Fall In Arterial Blood Pressure Research Articles

Fall in blood pressure produced from discrete regions of the ventral surface of the medulla by glycine and lesions

1. In cats anaesthetized with pentobarbitone sodium, atropinized by i.v. atropine methyl nitrate and artificially ventilated, experiments were carried out (a) to localize the site where glycine acts on the ventral surface of the medulla when, on topical application through paired Perspex rings caudal to the trapezoid bodies, it produces a fall in arterial blood pressure, (b) to compare the effects of uni- and bilateral application, and (c) to study the blood pressure effects produced by electrolytic lesions of the glycine-sensitive areas.2. Blood pressure fell only a little on unilateral application of glycine through one of the Perspex rings, but a pronounced fall occurred on its bilateral application. The fall was too large to be explained by two minimal responses added together. Thus the application of glycine to one side potentiated the depressor effect of glycine applied to the other side.3. By moving the paired Perspex rings rostrally or caudally to different positions on the medulla and determining for each position the effectiveness of glycine, the glycine-sensitive areas were found to be restricted to a 1.5 mm wide strip situated 1-2.5 mm caudal to the trapezoid bodies. By making electrolytic lesions within the limits of this strip the glycine-sensitive areas were found to be not wider than 1.5 mm in the mediolateral direction and to be situated about 4 mm lateral to the mid line. Histologically, such lesions involved the cells of the parvicellular part of the lateral reticular nucleus.4. Placing an electrode, with a diameter of 1 mm, under light pressure on the glycine-sensitive area produced a short-lasting steep rise in blood pressure. The same effect was produced when a current was passed through the electrode to destroy the underlying tissue, but after its destruction the passage of current no longer produced the pressor effect.5. Once the glycine-sensitive area of one side was destroyed, glycine applied to the destroyed area through one of the Perspex rings no longer produced its small depressor effect, but when applied to the intact area of the other side, a pronounced fall in blood pressure occurred. Thus unilateral destruction had the same effect as unilateral glycine application. It potentiated the depressor effect of glycine applied to the other side.6. Following unilateral destruction of the glycine-sensitive area there was only a small fall in blood pressure; following its bilateral destruction blood pressure fell to a low level.7. It is concluded that the cells in the small circumscribed glycine-sensitive areas on the ventral surface of the medulla may play a key role in the maintenance of arterial blood pressure and that the cells of one side are sufficient for this function.

Renin, aldosterone, body fluid volumes, and the baroreceptor reflex in the development and reversal of Goldblatt hypertension in conscious dogs.

The renal artery to a sole remaining kidney was constricted in unanesthetized dogs while renal arterial pressure was recorded distal to the occluder. Following the constriction, mean arterial blood pressure, which was continuously monitored 24 hours a day for 1 week, exhibited a biphasic increase. The first peak in pressure correlated with a large increase in plasma renin activity; the second peak correlated with an increase in plasma volume brought about by positive sodium and water balances. Renin activity was returning to normal when the second peak occurred. Increased drinking played a major role in the positive water balance. Plasma aldosterone concentration was moderately and transiently increased for only a few hours following the constriction. The experiment was repeated in sinoaortic baroreceptor-denervated dogs; apparently, the baroreceptor reflex significantly slows the time course of the arterial blood pressure increase during the first few days of constriction but does not alter the magnitude of the pressure increase after 1 week. After release of renal artery constriction, mean arterial blood pressure decreased progressively over a 3-day period, during which time significant negative sodium and fluid balance occurred. The slow return of the pressure back to normal correlated highly with a decrease in plasma volume. In the baroreceptor-denervated dogs, the initial fall in arterial blood pressure apparently also resulted at least partly from a decrease in plasma renin activity, but this effect was not observed in the intact dogs because the renin activities in these dogs had already decreased to normal prior to constrictor release. The effects of the baroreceptor reflex on the time course of the pressure decrease did not seem to be as significant as those on the time course of the pressure increase.

