High Pressure Baroreceptor Research Articles

Nitric oxide impacts on angiotensinAT2 receptor modulation of high‐pressure baroreflex control of renal sympathetic nerve activity in anaesthetized rats

AimNitric oxide (NO) interacts with the local brain renin-angiotensin system to modulate sympathetic outflow and cardiovascular homoeostasis. This study investigated whether NO influenced the ability of angiotensin AT2 receptor activation to modify the high-pressure baroreceptor regulation of renal sympathetic nerve activity (RSNA) and heart rate (HR).MethodsAnaesthetized (chloralose/urethane) rats were prepared to allow generation of baroreflex gain curves for RSNA or HR following intracerebroventricular (I.C.V.) CGP42112 (AT2 receptor agonist), PD123319 (AT2 receptor antagonist) or losartan (AT1 receptor antagonist), and then in combination with L-NAME (NO synthase inhibitor).ResultsI.C.V. PD123319, CGP42112, and Losartan did not change baseline mean arterial pressure, HR or RSNA. Baroreflex sensitivities for RSNA and HR were increased following AT2 receptor activation with CGP42112 by 112 and 157%, respectively, but were reduced following PD123319 by 20% (all P < 0.05). L-NAME alone increased baroreflex sensitivity for both RSNA and HR, by 62 and 158%, respectively, but when co-infused with either CGP42112 or PD123319, the baroreflex sensitivity fell to values comparable to those obtained during I.C.V. saline infusion. The baroreflex sensitivities for RSNA and HR were increased by losartan by 92% and 192%, respectively, but in the presence of L-NAME were no different from those obtained during I.C.V. saline infusion.ConclusionThere is an important facilitatory role for AT2 receptors in the high-pressure baroreflex regulation of RSNA and HR which is dependent on a functional NO/NOS system. Conversely, AT1 receptors have an inhibitory effect on the baroreflex, an action that relies on a tonic inhibition of NO.

Nitric oxide impacts on angiotensin AT2 receptors modulation of high‐pressure baroreflex control of renal sympathetic nerve activity in rats

To investigate the interaction of NO with AT2 receptor activation in the modulation of high‐pressure baroreceptor regulation of renal sympathetic nerve activity (RSNA). Experiments were carried out in chloralose/urethane anaesthetised rats and baroreflex gain curves were generated using intravenous phenylephrine and sodium nitroprusside following intracerebroventricular (I.C.V.) saline, CGP42112 (CGP), PD123319 (PD), AT2 receptor agonist and antagonist, and then in combination with L‐NAME, an NO synthase inhibitor. I.C.V. saline, PD and CGP did not change baseline mean arterial pressure (MAP), heart rate (HR) or RSNA (86±3 vs. 85±3 mmHg, 328±11 vs. 326±10 beat/min, 0.79±0.15 vs. 0.75±0.14 μV.s, respectively). The slope of the baroreflex gain curve for RSNA was increased by 64% and 107% following L‐NAME and CGP respectively but decreased by 19% following PD (all P&lt;0.05). In the group where PD preceded L‐NAME or when PD followed L‐NAME, the slope of the baroreflex gain curve during PD plus L‐NAME infusion was reduced by about 35% (P&lt;0.05) compared to the infusion of PD or L‐NAME alone. L‐NAME decreased the slope of the baroreflex gain curve following CGP I.C.V. administration by 33% (P&lt;0.05). These findings suggest that NO exerts a facilitatory action allowing the normal high‐pressure baroreceptor reflex regulation of RSNA mediated through central AT2 receptor activation.Funded by the Wellcome Trust

The impact of cisplatin induced renal failure on baroreflex regulation of renal sympathetic nerve activity (RSNA) in the male Wistar rat

Renal failure (RF) in man is associated with sympatho-excitation. We investigated whether low and high pressure baroreceptor regulation of RSNA was deranged in a cisplatin-induced rat RF model. Rat...

