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ROLE OF NITRIC OXIDE IN IMPAIRED CORONARY CIRCULATION AND IMPROVEMENT BY ANGIOTENSIN II RECEPTOR ANTAGONIST IN SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Fujita Hiroshi,
Takeda Kazuo,
Nakamura Kame,
Uchida Atsushi,
Takenaka Ken,
Itoh Hiroshi,
Nakata Tetsuo,
Sasaki Susumu,
Nakagawa Masao
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02858.x
Subject(s) - medicine , angiotensin ii , coronary circulation , nitric oxide , coronary flow reserve , angiotensin ii receptor type 1 , endocrinology , antagonist , blood pressure , cardiology , receptor antagonist , muscle hypertrophy , angiotensin ii receptor antagonist , candesartan , blood flow , angiotensin receptor , receptor
Summary 1. To determine whether coronary flow regulation by nitric oxide (NO) is impaired in the hypertensive heart (HTH), coronary perfusion was measured in isolated rat hearts using NO synthesis inhibitor L‐N G ‐monomethyl arginine (L‐NMMA) in Wistar‐Kyoto (WKY) rat and spontaneously hypertensive rat (SHR) with and without chronic N ω ‐nitro‐L‐arginine‐methylester (L‐NAME) treatment. Moreover, the effect of angiotensin 11 receptor antagonist (AT1 receptor antagonist) (TCV‐116) on the impaired coronary circulation in HTH was examined. 2. Coronary flow (CF) was decreased in HTH accompanied with cardiac hypertrophy. The decreased response of CF to L‐NMMA infusion was diminished in HTH. It is suggested that NO production was reduced in coronary vasculature in HTH. 3. In chronic L‐NAME treated SHR, blood pressure and cardiac hypertrophy were accelerated. Although coronary flow resistance (CFR) was increased, the increased response of CFR to L‐NMMA infusion was not altered. 4. The AT1 antagonist improved total minimal coronary flow resistance (MCFR) restoring CFR response in SHR, although it did not recover CFR response in chronic L‐NAME treated SHR. 5. Taken together the findings suggest that NO production was exhausted in the coronary artery even in the developing stage of hypertension and this exhaustion could contribute to the impairment of coronary circulation of HTH.