Sensitization of aortic and cardiac baroreceptors by arginine vasopressin in mammals.

Abboud, François M.; Aylward, Philip E.; Floras, John S.; Gupta, Badri N.

doi:10.1113/jphysiol.1986.sp016185

Cited by 50 publications

(6 citation statements)

References 19 publications

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“…(c) With direct nerve recordings from my elinated and nonmyelinated aortic depressor nerves in the rabbit, there was a significant enhancement of the slope relating nerve ac tivity to mean arterial pressure during eleva tion of arterial pressure while vasopressin was infused [15]. Similarly, there was a sig nificant enhancement of single nerve fiber discharge per cardiac cycle from left ventric ular mechanoreceptors in response to eleva tion of left ventricular end-diastolic pressure in the cat.…”

Section: Vasopressin Sensitizes Carotid Sinus Baroreceptors Aortic Dmentioning

confidence: 84%

“…This indicated that va-sopressin may also act directly on central pathoinhibitory baroreflexes [15,20] or inhibitory neurons and independently of the cause possibly a direct vasodilator effect [3, baroreflex to reduce sympathetic outflow. 7] resulting in increased renal blood flow, Similar observations were made by Bishop et decreased total vascular resistance, and inal.…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, there was a sig nificant enhancement of single nerve fiber discharge per cardiac cycle from left ventric ular mechanoreceptors in response to eleva tion of left ventricular end-diastolic pressure in the cat. The slope relating nerve activity to left ventricular end-diastolic pressure in creased significantly in both myelinated and nonmyelinated fibers (from 0.24 ± 0.07 to 0.32 ± 0.07 impulses/beat in the former and from 0.10 ± 0.01 to 0.15 ± 0.02 impulses/ beat in the latter) [15]. [13,21], The relationship between increased aortic baroreceptor activity and inhibition of lumbar sympathetic nerve activity was mea sured.…”

Section: Vasopressin Sensitizes Carotid Sinus Baroreceptors Aortic Dmentioning

confidence: 99%

“…4). [13,15]. (a) Vaso pressin was administered into the isolated carotid sinus of anesthetized rabbits.…”

Section: Vasopressin Augments the Cardiopulmo Nary Reflex Inhibition mentioning

confidence: 99%

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Role of Vasopressin in Cardiovascular and Blood Pressure Regulation

Abboud

Floras

Aylward³

et al. 1990

J Vasc Res

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At low concentrations and in physiologic states vasopressin is a potent antidiuretic hormone. Its cardiovascular effects have been more complex and their role in circulatory adjustments to hypovolemia and hypotension difficult to define with precision. Although recognized as a powerful vasoconstrictor, its pressor effect in intact animals, even at high concentrations, is minimal. The reasons for this blunted pressor response have been explored. This report is a review of previously published work from our laboratories which highlights the direct and indirect vasodilator actions of this hormone in animals and humans. The indirect vasodilator effect is caused by inhibition of sympathetic efferents, and facilitation of the baroreflex through a central action of the hormone and its sensitization of arterial baroreceptors as well as cardiac afferents.

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Section: Vasopressin Sensitizes Carotid Sinus Baroreceptors Aortic Dmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Vasopressin Sensitizes Carotid Sinus Baroreceptors Aortic Dmentioning

confidence: 99%

“…4). [13,15]. (a) Vaso pressin was administered into the isolated carotid sinus of anesthetized rabbits.…”

Section: Vasopressin Augments the Cardiopulmo Nary Reflex Inhibition mentioning

confidence: 99%

See 2 more Smart Citations

Role of Vasopressin in Cardiovascular and Blood Pressure Regulation

Abboud

Floras

Aylward³

et al. 1990

J Vasc Res

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“…We should consider the influence of peripherally secreted AVP on the results in this study. Because peripherally secreted AVP might affect the CNS through afferent baroreceptor input, circumventricular organs, and a ganglionic mechanism (50, 51), we cannot deny the possibility of the participation of peripheral AVP. Based on our previous reports that examined the effect of peripheral AVP on central neuronal activity, RSNA showed different results (16, 18).…”