Measuring high pressure baroreceptor sensitivity in the rat

IntroductionThe high pressure baroreceptor reflex rapidly buffers changes in systemic arterial pressure in response to postural changes, altered gravitational conditions, diseases, and pharmacological agents. Drug-induced exaggeration of changes in heart rate and in systemic arterial pressure is a leading cause of adverse events and of patients terminating use of drugs, particularly in the aging population. This paper presents a facile method for monitoring the high pressure baroreceptor reflex in rats, and presents an alternative to quantifying the magnitude of this reflex using 2 dependent variables, heart rate and systemic arterial pressure, rather than merely change in heart rate. MethodsTwenty-four rats were allocated to 3 groups: group I anesthetized with 100mg/kg thiopental, group II anesthetized with 2% isoflurane given by inhalation, group III anesthetized with thiopental but pretreated for 2weeks with 2μg/kg aldosterone given SQ bid. After induction to anesthesia, hair was clipped from the ventral aspect of the neck, and petrolatum was applied to the skin to permit an air-tight seal with a glass funnel attached to a source of variable and controllable negative pressure. Systemic arterial pressure, ECG, heart rate, and a force of suction applied to the neck were all recorded continuously. ResultsAfter baseline recordings, a force of −20mmHg was applied for 20s over the carotid artery. In rats receiving thiopental, the average changes in heart rate and systemic arterial pressure following the application of −20mmHg neck suction were 30±11bpm and 45±14mmHg, respectively. The ratios of change in heart and change in systemic arterial pressure to application of negative force over the carotid sinus are 1.5±0.6bpm/mmHg and 0.7±04mmHg/mmHg, respectively. Mean values for heart rate and for mean systemic arterial pressure during baseline and after application of neck suction for 20s showed little to no decrease (i.e., blunting) in rats anesthetized with isoflurane or pretreated with aldosterone. DiscussionThus this methodology was able to detect, in rats, blunting of baroreceptor function for at least 2 perturbations of this important homeostatic control system.

Cardiovascular Responses to Postural Changes: Differences with Age for Women and Men

The cardiovascular responses to postural change, and how they are affected by aging, are inadequately described in women. Therefore, the authors examined the influence of age and sex on the responses of blood pressure, cardiac output, heart rate, and other variables to change in posture. Measurements were made after 10 minutes each in the supine, seated, and standing positions in 22 men and 25 women who ranged in age from 21 to 59 years. Several variables differed, both by sex and by age, when subjects were supine. On rising, subjects' diastolic and mean arterial pressures, heart rate, total peripheral resistance (TPR), and thoracic impedance increased; cardiac output, stroke volume, and mean stroke ejection rate decreased; and changes in all variables, except heart rate, were greater from supine to sitting than sitting to standing. The increase in heart rate was greater in the younger subjects, and increases in TPR and thoracic impedance were greater in the older subjects. Stroke volume decreased less, and TPR and thoracic impedance increased more, in the women than in the men. The increase in TPR was particularly pronounced in the older women. These studies show that the cardiovascular responses to standing differ, in some respects, between the sexes and with age. The authors suggest that the sex differences are, in part, related to greater decrease of thoracic blood volume with standing in women than in men, and that the age differences result, in part, from decreased responsiveness of the high-pressure baroreceptor system.

Assessment of autonomic function in patients with neurally mediated syncope: Augmented cardiopulmonary baroreceptor responses to graded orthostatic stress

Objectives. The purpose of this study was to assess vagal tone and cardiopulmonary baroreceptor activity in patients with tiltinduced neurally mediated syncope.Background. The causes of individual susceptibility to orthostatic stress leading to recurrent neurally mediated syncope remain obscure. The trigger for sympathetic withdrawal and increased vagal activity is believed to be stimulation of ventricular mechanoreceptors.Methods. Seventeen patients (mean age 50.6 years) with recurrent syncope and a positive response on a 45-min 60 ° bead-up tilt test were compared with a control group of 17 patients (mean age 47.5 years) with unexplained syncope und negative tilt test findings. Vagal activity was assessed by high pressure baroreceptor testing and by temporal and spectral analysis of heart rate variability during Holter ambulatory electrocardiographic monitoring. Cardiopulmonary baroreceptor sensitivity was assessed by measurement of forearm vascular responses to lower body negative pressure.Results. Mean high pressure baroreceptor sensitivity was 16.4 ± 12.2 ms/mm Hg in the group with a positive tilt test response compared with 15.1 ± 13.0 ms/mm Hg in the control group (p = NS). There were no agnificant differences between the groups in any of the temporal or spectral measures of heart rate variability. The increase to forearm vascular résistance in response to lower body negative pressure was 11.5 ± 14.2 U in patents with tilt-inducetd syncope and 3.5 ± 3.2 U in the control group at -5 mm Hg, 16.8 ± 18.6 U and 4.8 ± 5.3 U, respectively, at -10 mm Hg and 26.4 ± 24.3 U and 10.2 ± 7.8 U, respectively, at -20 mm Hg (p < 0.001).Concisions. Patients with tilt-induced neurally mediated syncope have augmented cardiopulmonary baroreceptor responses to orthostatic stress. This finding sheds new light on the etiology of neurally mediated syncope.

