AJP - Heart and Circulatory Physiology, Vol 243, Issue 3 360-H364, Copyright © 1982 by American Physiological Society
Salt loading augments vascular responses to indomethacin in stroke-prone SHR
T. Imaizumi, A. Takeshita, T. Ashihara and M. Nakamura
We examined whether endogenous prostaglandins (PGs) participated in control
of hindquarters vascular resistance during salt loading in stroke-prone
spontaneously hypertensive rates (SHR-SP). SHR-SP and Wistar-Kyoto rats
(WKY) were fed either a normal (0.3% NaCl) or high (8% NaCl) salt diet for
5 wk. High salt increased blood pressure and hindquarter vascular
resistance (VR) in SHR-SP (P less than 0.01) but not in WKY. Indomethacin
given intravenously increased hindquarter VR in SHR-SP during high salt as
well as during normal salt (P less than 0.01) but not in either group of
WKY. In SHR-SP the increase in hindquarter VR by PG synthesis inhibitors
were two times greater during high salt than during normal salt (P less
than 0.01). In addition, hindquarter vasodilatation by bradykinin was
greater (P less than 0.05) in SHR-SP during high salt than that during
normal salt, but vasodilatation by prostaglandin E1 or nitroglycerin was
not different between the two groups. These results suggest that vascular
synthesis of endogenous PGs was greater in SHR-SP during high salt than
that during normal salt. Increased endogenous PGs may play an important
role in the regulation of hindquarter VR during high salt intake in SHR-SP.
