Organization of Differential Sympathetic Responses to Activation of Visceral Receptors and Arterial Baroreceptors

1986 ◽  
pp. 269-301
Author(s):  
Lynne C. Weaver ◽  
Robert L. Meckler ◽  
Jean C. Tobey ◽  
Reuben D. Stein
Keyword(s):  
Arterial Baroreceptors ◽  
Sympathetic Responses

Cardiac Sympathetic Responses to Acute Vasodilation

Circulation ◽  
1996 ◽  
Vol 94 (12) ◽  
pp. 3161-3167 ◽  
Author(s):  
Gary E. Newton ◽  
John D. Parker
Keyword(s):  
Sympathetic Responses

Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Negative Pressure ◽  
Enzyme Inhibitor ◽  
Lower Body Negative Pressure ◽  
Acute Effect ◽  
Acute Administration ◽  
Lower Body ◽  
Resistance Vessels ◽  
Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

Rilmenidine sympatholytic activity preserves mental stress, orthostatic sympathetic responses and adrenaline secretion

2004 ◽  
Vol 22 (8) ◽  
pp. 1529-1534 ◽  
Author(s):  
Murray Esler ◽  
Alan Lux ◽  
Garry Jennings ◽  
Jacqui Hastings ◽  
Flora Socratous ◽  
...  
Keyword(s):  
Mental Stress ◽  
Sympathetic Responses

Neurotransmission in the medulla mediating insular cortical and lateral hypothalamic sympathetic responses

1998 ◽  
Vol 76 (7-8) ◽  
pp. 737-746 ◽  
Author(s):  
Kenneth S Butcher ◽  
David F Cechetto
Keyword(s):  
Receptor Antagonist ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Bipolar Electrode ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Lateral Hypothalamic ◽  
Baseline Activity ◽  
Sympathetic Responses

Previous evidence has shown sympathetic nerve responses to insular cortical (IC) stimulation are mediated by synapses within the lateral hypothalamic area (LHA) and ventrolateral medulla (VLM). The present study was aimed at determining the neurotransmitter(s) and receptor(s) involved at the synapse in the VLM. Twenty male Wistar rats were instrumented for renal nerve, arterial pressure, and heart rate recording. The IC or the LHA was stimulated with a bipolar electrode (200-1000 µA; 2 ms; 0.8 Hz) to elicit sympathetic nerve responses. Antagonists were then pressure-injected into the VLM (300 nL). Bilateral and unilateral kynurenate (25 mM) resulted in 100% block of IC- and LHA-stimulated sympathetic nerve responses. Bilateral injection of the non-NMDA (N-methyl-D-aspartate) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 200 µM) also resulted in up to 100% block of IC and LHA sympathetic responses. In addition, unilateral injections of CNQX were made in two animals, resulting in 100 and 83% block of LHA sympathetic responses. Bilateral injection of the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5; 200µM) did not affect the response to IC or LHA stimulation. Kynurenate, CNQX, and AP5 all resulted in an elevation of baseline sympathetic nerve activity and a pressor response. Kynurenate resulted in a 263 ± 79% increase in baseline activity, while CNQX and AP5 resulted in 83 ± 19% and 91 ± 21% increases, respectively. Bilateral injections of antagonists for GABAA (bicuculline; 0.1 µM), acetylcholine (atropine; 0.1 µM) and catecholaminergic alpha and beta receptors (phentolamine and propranolol: 0.1 µM) had no effect on LHA sympathetic responses. Thus, sympathetic responses originating in the IC and LHA are mediated by a non-NMDA receptors in the VLM, which are likely AMPA receptors.Key words: insular cortex, ventrolateral medulla, glutamate, sympathetic activity.

Effects of water immersion on arginine vasopressin release in humans

1988 ◽  
Vol 64 (1) ◽  
pp. 1-10 ◽  
Author(s):  
P. Norsk ◽  
M. Epstein
Keyword(s):  
Water Intake ◽  
Arginine Vasopressin ◽  
Critical Review ◽  
Water Immersion ◽  
Base Line ◽  
Vasopressin Release ◽  
Arterial Baroreceptors ◽  
Lower Base

Since suppression of arginine vasopressin (AVP) appears to be a determinant of the diuresis of water immersion (WI) in humans, a further understanding of its responsiveness has important implications for normal physiology, pathophysiology, and space physiology. In recent years, discrepant measurements of AVP in plasma during WI have led to conflicting conclusions. In studies in which the subjects ingested water before or during WI, plasma AVP was reported to be unchanged or even increased. In contrast, plasma AVP was suppressed in studies in which the subjects remained hydropenic. A critical review discloses that water intake before and/or during the experiments introduces several new stimuli for AVP release. Furthermore the lower base-line levels of AVP in hydrated subjects complicate detection of small changes in plasma AVP. Although the mechanisms of AVP suppression during WI are incompletely defined, it appears that not only cardiopulmonary mechanoreceptors but also arterial baroreceptors mediate the response. Additional studies are proposed to delineate further the mechanisms governing AVP release during WI.

Mechanisms of Resetting of Arterial Baroreceptors: An Overview

1988 ◽  
Vol 295 (4) ◽  
pp. 327-334 ◽  
Author(s):  
Mark W. Chapleau ◽  
George Hajduczok ◽  
Francois M. Abboud
Keyword(s):  
Arterial Baroreceptors

scholarly journals Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

2009 ◽  
Vol 296 (2) ◽  
pp. H480-H488 ◽  
Author(s):  
Qi Fu ◽  
Shigeki Shibata ◽  
Jeffrey L. Hastings ◽  
Anand Prasad ◽  
M. Dean Palmer ◽  
...  
Keyword(s):  
Steady State ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Right Atrial ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Arterial Baroreceptors ◽  
Low Levels ◽  
Cardiopulmonary Baroreceptors

Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload “selectively” cardiopulmonary baroreceptors in humans, since steady-state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20–54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan-Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and −15- and −30-mmHg LBNP for 6 min each. Application of −15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at −5- and in all at −10-mmHg LBNP. The delay for left ventricular stroke volume to fall at −15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during −15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at −30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., −10 and −15 mmHg) of LBNP in humans. Thus “selective” unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

1982 ◽  
Vol 242 (2) ◽  
pp. H185-H190 ◽  
Author(s):  
B. G. Wallin ◽  
D. L. Eckberg
Keyword(s):  
Sympathetic Activity ◽  
Chamber Pressure ◽  
Reduced Pressure ◽  
Cardiac Responses ◽  
Carotid Baroreceptor ◽  
Sympathetic Responses ◽  
Nerve Muscle ◽  
Neck Pressure ◽  
Pressure Changes ◽  
Neck Chamber

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

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