AJP - Heart and Circulatory Physiology, Vol 253, Issue 6 1612-H1617, Copyright © 1987 by American Physiological Society
Effects of atriopeptin III on isolated mesenteric resistance vessels from SHR and WKY
C. Cauvin, M. Tejerina and C. van Breemen
Department of Pharmacology, University of Miami School of Medicine, Florida 33101.
The effects of atriopeptin III (AP III) were determined on agonist-induced
[i.e., 10(-4) M norepinephrine (NE)] and depolarization-induced (80 mM K+)
contractions of isolated mesenteric resistance vessels (ID approximately
100 microns) from spontaneously hypertensive rats (SHR) and from
normotensive control Wistar-Kyoto (WKY) rats. The vessels from both groups,
when activated by 80 mM K+, were unaffected by AP III. However, activation
of WKY vessels by 10(-4) M NE (both phasic and tonic contraction) was
inhibited quite effectively and potently by AP III, whereas that in SHR
vessels was much less inhibited. In the WKY rat vessels, the concentration
of AP III that inhibited contraction by 50% for NE-induced phasic tension
was 3.1 +/- 1.3 nM, whereas in SHR vessels it was nearly 1 microM.
Comparison of AP III inhibition of NE-induced phasic tension to that at 5
min of activation (tonic tension) indicated that the tonic contractions
were less sensitive to AP III than the phasic contractions in the vessels
from both strains. A similar experiment indicated that AP III was a potent
inhibitor of agonist-induced activation in a human renal resistance vessel
(ID 125 microns) and that this vessel depended virtually completely on
extracellular Ca2+ for NE-induced contraction. These studies contrast with
earlier reports (1, 30) that similar peptides inhibited tension only in rat
renal resistance vessels and not in resistance vessels from other vascular
beds. The decreased sensitivity and efficacy of AP III in inhibiting
tension in SHR compared with WKY mesenteric resistance vessels is discussed
in the context of the etiology of spontaneous hypertension.
