleen. Stimulation of splenic nerves produces normally splenoconstriction in Squalus, which can be blocked by phentolamine but not by atropine. The nervous control of the Scyliorhinus spleen seems to be poor or lacking. It is concluded that the dogfish spleen, and maybe also the arteries, are to a large extent controlled by circulating catecholamines and (in Squalus) also by sympathetic adrenergic fibres.     

Sympathetic Nerves Inhibit Conducted Vasodilatation Along Feed Arteries during Passive Stretch of Hamster Skeletal Muscle

Ascending vasodilatation is integral to blood flow control in exercising skeletal muscle and is attributable to conduction from intramuscular arterioles into proximal feed arteries. Passive stretch of skeletal muscle can impair muscle blood flow but the mechanism is not well understood. We hypothesized that the conduction of vasodilatation along feed arteries can be modulated by changes in muscle length. In anaesthetized hamsters, acetylcholine (ACh) microiontophoresis triggered conducted vasodilatation along feed arteries (diameter, 50-70 μm) of the retractor muscle secured at 100 % resting length or stretched by 30 %. At 100 % length, ACh evoked local dilatation (> 30 μm) and this response conducted rapidly along the feed artery (14 ± 1 μm dilatation at 1600 μm upstream). During muscle stretch, feed arteries constricted ≈10 μm (   P < 0.05  ) and local vasodilatation to ACh was maintained while conducted vasodilatation was reduced by half (   P < 0.01  ). Resting diameter and conduction recovered upon restoring 100 % length. Sympathetic nerve stimulation (4-8 Hz) produced vasoconstriction and attenuated conduction in the manner observed during muscle stretch, as did noradrenaline or phenylephrine (10 nM). Inhibiting nitric oxide production ( N ^ω-nitro-L-arginine, 50 μM) produced similar vasoconstriction yet had no effect on conduction. Phentolamine, prazosin, or tetrodotoxin (1 μM) during muscle stretch abolished vasoconstriction and restored conduction. Inactivation of sensory nerves with capsaicin had no effect on vasomotor responses. Thus, muscle stretch can attenuate conducted vasodilatation by activating α-adrenoreceptors on feed arteries through noradrenaline released from perivascular sympathetic nerves. This autonomic feedback mechanism can restrict muscle blood flow during passive stretch.     

Sympathetic nerve activation decreases the release of vasoactive intestinal polypeptide from the feline intestine

The splanchnic nerves to the small intestine were stimulated in anaesthetized cats. Activation of the sympathetic nerves caused vasoconstriction, increased net fluid absorption and decreased release of vasoactive intestinal polypeptide (VIP) in the small intestine. In the colon, parasympathetic nerve stimulation elicited vasodilatation and increased release of VIP. Additional stimulation of the sympathetic lumbar colonic nerves decreased the colonic blood flow and inhibited the release of VIP. These effects of the stimulation of the lumbar colonic nerves were blocked by phentolamine. It is concluded that, in the feline intestine, sympathetic nerve stimulation presynaptically decreased the release of VIP via an alpha-adrenergic mechanism.     

Contrasting reflex influences of cardiac afferent nerves during coronary occlusion

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

Correlation of the directly observed responses of mesenteric vessles of the rat to nerve stimulation and noradrenaline with the distribution of adrenergic nerves

1. The effects of nerve stimulation and of the topical application of noradrenaline on arteries, capillaries and veins of the mesentery of the anaesthetized rat were examined by direct observation under a microscope. The distribution of adrenergic nerves to the vessels of the mesentery was studied using the fluorescence histochemical method.2. Principal arteries, small arteries and terminal arterioles were all innervated by a network of adrenergic fibres and they all constricted in response to the stimulation of paravascular nerves and to exogenous noradrenaline. Few adrenergic fibres accompanied the smaller, precapillary arterioles; these vessels did not respond to nerve stimulation, although they were constricted by concentrations of noradrenaline as low as 10(-10) g/ml.3. The capillaries did not respond to nerve stimulation or to applied noradrenaline. All veins were constricted by noradrenaline, but only those veins greater than about 30 mum in internal diameter responded to nerve stimulation.4. At stimulus frequencies greater than 4 Hz the flow of blood through the microvasculature usually ceased, although there was never complete closure of these vessels. The maximum constriction observed in principal arteries was usually between 50 and 70% of the control internal diameter, and in small arteries and terminal arterioles was between 40 and 65% of the control internal diameter.5. It is concluded that the principal arteries and small arteries of the mesenteric vasculature are important in the control of blood flow through this vascular bed during sympathetic stimulation and following topical application of noradrenaline, and that the precapillary arterioles are important vessels determining the rate of blood flow through the capillary bed under resting conditions.     

