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Hypertension, Vol 7, 533-540, Copyright © 1985 by American Heart Association
RJ Tomanek, RD Wangler and CA Bauer
Spontaneously hypertensive rats (SHR) demonstrate an elevated minimal
coronary vascular resistance by the seventh month of age. In an attempt to
determine the role of long-standing hypertension in the etiological process
of the elevated minimal coronary vascular resistance, we treated SHR and
normotensive Wistar-Kyoto rats (WKY) with the vasodilator hydralazine from
the time of weaning (1 month) until they were 7 to 8 months of age. The
animals were instrumented 24 hours after their last drug dose and then
studied on the following day. Using microspheres we measured myocardial
perfusion in conscious rats at rest and during maximal coronary dilation
induced with dipyridamole infusion. Hydralazine maintained arterial blood
pressures in the normotensive range throughout the experimental period, but
had little effect on left ventricular weight/body weight ratios (control
SHR = 2.95 +/- 0.07, treated SHR = 2.73 +/- 0.08, control WKY = 2.39 +/-
0.09, mean +/- SEM). In treated SHR, left ventricular minimal coronary
vascular resistance (per 100 g of tissue) was markedly lower (0.10 +/-
0.01) than in the controls (0.16 +/- 0.01) and not significantly different
from that of WKY (0.11 +/- 0.01). Similar differences were noted in the
nonhypertrophic right ventricle (treated SHR = 0.08 +/- 0.01, control SHR =
0.16 +/- 0.01, control WKY = 0.10 +/- 0.01). Total minimal coronary
vascular resistance was also lower in both ventricles of the treated SHR
compared with their nontreated controls. In WKY, hydralazine treatment
significantly reduced blood pressure and total minimal coronary vascular
resistance (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Prevention of coronary vasodilator reserve decrement in spontaneously hypertensive rats
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