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Endocrinology, Vol 112, 653-658, Copyright © 1983 by Endocrine Society
ARTICLES |
JX Wilson and DG Butler
The extent to which the vasopressor action of angiotensin II (AII) in birds depends upon the sympathetic nervous system in not known. Therefore, we have tested whether the sympathetic neurotransmitter norepinephrine (NE) mediates the residual vasopressor response to AII in adrenalectomized ducks (Anas platyrhynchos). Treatment with 6- hydroxydopamine (6-OHDA) inhibited by up to 100% the pressor effect of exogenous AII in anesthetized adrenalectomized ducks. After high doses of AII, a transient drop in blood pressure (BP) often preceded or supplanted the pressor response. Systolic BP responses to injections of tyramine also were decreased by 6-OHDA, but responses to NE were increased (diastolic BP) or not affected significantly (systolic BP). Inhibition with SQ20881 of converting enzyme, to decrease endogenous production of AII, reduced pressor responses to AI, but did not affect either baseline BP or responses to AII. Thus, the diminished responsiveness to AII in these catecholamine-depleted ducks was not due to competition from endogeneous AII. Furthermore, the increases in plasma NE and E concentrations that normally follow AII injection were abolished by adrenalectomy and 6-OHDA treatment. The coincident extinction of both cathecholamine and vasopressor responses comprises new evidence that AII raises BP in the Pekin duck by stimulating the sympathetic nervous system. The vasopressor response is mediated by extraadrenal as well as adrenal sources of NE.
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D. G. Butler Mecamylamine blocks the [Asp1,Val5]-ANG II-induced attenuation of salt gland activity in Pekin ducks Am J Physiol Regulatory Integrative Comp Physiol, September 1, 1999; 277(3): R836 - R842. [Abstract] [Full Text] [PDF] |
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