Influence of vasopressin and angiotensin on baroreflexes in the dog.

Cowley, Allen W.; Merrill, David; Osborn, John W.; Barber, Brent J.

doi:10.1161/01.res.54.2.163

Cited by 66 publications

(28 citation statements)

References 36 publications

(41 reference statements)

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“…Because the reflex response produced by vasopressin is of such a magnitude as to oppose almost completely the direct effect, and because the response is markedly greater than that seen with other pressor agents, it has been postulated that vasopressin specifically facilitates the baroreflex. This hypothesis has been confirmed in our laboratory (Sharabi et al 1985;Guo et al 1986) and by Cowley, Merrill, Osborn & Barber (1984) who showed that vasopressin increased the gain of the reflex control of vascular resistance in hypophysectomized, anaesthetized, carotid sinus-isolated dogs.…”

Section: Evidence That Vasopressin Facilitates the Baroreflexsupporting

confidence: 56%

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

Abboud¹,

Aylward²,

Floras³

et al. 1986

The Journal of Physiology

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SUMMARY1. Vasopressin facilitates the baroreflex control ofthe circulation. The peptide may act at several sites to augment the baroreflex. In this study we examined the effect of vasopressin on aortic baroreceptors in anaesthetized rabbits and on left ventricular mechanoreceptors in anaesthetized cats.2 Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from aortic baroreceptors.3. Vasopressin (16 mu./kg. min) significantly enhanced the response of single aortic nerve fibre discharge to elevation in arterial pressure. The slope relating nerve activity to mean arterial pressure increased from 0-24 + 0'05 (mean + S.E. of mean) to 0'50+0-16 impulses/cardiac cycle . mmHg (P < 0-05) in ten aortic medullated fibres and from 0-06 + 0 03 to 0-18 + 0-04 impulses/cardiac cycle . mmHg (P < 0-05) in three non-medullated fibres.4. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from left ventricular mechanoreceptors.5. Vasopressin (16 mu./kg. min) significantly enhanced the response ofsingle nerve fibre discharge from left ventricular mechanoreceptors in response to elevation of left ventricular end-diastolic pressure. The slope relating nerve activity to left ventricular end-diastolic pressure increased from 0-24 + 0-07 to 0-32 + 0-07 impulses/cardiac cycle. mmHg (P < 005) in six medullated fibres and from 0 10 +0-01 to 0 15 + 0-02 impulses/cardiac cycle . mmHg (P < 0-05) in four non-medullated fibres.6. These data show that vasopressin sensitizes high and low pressure baroreceptors and suggest a mechanism by which vasopressin may facilitate the baroreflex control of the circulation.

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Section: Evidence That Vasopressin Facilitates the Baroreflexsupporting

confidence: 56%

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

Abboud¹,

Aylward²,

Floras³

et al. 1986

The Journal of Physiology

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“…Moreover, endogenous and exogenous opioid peptides modulate baroreceptor reflex (12, 13), and intravenous naloxone acts at central p-receptors to attenuate the baroreflex control of RSNA (13). Ang II also modulates the baroreceptor reflex (1,5,27,28), while AVP has been shown to augment it (29). In the present study, pretreatment with V1-receptor antagonist caused a significant increase in RSNA in response to ICV Ang II; furthermore, combined pretreatment with naloxone and V1-receptor antagonist elicited further increases in blood pressure and RSNA in response to ICV infusion of Ang II.…”

Section: Combined Effects Of Naloxone and Vasopressin Vireceptor Antasupporting

confidence: 54%

Interaction of Opioids and Vasopressin in Central Action of Angiotensin II in Consciour Rabbits.

et al. 1998

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It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICY) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICY Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 pg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9 ± 2.2 vs. 16.2 ± 0.7% , p < 0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICY Ang II (20 ± 1 vs. 16 ± 2 mmHg, p < 0.05, and 30.9 ± 3.7 vs. 16.2 ± 0.7% , p < 0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central pressor action of Ang II in conscious rabbits. (Hypertens Res 1998; 21: 89-95)