A CENTRAL VASODEPRESSOR EFFECT OF DYFLOS

1 Cats were anaesthetized with pentobarbitone sodium and atropinized peripherally by intravenous injection of atropine methyl nitrate; the effect was examined of topical bilateral application of dyflos to the ventral surface of the medulla oblongata at a region lateral to the pyramids and caudal to the trapezoid bodies. Dyflos was applied by means of perspex rings; the volume of fluid placed in each ring was 10 mul.2 The topical application of dyflos (1-20 mg/ml) produced a fall in arterial blood pressure without changes in heart rate and, in experiments without artificial ventilation, tachypnoea with dissociation of thoracic and abdominal respiration.3 Atropine methyl nitrate (50 mg/ml) applied topically in the same way as dyflos, prevented or abolished its vasodepressor effect.4 The two reactivators of acetylcholinesterase, obidoxime (100-200 mg/ml) and pralidoxime mesylate (100-200 mg/ml), applied topically in the same way as dyflos, abolished its vasodepressor effect. The reactivator compound 30 (100 mg/ml), also a pyridinium aldoxime, did not have this effect.5 Obidoxime and pralidoxime mesylate also reversed the vasodepression produced by carbachol applied to the ventral surface of the brain stem but not the vasodepression produced by glycine similarly applied.6 The problem is discussed as to whether the reversal of the dyflos and carbachol-induced vasodepression by obidoxime and pralidoxime is due to acetylcholinesterase reactivation by dephosphorylation and decarbamylation respectively, to a central atropine-like action of these compounds or to a combination of both.

Equinatoxin, a lethal protein from Actinia equina—II. Pathophysiological action

Effects of lethal doses of a toxic protein from Actinia equina were studied on anesthetized rats. The electrical activity of the phrenic nerves, the respiratory movements, the mechanical activity of the heart, the ECG, and the arterial blood pressure on intact, vagotomized and artificially respired animals were recorded. Shortly (15–50 sec) after beginning the i.v. injection of equinatoxin, the trains of action potentials in the phrenic nerve disappeared and respiration stopped. Bradycardia was observed, indicating elevated vagal tone. A transient fall of arterial blood pressure in vagotomized and in intact animals was registered for 10–15 sec, simultaneously with the block of respiration; thereafter an elevation of arterial blood pressure was registered for 3–7 min. The elevation of the arterial blood pressure was also observed in artificially respired animals. No spontaneous respiratory movements were registered during the period of elevated arterial blood pressure. The diaphragm remained excitable when stimulated indirectly via the phrenic nerve. Conduction disturbances, ectopic foci, myocardial ischemia, negative inotropic and negative chronotropic actions were followed on the ECG and on the in situ exposed heart.

Prevention of heart failure in dogs during arterial hypoxaemia by means of intra-aortic balloon pumping.

<h2>Abstract</h2> In dogs intra-aortic balloon pumping (IABP) under control conditions resulted in a significant decrease of cardiac and stroke work index, systolic aortic pressure, and diastolic aortic pressure, and dpdtmax. After continuous circulatory breakdown during cardiogenic shock conditions the progressive fall in arterial blood pressure,dpdt values, and stroke volume, and the continuous rise in left ventricular end diastolic pressure and pulmonary artery pressure was interrupted by means of IABP, and values remained at their levels for the period of observation for 20 min or were slightly improved. In contrast, interruption of IABP resulted in circulatory breakdown within 2–7 min. However, repetitive IABP treatment, started early enough with an arterial pressure above 60-mmHg, was able to restore cardiac haemodynamics in most instances. In accordance with other investigators, we conclude that IABP reduced the energy demand of myocardium. However, maximal benefit of this cirulatory assistance device can be expected only if IABP is initiated early enough.

Hemodynamic effects of group A Streptococcus mucopeptide.

Streptococcal cell wall mucopep–tide administered intravenously to experimental animals provoked marked circulatory changes. A fall of arterial blood pressure and a decrease of cardiac output were observed. These changes are similar to those reported after the administration of bacterial lipopoly–saccharide. Some evidence suggests that both a direct effect of mucopeptide on sensitive structures and a release of pharmacologically active substances may play a role in the hemodynamic disturbances. On the other hand, the central nervous system probably plays no important role in the circulatory effect of the mucopeptide.

Localization of the central cardiovascular action of clonidine.

