AJP - Heart and Circulatory Physiology, Vol 266, Issue 2 491-H495, Copyright © 1994 by American Physiological Society
Potassium channels are not involved in vasopressin-induced vasodilation in the rat lung
M. R. Eichinger, R. D. Russ and B. R. Walker
Department of Physiology, School of Medicine, University of New Mexico, Albuquerque 87131.
We have previously observed that arginine vasopressin (AVP)-induced
pulmonary vasodilation is attenuated by nitric oxide (NO) synthesis
inhibition; however, blockade of the response is incomplete even at very
high doses of the inhibitor. Thus it was hypothesized that the remaining
vasodilation might be due to release of an endothelium-derived
hyperpolarizing factor acting to open vascular smooth muscle K+ channels.
Lungs were isolated from male Sprague-Dawley rats and perfused at constant
flow with physiological saline solution containing 4% albumin. After
equilibration, lungs were treated with either glibenclamide (50 microM),
Ba2+ (100 microM), tetraethylammonium (10 mM), or the respective vehicle
and were then constricted with the thromboxane mimetic U-46619. Upon
development of a stable degree of vasoconstriction, AVP (2.5 x 10(-9) M)
was administered and its vasodilator action noted. AVP caused an
approximately 60% reversal of U-46619 vasoconstriction in control lungs,
and this response was not affected by any of the K+ channel blockers. In
contrast, administration of the NO synthesis inhibitor N
omega-nitro-L-arginine (L-NNA; 300 microM) significantly attenuated
AVP-induced dilation to approximately 25%. The addition of K+ channel
blockers did not further diminish the vasodilatory response in
L-NNA-treated lungs. In conclusion, these results suggest that ATP- and
Ca(2+)-sensitive K+ channels are not involved in the pulmonary vasodilatory
response to AVP.