Sympathetic baroreflex control of vascular resistance in comfortably warm man. Analyses of neurogenic constrictor responses in the resting forearm and in its separate skeletal muscle and skin tissue compartments

Resting forearm vascular resistance changes elicited in male volunteers by graded reflex sympathetic activation evoked by graded lower body negative pressure (LBNP) were studied at room temperatures of 24-25 and 20-21 degrees C. The latter condition caused strong suppression of skin flow and permitted preferential analysis of muscle responses and, by comparison with responses at 24-25 degrees C, secondary estimation of circulatory reactions in the skin. Short-lasting LBNP-bouts (1.5 min) allowed analyses of reflex vascular reactions to high and barely tolerated LBNP (85 mmHg) and thereby to high levels of circulatory stress and sympathetic nerve discharge, yet without risks for the subjects under study. Both muscle and skin reacted intensely and in a graded manner to graded sympathetic activation with very pronounced resistance change (74-77% flow decline; 350-400% resistance rise above control level) at high LBNP. Therefore, the sympathetic vasomotor fibres can exert a very potent control of vascular resistance both in skeletal muscle and in skin under thermoneutral conditions, and both tissues apparently can serve as major targets for powerful sympathetic homeostatic baroreflexes. Evidence indicated that this control is exerted from both low-pressure cardiopulmonary and high-pressure arterial baroreceptor areas. These conclusions deviate from previous literature, in which baroreflex sympathetic vasoconstriction in the human limb has been proposed to be more or less selectively mediated from cardiopulmonary receptors and, further, muscle to respond fully already at mild circulatory stress without further constriction if the stimulus is increased.

Disturbed Fluid and Electrolyte Homoeostasis Following Dehydration in Elderly People

Disturbances in homoeostatic capacity are typical of the ageing process. Changes in the neuroendocrine controls of salt and water homoeostasis with age make elderly people more susceptible to fluid and electrolyte disturbances such as dehydration and overhydration. Not only do elderly subjects show reduced thirst and water intake following dehydration, but their kidneys are less able to retain water. This reduced thirst and water intake is not dependent on palatability of the liquids offered as the amounts drunk are no different if water alone or a variety of beverages are offered to healthy elderly dehydrated men. It is of interest that the arginine vasopressin (AVP) response to dehydration is maintained in elderly subjects, indicating that their reduced renal water retentive capacity is due to relative renal resistance to vasopressin. The mechanism underlying the reduced thirst is unclear. Dehydration causes plasma hypertonicity and reduced extracellular fluid (ECF) volume, both of which stimulate thirst and AVP secretion. Elderly subjects show deficits in sensing the reduced ECF volume through reduced low and high pressure baroreceptor sensitivity. In contrast, while the AVP responses to hypertonicity are maintained, the thirst responses seem to be reduced. It seems unlikely that the primary sensing 'osmoreceptor' neurons in the hypothalamus leading to AVP secretion or thirst would be differentially affected by age. Therefore the thirst deficit may result from changes with age in the more poorly defined pathways that bring thirst to consciousness. Following rehydration, thirst and AVP secretion are inhibited in young individuals thus avoiding overhydration.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreceptor sensitivity in prehypertensive young adults.