1. The fall in arterial blood pressure with bradycardia that occurs on injection of clonidine into the cerebral ventricles and into the cisterna magna is attributed to an action on ;chemosensitive zones' situated at the ventral surface of the brain stem. This conclusion is based on the following results obtained in cats anaesthetized with pentobarbitone sodium.2. The fall in blood pressure no longer occurs on injection of clonidine (10 to 100 mug) into the cerebral ventricles when the passage of clonidine into the subarachnoid space is prevented by cannulation of the aqueduct. In this condition, the injections produce instead a rise in blood pressure.3. Applied bilaterally, by means of perspex rings, to the ventral surface of the brain stem, clonidine (10 mul of a 50 to 1,000 mug/ml solution placed in each ring) produces a fall in blood pressure with bradycardia, but only when the perspex rings cover the ;chemosensitive zones' from which changes in blood pressure and heart rate are obtained with various drugs.

Differential sympathetic response during coronary occlusion.

Occlusion of the circumflex branch of the left coronary artery in rabbits induces a differential response of regional sympathetic activity. The discharges of the splanchnic nerve are increased, and the discharges of a sympathetic nerve twig to the ear are inhibited. This pattern of sympathetic response is accompanied by a fall in arterial blood pressure.

Respiratory and cardiovascular responses resulting from intravenous injection of sheep hydatid cyst fluid to dogs

Effects of intravenous injection of sheep hydatid cyst fluid on respiratory and cardiovascular systems were studied in sodium pentobarbital-anesthetized dogs. Under sterile conditions, the fluid was drawn from the liver and lung hydatid cysts of sheep, and centrifuged for 20 min at 500 g. The supernatant fluid was used as the test solution. In a majority of animals, administration of 5 ml of the cyst fluid caused a sharp fall in arterial blood pressure, with or without respiratory changes. The latter, when present, included temporary cessation of respiration followed by rapid shallow breathing. There was usually an increase in the heart rate as the arterial blood pressure dropped. Atropine, 0.5 mg/kg body wt, given subcutaneously prior to the cyst fluid administration, did not block the responses. Cardiovascular responses produced by intravenous injection of cyst fluid were similar in dogs with positive pressure breathing and with spontaneous breathing. In 7 out of 10 responsive dogs, pretreatment with the antihistamine, chlorpheniramine, abolished the respiratory and cardiovascular responses.

Action and metabolism of bradykinin in dog lung.

ArticleAction and metabolism of bradykinin in dog lung.B W Levine, R C Talamo, and H KazemiB W Levine, R C Talamo, and H KazemiPublished Online:01 Jun 1973https://doi.org/10.1152/jappl.1973.34.6.821MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByLung Circulation15 March 2016Role of NO and EDHF-mediated endothelial function in the porcine pulmonary circulation: Comparison between pulmonary artery and veinVascular Pharmacology, Vol. 44, No. 3Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbitY. Wang, G. Soukhova, M. Proctor, J. Walker, and J. Yu1 July 2003 | Journal of Applied Physiology, Vol. 95, No. 1Evidence for specific regional patterns of responses to different vasoconstrictors and vasodilators in sheep isolated pulmonary arteries and veins10 February 2009 | British Journal of Pharmacology, Vol. 121, No. 3Cyclophilin-facilitated bradykinin inactivation in the perfused rat lungBiochemical Pharmacology, Vol. 50, No. 12Beneficial Effects of a Bradykinin Antagonist in a Model of Gram-Negative SepsisThe Journal of Trauma: Injury, Infection, and Critical Care, Vol. 39, No. 1Afferent pathways involved in reflex regulation of airway smooth musclePharmacology & Therapeutics, Vol. 42, No. 1The kallikrein kinin system in pulmonary lavage fluid of reserpinized ratsPharmacological Research Communications, Vol. 20, No. 8Attenuation of arterial blood pressure fall in endotoxin shock in the rat using the competitive bradykinin antagonist Lys-Lys-[Hyp2, Thi5,8, DPhe7]-Bk (B4148)19 July 2012 | British Journal of Pharmacology, Vol. 94, No. 2Cellular and humoral mediators of pulmonary edemaLung, Vol. 163, No. 1Afferent vagal C fibre innervation of the lungs and airways and its functional significance21 June 2005The adult respiratory distress syndromeDisease-a-Month, Vol. 27, No. 4Method for Measurement of Human Urinary Kininase Activity22 October 2012Effects of Kinins on Organ SystemsKininasesBradykinin RadioimmunoassayRole of prostaglandins in alveolar hypoxic vasoconstrictionRespiration Physiology, Vol. 29, No. 2Plasma Factors: The Hageman-Factor-Dependent Pathways and the Complement SequenceBRADYKININASE AND CONVERTING ENZYME IN LUNG More from this issue > Volume 34Issue 6June 1973Pages 821-6 https://doi.org/10.1152/jappl.1973.34.6.821PubMed4711592History Published online 1 June 1973 Published in print 1 June 1973 Metrics

Blood pressure effects obtained by drugs applied to the ventral surface of the brain stem.