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“…Recent studies in dogs, rabbits, and humans, have demonstrated that elevations of the circulating levels of AVP are associated with increased sensitivity of baroreceptor reflex activity, thereby buffering the pressor activity of the peptide. 6 In rats, the baroreceptor reflex control of heart rate may be enhanced by AVP through V 2 receptors, 22 whereas the pressor activity of AVP may be buffered through a nonbaroreceptor reflex withdrawal of sympathetic tone. 23 Interestingly, sympathetic hyperactivity 24 and impairment of baroreceptor reflex function 25 are found in SHR.…”

Section: Discussionmentioning

confidence: 99%

“…The specificity in AVP may lie in the fact that AVP, among pressor agents, has the strongest vasoconstrictor activity, 4 has a natriuretic action, 5 and enhances baroreceptor reflex activity 6 ; one or more of these actions of AVP may form the basis of the mechanism for the WAP. Because there is no evidence that these actions of AVP exist in SHR alone, one needs to postulate that SHR are more sensitive than WKY to these actions of AVP.…”

Section: Antihypertensive Effect Of Vasopressin Withdrawal In Young Amentioning

confidence: 99%

Antihypertensive effect of vasopressin withdrawal in young and adult spontaneously hypertensive rats.

Chiu

McNeill

1989

Hypertension

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The extent to which age influences the effect of prolonged intravenous infusion and withdrawal of arginine vasopressin (AVP) on blood pressure was investigated in spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY) of 6-, 10-, 14-, 18-, and 22-week age groups. The pressor response to AVP (20 ng/kg/min for 3 hours) was relatively well maintained in WKY but showed an age-dependent tachyphylaxis in SHR. After cessation of the infusion, arterial pressure of SHR fell in all age groups. In contrast, withdrawal of AVP in WKY resulted in little or no hypotensive response. Thus, a withdrawal-induced antihypertensive phenomenon (WAP) to AVP was specific to SHR. The magnitude of the WAP was significantly correlated with the level of initial blood pressure in SHR (r=-0.81,p<0.001). The magnitude of the tachyphylaxis during the AVP infusion was also correlated with the level of initial blood pressure in SHR (r=-0.66, p<0.001). Accordingly, a significant correlation was found between the magnitude of the WAP and the degree of tachyphylaxis to the pressor activity of AVP in SHR (r=0.69, p< 0.001). The significance of this is unknown, but it might mean that a common underlying mechanism existed in the expression of the tachyphylactic phenomenon and the WAP in SHR. Finally, an apparent enhancement in the baroreceptor reflex sensitivity was observed in both SHR and WKY during the infusion of AVP, but the magnitude of this enhancement appeared to be greater in SHR than in WKY. We conclude that in all age groups, a WAP to AVP is observed in SHR but not in WKY; the magnitude of the WAP appears to depend on the level of the hypertension in SHR. (Hypertension 1989;14:66-72) P reviously, 1 -2 we described a hypotensive response that occurred in spontaneously hypertensive rats (SHR) after the cessation of a prolonged intravenous infusion of a pressor dose of arginine vasopressin (AVP). This fall of arterial pressure below basal control levels did not occur in normotensive Wistar-Kyoto rats (WKY). Furthermore, the hypotensive response in SHR was of a magnitude (approximately 45-50 mm Hg) sufficient to reduce arterial pressure in these SHR to normotensive levels. Thus, a withdrawal-induced antihypertensive phenomenon (WAP) was specific to SHR. The WAP was reduced or absent when angiotensin II or phenylephrine was infused at pressor doses.1 " 3 Accordingly, the WAP appeared to be specific for AVP in SHR. The specificity in

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Influence of vasopressin and angiotensin on baroreflexes in the dog.

Cited by 66 publications

References 36 publications

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

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

Interaction of Opioids and Vasopressin in Central Action of Angiotensin II in Consciour Rabbits.

Antihypertensive effect of vasopressin withdrawal in young and adult spontaneously hypertensive rats.

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