Decreased baroreceptor reflex sensitivity has been implicated in the pathogenesis of hypertension. The purpose of this study is to determine if alterations of baroreceptor function precede the development of hypertension in humans. Baroreceptor function was evaluated in 13 young adult white men with relatively high blood pressures sustained for 12 to 15 years and 12 age-matched men with sustained relatively low blood pressures. High pressure baroreceptor activity was evaluated by measuring change in pulse interval in response to decreases and increases of arterial pressure, induced by graded infusions of nitroprusside and angiotensin II, respectively. In response to both agents, baroreceptor slopes did not differ in the high and low blood pressure groups. Plasma norepinephrine also increased similarly in both blood pressure groups in response to nitroprusside. To study low-pressure baroreceptor function, responses to graded levels of lower-body negative pressure (LBNP) were measured. Comparing both blood pressure groups, there were similar increases of heart rate, total peripheral resistance, and plasma norepinephrine in response to LBNP. Both blood pressure groups also had similar increases of heart rate and blood pressure in response to isometric (handgrip) exercise. Thus, high-pressure and low-pressure baroreceptor function is not altered in prehypertensive young adults. However, continued follow-up will be required to determine if these individuals with sustained relatively high blood pressures are truly prehypertensive.

Contributions of the sympathetic nervous system, vasopressin and baroreceptor function in brain angiotensin II excess-induced hypertension in the dog.

To determine the principal effects of brain angiotensin(Ang) II on the sympathetic nervous system, vasopressin (AVP), and the high and low pressure baroreceptor systems, we observed the hemodynamic and neurohumoral characteristics induced by the acute(1-hr) and chronic(1-wk) infusion of Ang II into the brain ventricle in conscious dogs, and then evaluated the hemodynamic responses to sole-innervated carotid artery occlusion(COR) after Ang II infusion and again after vagotomy in anesthetized dogs. Both acute(50ng/kg/min) and chronic(15ng/kg/min) infusion of Ang II caused a significant rise in arterial pressure without changes in heart rate. Neither acute nor chronic Ang II treatment produced significant changes in plasma renin activity and norepinephrine in plasma and cerebrospinal fluid(CSF), while the plasma and CSF level of AVP was increased in the acute Ang II treatment, but not in the chronic Ang II treatment. The COR was blunted in the acute Ang II treatment compared with those obtained in the chronic Ang II or sham treatment. The blunted pressor response to carotid occlusion in the acute Ang II treatment was restored by cutting the remaining vagus nerve. These results suggest that baroreceptor reflexes are impaired by the acute excess of Ang II in the brain, and it might be mediated through increased vagal afferent activity, changes in the central integration of low and high pressure baroreceptors, and a combination of both.

Evidence that the arterial baroreceptors influence muscle blood flow and not subcutaneous flow in man.

Studies in man indicate that skeletal muscle blood flow is modulated via high pressure baroreceptors located in the carotid body. However, whether subcutaneous blood flow is influenced in this way remains controversial. Therefore, the aim of the present study was to determine whether subcutaneous as well as skeletal muscle blood flow was influenced by direct carotid body stimulation; this was done by means of neck suction. Six young healthy males were investigated. Subcutaneous and skeletal muscle blood flow in the forearm was measured by the local 133Xe washout technique. Neck suction of -20 mmHg was applied through a tight helmet covering the head and neck. In the supine position heart rate increased about 10%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged, but skeletal muscle blood flow increased about 70%. Measurements were repeated during neck suction, -20 mmHg, and 45 degrees head-up tilt (which is known to decrease subcutaneous blood flow and skeletal muscle blood flow by increasing sympathetic vasoconstrictor activity). Heart rate increased by about 20%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged and skeletal muscle blood flow increased about 100%. These results indicate that skeletal muscle blood flow is modulated through carotid baroreceptors. Subcutaneous blood flow seems not to be influenced by high pressure baroreceptor modulation, although a vasoconstrictor response to head-up tilt was demonstrated in this as well as other recent studies.

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

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

Characterization of high and low pressure baroreceptor influences on renal nerve activity in the primate Macaca fascicularis.

We characterized the influence of high pressure and low pressure intravascular receptors on renal nerve activity in the pentobarbital sodium-anesthetized nonhuman primate Macaca fascicularis. Epinephrine-induced increases in arterial pressure were used to stimulate high pressure receptors, and intravascular volume expansion was used to stimulate both high and low pressure receptors. In addition, the intravascular mechanoreceptors were stimulated directly by intravenous veratrine administration. All interventions produced large decreases in renal nerve activity in the intact state. Denervation of the carotid sinus or bilateral cervical vagal section dimished, whereas sinoaortic denervation with vagotomy completely abolished all responses of renal activity to these interventions. We conclude that the nonhuman primate possesses very sensitive renal nerve sympathetic reflexes that are modulated by intravascular mechanoreceptors whose afferents traverse the carotid sinus nerves and the vago-aortic trunks. The carotid sinus nerves and the vago-aortic trunks appear to be equally effective in inhibiting renal nerve activity in response to increases in arterial pressure. In addition, there are no afferent pathways mediating intravascular mechanoreceptor modulation of renal nerve activity outside the carotid sinus nerves and the vago-aortic trunks.