1. In cats anaesthetized with pentobarbitone sodium the effect on arterial blood pressure was examined of substances applied bilaterally to the exposed ventral surface of the brain stem by means of Perspex rings placed lateral to the pyramids and caudal to the trapezoid bodies. Routinely, atropine methyl nitrate, which does not pass the blood-brain barrier, was injected I.V.2. The cholinomimetic substances carbachol and physostigmine, and the amino acids glycine and GABA, caused a fall in arterial blood pressure.3. Atropine produced a small but definite rise in arterial blood pressure, antagonized the depressor effects of the cholinomimetic substances, but not those of the amino acids.4. Strychnine, leptazol and tubocurarine, caused a rise in arterial blood pressure.5. The depressor and pressor effects are due to changes in vasomotor tone. They are central effects brought about by penetration of the substances into the brain tissue from the ventral surface of the brain stem. They are not due to their absorption into the blood stream.6. The depressor effects of the cholinomimetic substances may imitate the action of cholinergic neurones, and those of the amino acids that of central inhibitory neurones ending on cells near the ventral surface of the brain stem and exerting an inhibitory influence on vasomotor tone. The pressor effects of strychnine and tubocurarine may in part result from ;disinhibition', i.e. from an antagonistic action produced by these drugs on the amino acids released from the central inhibitory neurones.

Failure of intracoronary nitroglycerin to alleviate pacing-induced angina.

Relief of angina by nitroglycerine has been attributed to two possible mechanisms: (1) Increase in myocardial blood supply by direct action of the drug on the coronary arteries. (2) Reduction in myocardial oxygen demand by action of the drug on the systemic circulation. Sublingual application of nitroglycerin in previous studies did not allow the ruling out of the operation of either or both mechanisms. This study was, therefore, designed in such a way that the effect of the direct action of nitroglycerin on the coronary bed on angina could be studied in the absence of changes in the systemic circulation. In 25 patients undergoing cardiac catheterization and coronary arteriography as possible candidates for revascularization surgery, nitroglycerin, 0.075 mg in 1 ml of 5% dextrose, was injected into the left coronary artery through the angiographic catheter during angina pectoris induced by pacing. Coronary sinus blood flow by the continuous thermodilution method, femoral artery blood pressure, and lead V 5 were recorded continuously. In 20 patients the procedure was repeated with injection into the right coronary artery. In none of the 25 patients did the intracoronary injection of nitroglycerin alleviate the angina during the 1-min observation period, whether injected into the obstructed artery or into the artery supplying collaterals to the obstructed artery. The intracoronary injection was ineffective despite a significant increase in coronary sinus blood flow in 14, lasting 26 sec on the average. This suggests that the increase in blood flow did not occur in the ischemic areas where it was needed, but in other areas where the arterioles were not maximally dilated by ischemia. This explanation is further supported by the fact that in five patients with very severe restriction of the left coronary artery system the coronary sinus blood flow failed to increase in response to intracoronary nitroglycerin during angina, but increased significantly in response to nitroglycerin after discontinuation of pacing and disappearance of angina. In six patients, 0.2 mg nitroglycerin injected intravenously 1 min following the intracoronary injection relieved the angina unaffected by the preceding intracoronary injection. The relief was associated with a fall in arterial blood pressure and coronary sinus blood flow. The study indicates that the direct action of nitroglycerin on the coronary bed plays little, if any, role in the antianginal effect of the drug, which appears to be due entirely to the action of the drug on the systemic circulation.

Effect of endotoxin on hemodynamics and norepinephrine metabolism in the dog.

