J. Tsoporis et al., EFFECTS OF THE ARTERIAL VASODILATOR MINOXIDIL ON CARDIOVASCULAR STRUCTURE AND SYMPATHETIC ACTIVITY IN SPONTANEOUSLY HYPERTENSIVE RATS, Journal of hypertension, 11(12), 1993, pp. 1337-1345
Objective and design: In spontaneously hypertensive rats (SHR) arteria
l vasodilators do not cause regression and might cause further progres
sion of cardiac hypertrophy. To assess whether these effects extend to
the vasculature, and to examine the possible mechanisms involved, car
diac and mesenteric arterial structure was evaluated with respect to c
hanges in cardiac volume load and cardiac and arterial sympathetic act
ivity during long-term (5- and 10-week) treatment of 16-week-old SHR w
ith the arterial vasodilator minoxidil, alone or in combination with t
he diuretic hydrochlorothiazide. Results: Despite causing a persistent
decrease in blood pressure in SHR, minoxidil further increased left a
nd right ventricular weights and left ventricular internal diameter. I
n combination with hydrochlorothiazide, minoxidil caused concentric, r
ather than eccentric, left ventricular hypertrophy. In the mesenteric
arterial bed of SHR, minoxidil increased the lumen of the superior mes
enteric artery, and prevented further increases in the medial area of
the large and small mesenteric arteries. The increase in lumen size of
the superior mesenteric artery by minoxidil was abolished when hydroc
hlorothiazide was added to the treatment. After 10 weeks' treatment wi
th minoxidil, noradrenaline turnover rates were still significantly in
creased in the left ventricle but were decreased in the mesenteric art
eries in the SHR. Minoxidil increased plasma and blood volumes, the in
creases being largely prevented by concomitant diuretic treatment. Con
clusions: We conclude that there are regional differences in the respo
nse of the cardiovascular system to minoxidil in SHR. Some of these di
fferences may be related to differences in regional sympathetic activi
ty, whereas volume load appears to play a modulatory role.