Influence of low- and high-pressure baroreceptors on plasma renin activity in humans.

We evaluated effects of the low- and high-pressure baroreceptors on plasma renin activity (immunoassay) using graded lower body suction (LBS) in six healthy men. LBS at -10 and -20 mmHg for 10 min decreased central venous pressure without changing arterial pressure and thereby presumably reduced low- but not high-pressure baroreceptor inhibition of renin release. LBS at these levels produced forearm vasoconstriction, but did not increase renin. LBS at -40 mmHg decreased central venous and arterial pulse pressure and thus reduced both low- and high-pressure baroreceptor inhibition. LBS at this level produced forearm vasoconstriction and tachycardia and increased renin from 2.1 +/- 0.4 (mean +/- SE to 7.4 +/- 1.4 ng.ml-1.h-1 (P less than 0.05). In summary, reduction in low-pressure baroreceptor inhibition in humans did not increase renin in the presence of physiological tonic inhibition from high-pressure baroreceptors. Increases in renin did not occur until there was combined reduction of high- and low-pressure baroreceptor inhibition on plasma renin activity.

Effect of beta adrenoceptor antagonists on baroreceptor reflex sensitivity in hypertension

High-pressure baroreceptor reflex sensitivity (BRS) was estimated by measuring the reflex heart rate response to pharmacologic elevation of blood pressure (phenylephrine, 150 to 200 microgram intravenously) in 18 patients with essential hypertension on two occasions: after a 4-wk placebo period and after 9 wk of incremental doses of oral timolol (20, 40, and 60 mg daily). On placebo, measurements were performed both before and after propranolol (0.2 mg/kg intravenously). The level of cardiac vagal inhibition, estimated by the heart rate change after atropine (0.04 mg/kg intravenously), was similar in placebo and on timolol, thereby permitting comparisons of BRS. BRS on placebo (before and after propranolol) correlated with BRS on timolol ( r = 0.87 and 0.90, p less than 0.001), attesting to the reproducibility of BRS measurements. BRS was unchanged by either short-term (propranolol) or long-term (timolol) beta adrenoceptor inhibition. Results were similar in responders (n = 10), whose mean arterial blood pressure on timolol fell by 10 mm Hg or more, and in nonresponders. The findings do not provide evidence for a change in gain of the baroreceptor reflex arc under conditions of short- or long-term beta adrenoceptor inhibition.

Sympathetic nerve activity: role in regulation of blood pressure in the spontaenously hypertensive rat.

Sympathetic nerve activity (SNA) and high pressure baroreceptor regulation of SNA were studied in the Okamoto strain of spontaneously hypertensive rat (SHR). Mean arterial pressure (MAP) and SNA were not significantly affected by anesthesia with low doses of pentobarbital (20-25 mg/kg). Thus, most of these studies were performed in anesthetized rats. SNA in visceral sympathetic nerves increased rapidly with age up to 24 weeks and slowly thereafter. MAP increased with SNA, following the same time course. Both SNA and MAP in SHR were significantly greater than that found in normotensive Wistar control rats of comparable ages. Abolition of ganglionic transmission with hexamethonium in both SHR and normotensive controls reduced postganglionic SNA and MAP to comparable levels. In SHR less than 16 weeks old, increased baroreceptor stimulation effectively inhibited SNA with the same sensitivity as found in Wistar control rats. However, older SHR appeared to lose their ability to completely inhibit SNA during induced hypertension, whereas in Wistar control rats as old as 52 weeks, elevation of blood pressure to 165.3 +/- 2.3 mm Hg completely suppressed SNA. These results suggest that SNA may play an important role in the development and maintenance of hypertension in SHR, and that central sympathetic centers, uninhibited by baroreceptor afferents, become active during the development of hypertension in the SHR.

High pressure baroreceptor regulation of sympathetic nerve activity in spontaneously hypertensive rats

High pressure baroreceptor regulation of sympathetic nerve activity in spontaneously hypertensive rats

The role of low pressure baroreceptors in reflex vasoconstrictor responses in man.

