H. Nishimura et al., LEFT-VENTRICULAR FUNCTION OF THE HEART REGRESSED BY NIFEDIPINE IN SPONTANEOUSLY HYPERTENSIVE RATS, Japanese Circulation Journal, 58(2), 1994, pp. 116-122
Left ventricular (LV) performance of the pharmacologically regressed h
eart in hypertension is still unclear. We compared LV function of the
heart regressed by nifedipine with that of the hypertrophied heart in
spontaneously hypertensive rats (SHR). Nifedipine (30 mg/kg/day in foo
d) was given to 15-week-old male SHR for 20 weeks (n=12). Age- and sex
-matched SHR served as controls (n=12). LV catheterization was perform
ed using a micromanometer and cardiac output was determined by the the
rmodilution method. Hemodynamic studies were performed after washout o
f nifedipine (24 h), when blood pressure had returned to the untreated
level. Peak pumping ability was assessed during acute volume loading
with saline. Nifedipine significantly decreased blood pressure in cons
cious animals (222+/-11 to 201+/-12mmHg, p<0.01) and reduced LV weight
(1.20+/-0.07 to 1.07+/-0.05g, p<0.01). After washout of nifedipine, L
V systolic and end-diastolic pressures, dp/dt(max) and cardiac output
determined under pentobarbital anesthesia were similar in the treated
and untreated groups. Peak pumping ability during acute preload elevat
ion was also similar in the 2 groups. Plasma norepinephrine was unalte
red, and plasma renin activity was significantly lower in the treated
rats (p<0.05). These results indicate that nifedipine regressed LVH wi
th a minimal reduction of blood pressure and without evidence of neuro
humoral activation or volume retention. In conclusion, LV function of
the heart regressed by nifedipine was preserved after a spontaneous ri
se in blood pressure and during acute preload elevation.