Effects of drugs and nerve stimulation on the spleen and arteries of two species of dogfish, Scyliorhinus canicula and Squalus acanthias.

The effects of drugs and nerve stimulation on the spleen of 2 species of dogfish have been examined by experiments with perfused spleens and isolated spleen and artery strips. Adrenaline, noradrenaline and phenylephrine, acting via alpha adrenoceptors, constrict the perfused spleen of both species, thereby releasing erythrocytes, and contract the isolated spleen and artery strips. Phenotolamine competitively antagonizes the excitatory effects of adrenergic agonists. The responses of the spleen to acetylcholine are very irregular, and a rapid desensitization makes evaluation of the mode of action of this drug difficult. In the artery strips acetylcholine produces a dose-dependent contraction. Fluorescent histochemistry reveals well developed adrenergic innervation of the arteries, and a few adrenergic terminals in the spleen. Stimulation of splenic nerves produces normally splenoconstriction in Squalus, which can be blocked by phentolamine but not by atropine. The nervous control of the Scyliorhinus spleen seems to be poor or lacking. It is concluded that the dogfish spleen, and maybe also the arteries, are to a large extent controlled by circulating catecholamines and (in Squalus) also by sympathetic adrenergic fibres.     

Synaptically mediated potentials elicited by the stimulation of post-ganglionic trunks in the guinea-pig superior cervical ganglion

Summary Stimulation of a post-ganglionic nerve trunk (internal carotid nerve) leads to synaptic activation of the majority of the sympathetic neurons in the superior cervical ganglion of the guinea-pig. Curarization of the ganglion and the section of the cervical sympathetic trunk eliminate any sign of synaptic activation in the ganglion cells produced by stimulating the internal carotid nerve. Stimulation of other post-ganglionic nerve trunks (superior cardiac nerve) gives rise only to pure antidromic responses in the cells. A compound action potential of considerable amplitude, which is completely cancelled by curarization of the ganglion, may be led off from the superior cardiac nerve after stimulating the internal carotid nerve; no propagated potential in the opposite direction was recorded at all. The conclusion is drawn that pre-ganglionic fibres projecting into the internal carotid nerve give rise to an elaborate system of collateral endings impinging onto most of the ganglion neurons and are responsible for synaptic activation of the ganglion cells observed after stimulating post-ganglionic nerves. The characteristics of action potentials evoked antidromically in the sympathetic neurons are also described.     

The influence of the pelvic nerves on anorectal motility in the cat

The influence of the parasympathetic pelvic nerves on anorectal motility was studied in anaesthetized cats. Anal pressure and rectal motility were recorded by a manometric and a volumetric method, respectively. Severing of the pelvic nerves did not cause any pressure change in the anus, indicating that these nerves are not significantly tonically active. Efferent low intensity (0.05-0.5 ms, 8 V at 5 Hz) electrical stimulation of the pelvic nerves (PNS) elicited a contraction of the internal anal sphincter (IAS), while high intensity stimulation (greater than 1 ms, 8 V at 5 Hz) caused a sphincter relaxation. A rectal contraction was noted on both low and high intensity stimulation. After sectioning of the sympathetic nerves, PNS elicited a contraction in both the anus and the rectum irrespective of stimulation intensity. PNS inhibited the anal contraction elicited by simultaneous stimulation of the sympathetic nerves or noradrenaline infusion. The inhibitory anal responses to PNS were unaffected or augmented by atropine, unaffected by propranolol and abolished by hexamethonium. The excitatory anal effects of PNS were reduced or abolished by atropine and abolished by phentolamine. The rectal contraction induced by low intensity PNS was abolished by atropine or converted to a relaxation. In half of the experiments an atropine resistant rectal contraction was observed in response to high intensity PNS. The results are consistent with a pelvic nerve influence on IAS pressure through several mechanisms, including modulation of the activity in the sympathetic nerves and activation of inhibitory non-adrenergic, non-cholinergic neurons. The pelvic nerves convey both cholinergic and non-cholinergic excitatory, as well as non-adrenergic, non-cholinergic inhibitory fibres to the rectum.     