Studies were performed on 11 healthy men to evaluate the role of low pressure baroreceptors in the reflex forearm vasoconstrictor responses (plethysmography) to venous pooling produced by lower body negative pressure. Lower body negative pressure (LBNP) at - 5, - 10, - 20, and - 40 mm Hg lowered central venous pressure by 42, 59, 74, and 93%, respectively, and decreased forearm vascular conductance by 24, 29, 34, and 40%, respectively. The decreases in forearm blood flow and conductance during the low levels of venous pooling (LBNP - 5 and - 10 mm Hg) occurred without significant changes in arterial pressure, arterial dP/dt. and heart rate. These results with the low levels indicate that maneuvers which decrease venous return and central venous pressure in man can influence forearm vascular tone without significant changes in the determinants of carotid and aortic baroreceptor activity. During high levels of venous pooling (LBNP - 20 and - 40 mm Hg), significant decreases in arterial pressure and dP/dt and significant increases in heart rate accompanied the further reductions in central venous pressure, forearm blood flow, and forearm vascular conductance. About 73% of the decrease in conductance during venous pooling at LBNP - 40 mm Hg, which was sufficient to decrease arterial pressure and activate high pressure baroreceptor reflexes, occurred during low levels of venous pooling at LBNP - 10 mm Hg without changes in arterial pressure. This suggests that much of the forearm vasoconstriction with the high levels of venous pooling, which were sufficient to decrease arterial pressure, may be accounted for by reflexes originating in areas other than high pressure baroreceptors. The results of these studies suggest that low pressure baroreceptors exert an important influence on forearm vascular tone during decreases in venous return and central venous pressure in man.

HEMODYNAMIC EFFECTS OF NOREPINEPHRINE IN SEVERE HYPNOTIC DRUG POISONING WITH ARTERIAL HYPOTENSION

Abstract The hemodynamic response to infusion of norepinephrine (NE) has been measured in 12 patients with severe hypnotic drug poisoning. All patients had a mean arterial blood pressure (B.P.) of 70 mmHg or less initially. As evaluated from central venous pressure no marked hypovolemia was present. Cardiac output (C.O.) was determined by the dye dilution method and right heart catheterization by a “floating” catheter technique. Following infusion of NE the arterial B.P. and C.O. increased. The increase in C.O. resulted from increases in stroke volume and to a less extent also in heart rate (HR). There was no significant change of peripheral vascular resistance index (PVRI), in contrast to the NE effect in cardiogenic, hemorrhagic and septic shock states. The increase in arterial B.P. was accompanied by an increase in HR, which implies a disturbed function of the high pressure baroreceptor system. The rise in B.P. is primarily due to the increase in C.O. No adverse effects were noted during the NE infusion. It is concluded that NE is beneficial in the treatment of severe hypnotic drug poisoning complicated by hypotension.

Summation of baroceptor reflex effects on sympathetic nerve activities.