SummaryIntravenous administration of E. coli endotoxin to anesthetized dogs caused a precipitous fall in arterial blood pressure and renal artery flow within 3 min. With the fall in blood pressure, plasma 3H-norepinephrine fell to 63% of control levels. Five minutes after endotoxin administration, the 3H-norepinephrine level increased to 90% of the control value. Thirty minutes after endotoxin administration, blood pressure had risen to 75% of control levels and 3H-norepinephrine remained unchanged. 3H-Norepinephrine concentration in the atria, ventricle and kidneys remained unchanged, but the levels in the spleen and adrenals were significantly increased. In all cases 3H-normetanephrine levels increased suggestive of increased release and metabolism of catecholamines. It is suggested that endotoxin exerts certain changes in cellular permeability resulting in increased extraction of norepinephrine from the circulating blood.

Prostaglandin action on pancreatic blood flow and on electrolyte and enzyme secretion by exocrine pancreas in vivo and in vitro.

1. Intra-arterial injection or infusion of prostaglandins E(1) and E(2) into anaesthetized cats caused a fall in arterial blood pressure, a reduction in pancreatic blood flow and an inhibition of secretin-stimulated pancreatic electrolyte secretion. In some experiments these effects were preceded by a transient increase in blood flow and secretion.2. The fall in blood pressure and reduction in blood flow, but not the inhibition of secretion, were much less marked following administration of the alpha-adrenergic blocking agent phenoxybenzamine.3. Prostaglandins F(1alpha) and F(2alpha) caused only a slight reduction in blood pressure and had very little effect on pancreatic blood flow or electrolyte secretion.4. Addition of prostaglandins to the perfusate of the saline-perfused cat pancreas stimulated electrolyte secretion, with E(1) = E(2) >> F(1alpha) = F(2alpha). This stimulatory action was markedly potentiated by theophylline.5. Enzyme secretion was not stimulated by any of the prostaglandins, even in the presence of theophylline.6. It is concluded that prostaglandins can stimulate electrolyte transport by exocrine pancreas, perhaps through a mechanism involving adenylate cyclase, but that in vivo this action is masked by a secondary inhibition resulting either from vasoconstriction, or from the libration of an antisecretory agent, or both.

The response of the unanesthetized sheep fetus to sympathomimetic amines and adrenergic blocking agents

The response of the unanesthetized intrauterine sheep fetus to sympathomimetic amines was investigated before and after administration of adrenergic blocking agents. Epinephrine, norepinephrine, and methoxamine elicited a prompt increase in systolic and diastolic blood pressures and a decrease in heart rate which tended to be proportional to the rise in mean blood pressure. Isoproterenol, in contrast, produced a fall in arterial blood pressure and a rise in fetal heart rate. The relative changes in blood pressure and in heart rate following the administration of sympathomimetic amines were unaffected by increasing maturity although there was a continuous increase in fetal blood pressure throughout the last trimester of gestation. Phenoxybenzamine (an alpha-receptor-blocking agent) or propranolol (a beta-receptor-blocking agent) exerted only a minor effect on fetal heart rate and blood pressure and did not alter the oxygenation and acid-base state of the fetus. The response to sympathomimetic amines was obliterated. In contrast to the adult of most species, alpha blockade of the fetal sheep did not lead to epinephrine reversal.

A vasodepressor effect of pentobarbitone sodium

1. In anaesthetized cats under artificial ventilation, a few milligrams of pentobarbitone sodium injected into the cerebral ventricles produced a pronounced fall in arterial blood pressure, which was central in origin and resulted from inhibition of vasomotor tone.2. Pentobarbitone sodium was more effective in lowering blood pressure when injected into the cerebral ventricles than when injected into the cisterna magna, yet the pentobarbitone sodium did not act on structures in the ventricular wall, but acted on structures reached from the subarachnoid space.3. To produce its vasodepressor effect, the pentobarbitone sodium had to pass through the foramina of Luschka into the subarachmoid space beneath the medulla oblongata and to penetrate its ventral surface in a region caudal to the trapezoid bodies and lateral to the pyramids. This was the outcome of experiments in which the pentobarbitone sodium was injected into or perfused through the cerebral ventricles with or without an outflow cannula inserted into the aqueduct or into the fourth ventricle, and of experiments in which pentobarbitone sodium solutions were applied by means of Perspex rings to this region of the exposed ventral surface of the medulla. Whereas the application of pentobarbitone sodium to this region on one side had a weak vasodepressor effect only, its application on both sides produced a pronounced fall in arterial blood pressure.4. The region where pentobarbitone acted on topical application covers the region where nerve cells are found in the marginal glia immediately under the pia mater. The possibility is discussed that these cells are the morphological substrate on which the pentobarbitone acts, that arterial blood pressure is maintained by their activity which is suppressed by the pentobarbitone sodium.

