A. Robert et al., MYOPLASMIC CALCIUM-VASOCONSTRICTION COUPL ING IN THE PERFUSED TAIL ARTERY OF THE ADULT SHR - EFFECT OF ANTIHYPERTENSIVE TREATMENT, Therapie, 48(4), 1993, pp. 345-349
In order to investigate whether smooth muscle intracellular calcium le
vels ([Ca2+]i) are related to hypertension and drug-induced changes in
blood pressure, we studied basal perfusion resistance and basal [Ce+]
i and increases in perfusion pressure and [Ca2+]i using the fluorescen
t dye, fura-2 (dual wavelength excitation) in perfused tail artery. Th
ese were removed from 6 month old SHR previously treated (CAP + HCZ) f
or 10 weeks with captopril plus hydrochlorothiazide (44 and 22 mg/kg/d
ay po, respectively). Separate groups received captopril (CAP) or hydr
ochlorothiazie (HCZ) alone, at similar doses, or no treatment (SHR). A
fifth group of WKY normotensive rats did not receive any drug. Follow
ing determination of systolic arterial pressure (SAP) in awake rats, t
ail artery segments were removed and perfused at a constant flow rate
with physiological salt solution plus fura-2/AM. Basal resistance and
[Ca2+]i were determined. Then a dose-response curve for calcium chlori
de in the presence of a depolarizing concentration of potassium chlori
de was constructed. SAP was lowered in groups CAP + HCZ or CAP, but no
t in the group HCZ. Basal [Ca2+]i were similar in treated and untreate
d SHR and in WKY. Basal resistance to flow was lower in groups CAP + H
CZ or CAP, and in WKY, than in untreated SHR. In depolarized arterial
segments, vasoconstrictor responses to perfusion with calcium chloride
were lower in groups CAP + HCZ or CAP, and in WKY. Increases in [Ca2]i were diminished in WKY rats. SAP measured in awake SHR and WKY was
significantly correlated to basal and stimulated intracellular calcium
-vasoreactivity coupling measured in vitro.