ARTICLESSummation of baroceptor reflex effects on sympathetic nerve activitiesI Ninomiya, and H IrisawaI Ninomiya, and H IrisawaPublished Online:01 Jun 1969https://doi.org/10.1152/ajplegacy.1969.216.6.1330MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDifferential contribution of aortic and carotid sinus baroreflexes to control of heart rate and renal sympathetic nerve activity10 July 2015 | The Journal of Physiological Sciences, Vol. 65, No. 5Central command differentially affects aortic and carotid sinus baroreflexes at the onset of spontaneous motor activityAutonomic Neuroscience, Vol. 179, No. 1-2An optimal control model of 1/f fluctuations in heart rate variabilityIEEE Engineering in Medicine and Biology Magazine, Vol. 20, No. 2Cardiac vagal and sympathetic efferent discharges are differentially modified by stretch of skeletal muscleJun Murata, and Kanji Matsukawa1 January 2001 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 280, No. 1Influence of sympathetic blockade on the acute hypertensive response to aortic constrictionR. Fazan, J. A. Castania, G. Ballejo, M. C. O. Salgado, and H. C. Salgado1 December 1997 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 273, No. 6Electrophysiological evidence of ipsilateral reno–renal reflexes in the catJournal of the Autonomic Nervous System, Vol. 65, No. 1Vasopressor mechanisms in acute aortic coarctation hypertensionBrazilian Journal of Medical and Biological Research, Vol. 30, No. 4Renal sympathetic nerve activity and the weight of the remaining kidney in unilateral nephrectomized ratsJournal of the Autonomic Nervous System, Vol. 63, No. 1-2Unilateral carotid sinus stimulation and muscle sympathetic nerve activity in manMedicine &amp Science in Sports &amp Exercise, Vol. 28, No. 7Arterial Baroreceptor Regulation of Peripheral Resistance and of Cardiac PerformanceOrganization of Differential Sympathetic Responses to Activation of Visceral Receptors and Arterial BaroreceptorsNucleus Tractus Solitarii (NTS): Does It Mask the Interaction of Blood Pressure and Thermal Energetics?Sympathetic nerve activity: a link to stroke?Stroke, Vol. 16, No. 1Baroreflex suppression on non-shivering thermogenesis in restrained and non-restrained ratsJournal of Thermal Biology, Vol. 9, No. 1-2Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Interaction of Cardiovascular Reflexes in Circulatory Control1 January 2011Differential interaction between hypothalamic and bulbar mechanisms in blood flow regulation in skeletal musclesBulletin of Experimental Biology and Medicine, Vol. 96, No. 2Arterial baroreflexes in renal hypertensive rabbits. Selectivity and redundancy of baroreceptor influence on heart rate, vascular resistance, and lumbar sympathetic nerve activity.Circulation Research, Vol. 53, No. 2Segmental distribution and central projectionsof renal afferent fibers in the cat studied by transganglionic transport of horseradish peroxidaseThe Journal of Comparative Neurology, Vol. 216, No. 2Vasomotor Response in Acute Intracranial HypertensionAssociation between sympathetic nerve activity and cerebrovascular protection in young spontaneously hypertensive rats.Stroke, Vol. 14, No. 1Cardiac and Sinoaortic Reflexes During Aortic Constriction in Awake Calves11 July 2009 | Biomaterials, Medical Devices, and Artificial Organs, Vol. 11, No. 2-3Altered neural control of cardiovascular function in sodium-depleted dogs.Hypertension, Vol. 4, No. 3_pt_2Differential baroreflex control of heart rate and vascular resistance in rabbits. Relative role of carotid, aortic, and cardiopulmonary baroreceptors.Circulation Research, Vol. 50, No. 4Characteristics and functions of two types of efferent fibers in the adrenal nerveJournal of the Autonomic Nervous System, Vol. 4, No. 4Neuronal Regulation of Blood PressureInfluence of the input from left and right arterial baroreceptors on left inferior cardiac nerve activity in catsJournal of the Autonomic Nervous System, Vol. 2, No. 4Characterization of high and low pressure baroreceptor influences on renal nerve activity in the primate Macaca fascicularis.Circulation Research, Vol. 46, No. 5Epinephrine suppression of efferent activity of the adrenal nerveJournal of the Autonomic Nervous System, Vol. 1, No. 3Arterial baroreceptor reflex control of sympathetic nerve activity in the spontaneously hypertensive rat.Hypertension, Vol. 1, No. 6Antihypertensive effect of cardiovascular Ca2+-antagonist in hypertensive patients in the absence and presence of beta-adrenergic blockadeAmerican Heart Journal, Vol. 96, No. 2Regulation of arterial blood pressure by aortic baroreceptors in the unanesthetized dog.Circulation Research, Vol. 42, No. 2Depressant action of the posterior lobe of the cerebellum upon renal sympathetic nerve activityBrain Research, Vol. 133, No. 2The Pathogenesis of Experimental Acute Renal Failure: The Role of Membrane DysfunctionSympathetic nervous response to induced fall and rise of arterial blood pressure in anesthetized rabbitsPfl�gers Archiv European Journal of Physiology, Vol. 326, No. 3Untersuchungen zur Bahnung und Konvergenz pressoreceptorischer Afferenzen mit Hilfe der Konditions-TestreiztechnikPfl�gers Archiv European Journal of Physiology, Vol. 320, No. 3 More from this issue > Volume 216Issue 6June 1969Pages 1330-1336 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.216.6.1330PubMed5786719History Published online 1 June 1969 Published in print 1 June 1969 Metrics