[Captopril in improving vascular structure and lowering blood pressure]

SHRs were given captopril 20 mg/kg/day (group A, n = 13) and 100 mg/kg/day (group B, n = 17) from intrauterus period to 16 weeks of age, then the treatment was removed. Experiments were carried out at 40 weeks. SBP, left ventricular mass/body weight ratio, wall/lumen ratio of branch III mesenteric and renal artery were determined. The perfusion pressure response to alpha 1 adrenergic agonist (phenylephrine) of resistance blood vessels in a hindquarter model in the presence of Nw-nitro-1-arginine-methyl ester (LNAME) or L-arginine were examined. Untreated SHR (n = 16) and untreated WKY (n = 17) served as controls. Both doses of captopril treatment completely prevented hypertrophy of vascular vessels to some extent comparable to that of the untreated WKY. But their SBP was still significantly higher than that of the untreated WKY. The curves of perfusion pressure responding to incremental doses of phenylephrine shifted rightward in the captopril treatment groups in a dose dependent manner. The curves of high dose group were almost identical to those of WKY, markedly different from that of the untreated SHR. Captopril decreased the over enhanced vasoconstrictor effect of LNAME in SHR. The attenuated vasoconstrictor effect by L-arginine was greatly augmented by captopril, suggesting that captopril improves the function of resistance of vessels by mediating endothelial cells. Captopril-induced alteration in vascular structure and function may be separated from its hypotensive effect. Clinically, continuing administration of captopril may be beneficial to the improvement of the vascular system in those blood pressure unresponsive patients.