Platelet aggregation induced by ADP in vivo: Continuous and quantitative measurements in different vascular beds

Platelet aggregates induced by infusion of ADP are recorded in arteries and veins by a previously described photoelectric technique. Two parameters are mainly responsible for the degree of aggregation, (1) the concentration of ADP and (2) the platelet count. The lower the concentration of ADP, the lower the number of aggregates counted. Maximum effect was achieved at 0.35 mg ADP/kg body wt/min. Larger doses of ADP proved to be impractical because of the vasodilatory action with extreme fall in arterial blood pressure. There is a correlation between platelet count in the range from 180,000 to 260,000/mm 3 and the number of aggregates formed, however, beyond 300,000/mm 3 the degree of aggregation seems to be independent of the number of platelets. When blood containing a well-defined number of aggregates passes the minute vessels of kidney, lung, brain, mesentery, and hind leg the aggregate count is reduced significantly. The reduction in aggregate count seems to be most marked in the renal and pulmonary system. This could be due to anatomical and/or hemodynamical differences in the microvascular systems of the organs investigated.

Participation of the anterior hypothalamus in the baroreceptor reflex

1. On the basis of discrete electrical stimulation in the pre-optic region and anterior hypothalamus of anaesthetized cats, a depressor area has been defined, stimulation of which elicits a fall of arterial blood pressure of 30-50 mm Hg and a bradycardia of some 25%, caused by inhibition of sympathetic vasomotor tone and by vagal activation respectively. These are accompanied by a reduction in rate and depth of respiration.2. The depressor area, from which this pattern of response is elicited, lies ventral and caudal to the anterior commissure, and extends caudally in the dorsal hypothalamus, dorsal to the fornix.3. The pattern of response elicited from identified points in the depressor area was shown to be indistinguishable from that to baroreceptor afferent stimulation.4. A lesion destroying the hypothalamic depressor area bilaterally reduced the response to baroreceptor afferent stimulation. Lesions in the medullary depressor area which spared a large part of the nucleus of the tractus solitarius also reduced, but did not abolish, the baroreceptor reflex response. The two lesions combined abolished the reflex.5. It is concluded that the whole brain-stem depressor area, from the hypothalamus through the mid-brain to the medulla, constitutes a functional unit which integrates the response to baroreceptor afferent stimulation.

Early histamine release and death due to endotoxin.

SummaryThe intravenous injection of a lethal dose of E. coli endotoxin into anesthetized dogs produces a precipitous fall in arterial blood pressure, a sharp increase in plasma histamine and an abrupt decrease in circulating platelets. The increase in histamine, like the fall in arterial pressure, occurs within 30-60 sec following the administration of a lethal dose of endotoxin. In contrast, sublethal doses of endotoxin produce only modest decreases in arterial blood pressure, no significant elevation in plasma histamine levels, and a slight fall in circulating platelets. In this study an increase in plasma histamine was always associated with a lethal outcome. In no instance was there death with no prior elevation in histamine. Results indicate that an early and marked increase in histamine seems to follow the injection of a lethal dose of endotoxin, and it is highly probable that this early release of histamine is in some way involved in both the cardiovascular changes and the ultimate lethality of thi...

Sympathetic nervous response to induced fall and rise of arterial blood pressure in anesthetized rabbits

The baroreceptor reflex is thought to counteract both a rise and a fall in arterial blood pressure, but the evidence for this is incomplete. In 19 anesthetized rabbits, the relationship between blood pressure/aortic nerve activity and efferent sympathetic activity in renal and splanchnic nerves was therefore investigated during induced rise and fall of arterial pressure. Baroreceptor activity increased and sympathetic activity decreased with raised pressure. In contrast, reduction of baroreceptor activity during acute hemorrhagic hypotension had little or no effect on activity in the two sympathetic nerves. Following complete barodenervation, however, sympathetic activity rose on average to 238% of control values. We therefore conclude that the baroreceptor reflex mainly counteracts a rise in arterial blood pressure. Reduction of baroreceptor activity in the first few minutes of acute hemorrhagic hypotension does not lead to increased sympathetic activity. The small activity remaining in baroreceptor nerves at low pressures had a very potent sympathetic inhibitory effect.