Section: Discussionmentioning

confidence: 99%

Central Endogenous Vasopressin Induced by Central Salt‐Loading Participates in Body Fluid Homeostasis through Modulatory Effects on Neurones of the Paraventricular Nucleus in Conscious Rats

Kato

Kannan

Ohta

et al. 2009

J Neuroendocrinology

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Peripherally secreted arginine vasopressin (AVP) plays a role in controlling body fluid homeostasis, and central endogenous AVP acts as a neurotransmitter or neuromodulator. The limbic system, which appears to exert an inhibitory effect on the endocrine hypothalamus, is also innervated by fibres that contain AVP. We examined whether central endogenous AVP is also involved in the control of body fluid homeostasis. To explore this possibility, we examined neuronal activity in the paraventricular nucleus of the hypothalamus (PVN), periventricular parts of the PVN and limbic brain areas, as well as AVP mRNA expression in the PVN and the peripheral secretion of AVP after central salt-loading in rats that had been pretreated i.c.v. with the AVP V(1) receptor antagonist OPC-21268. Neuronal activity in the PVN evaluated in terms of Fos-like immunoreactivity (FLI), especially in the parvocellular subdivisions, was suppressed. On the other hand, FLI was enhanced in the lateral septum, the bed nucleus of the stria terminalis and the anterior hypothalamic area. Similarly, AVP mRNA expression was enhanced in the magnocellular subnucleus of the PVN, despite the lack of a significant difference in the peripheral AVP level between OPC-21268- and vehicle-pretreated groups. We recorded renal sympathetic nerve activity (RSNA) as sympathetic nerve outflow during central salt-loading. The suppression of RSNA was significantly attenuated by i.c.v. pretreatment with OPC-21268. These results suggest that the suppression of RSNA during central salt-loading might be the result of a decrease in neuronal activity in the parvocellular subdivisions of the PVN via the inhibitory action of central endogenous AVP. The parvocellular and magnocellular neurones in the PVN might show different responses to central salt-loading to maintain body fluid homeostasis as a result of the modulatory role of central endogenous AVP.

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Abnormal pressor response to vasopressin in patients with cirrhosis: Evidence for impaired buffering mechanisms

et al. 1990

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In patients with cirrhosis, vasopressin infusion induces sustained vasoconstriction and elevation of arterial pressure. The vasopressor effect could be caused by impairment of mechanisms normally aimed at buffering increases in arterial pressure (reflex bradycardia and decreases in arteriolar resistance). We studied the acute effects of continuous vasopressin infusion (0.4 IU/min) on systemic hemodynamics in seven patients with cirrhosis and in six patients without cirrhosis (controls). Vasopressin effects on systemic O2 consumption were also studied. In both groups, vasopressin infusion induced similar peak increases in arterial pressure, followed by similar decreases in heart rate and cardiac output. However, cirrhotic patients and controls differed 30 min after the start of vasopressin infusion. At 30 min, mean arterial pressure, diastolic arterial pressure and systemic vascular resistance remained significantly higher than preinfusion values in patients with cirrhosis. No decrease in systemic O2 consumption occurred in cirrhotic patients. In controls, at 30 min, mean arterial pressure and diastolic arterial pressure had returned to baseline. Systemic vascular resistance was not significantly higher than the preinfusion value and systemic O2 consumption had significantly decreased to below preinfusion values. We conclude that the vasopressor effect of vasopressin is abnormally sustained in patients with cirrhosis. This might be caused by insufficient buffering of vasopressin-induced arteriolar constriction rather than by abnormal vagal control of heart rate. In turn, as suggested by the lack of a decrease in systemic O2 consumption, persistent arteriolar constriction might be related to abnormally sustained sympathetic vascular tone in patients with cirrhosis.

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Sensitization of aortic and cardiac baroreceptors by arginine vasopressin in mammals.

Cited by 50 publications

References 19 publications

Role of Vasopressin in Cardiovascular and Blood Pressure Regulation

Role of Vasopressin in Cardiovascular and Blood Pressure Regulation

Central Endogenous Vasopressin Induced by Central Salt‐Loading Participates in Body Fluid Homeostasis through Modulatory Effects on Neurones of the Paraventricular Nucleus in Conscious Rats

Abnormal pressor response to vasopressin in patients with cirrhosis: Evidence for impaired buffering mechanisms

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