The influence of the pelvic nerves on. anorectal motility in the cat

The influence of the parasympathetic pelvic nerves on anorectal motility was studied in anaesthetized cats. Anal pressure and rectal motility were recorded by a manometric and a volumetric method, respectively. Severing of the pelvic nerves did not cause any pressure change in the anus, indicating that these nerves are not significantly tonically active. Efferent low intensity (0.05–0.5 ms, 8 V at 5 Hz) electrical stimulation of the pelvic nerves (PNS) elicited a contraction of the internal anal sphincter (IAS), while high intensity stimulation (> 1 ms, 8 V at 5 Hz) caused a sphincter relaxation. A rectal contraction was noted on both low and high intensity stimulation. After sectioning of the sympathetic nerves, PNS elicited a contraction in both the anus and the rectum irrespective of stimulation intensity. PNS inhibited the anal contraction elicited by simultaneous stimulation of the sympathetic nerves or noradrenaline infusion. The inhibitory anal responses to PNS were unaffected or augmented by atropine, unaffected by propranolol and abolished by hexamethonium. The excitatory anal effects of PNS were reduced or abolished by atropine and abolished by phentolamine. The rectal contraction induced by low intensity PNS was abolished by atropine or converted to a relaxation. In half of the experiments an atropine resistant rectal contraction was observed in response to high intensity PNS. The results are consistent with a pelvic nerve influence on IAS pressure through several mechanisms, including modulation of the activity in the sympathetic nerves and activation of inhibitory non-adrenergic, non-cholinergic neurons. The pelvic nerves convey both cholinergic and non-cholinergic excitatory, as well as non-adrenergic, noncholinergic inhibitory fibres to the rectum.     

The role of the cervical sympathetic nerve in the regulation of oxygen consumption of the carotid body of the cat

1. Carotid body blood flow (c.b.f.) and carotid arterial-carotid body venous oxygen (A-V O(2)) difference were measured and carotid body oxygen consumption calculated in twenty-six cats anaesthetized with pentobarbitone sodium, paralysed with gallamine triethiodide and ventilated mechanically.2. With the sinus nerves intact and with blood gas tensions and carotid sinus pressure within physiological limits, section of either the pre- or post-ganglionic cervical sympathetic nerve on the same side caused an average rise in c.b.f. of 9.2 mul./min, in A-V O(2) difference of 0.09 ml./100 ml. and in carotid body oxygen consumption of 0.075 mul./min.3. When the pre- or post-ganglionic cervical sympathetic nerves were stimulated, c.b.f. and A-V O(2) difference fell. The fall in c.b.f. was enhanced at high P(a, CO2); the fall in A-V O(2) difference and in calculated oxygen consumption was enhanced at low mean arterial pressure (M.A.P.) or P(a, O2).4. Following sympathectomy, a reduction of M.A.P. at constant P(a, O2) and P(a, CO2) caused a fall in c.b.f. and a commensurate rise in A-V O(2) difference so that carotid body oxygen consumption remained approximately constant.5. When P(a, O2) was altered over the range 35 to > 400 mm Hg, or P(a, CO2) over the range 27-70 mm Hg at constant M.A.P., c.b.f. changed by amounts which were similar to those observed when the sympathetic nerves were intact and A-V O(2) difference changed in the opposite direction so that carotid body oxygen consumption similarly remained constant.6. Comparison of these results with those observed when the sympathetic nerves were intact indicates that the sympathetic nerves exert a vasoconstrictor effect upon carotid body blood vessels over a wide range of blood gas tensions and arterial pressure and that they also tend to diminish the rate of carotid body oxygen consumption. The mechanisms which may be involved in this regulation are discussed.