HRs were given
captopril 20 mglkglday (groupA , n= 13) and
100 mg/kg/day (group B , n=17) fromintrauterus peritxl
to 16 weeks of age, then the treat-ment
was removed. Experiments were carried out at 40weeks. SBP, left ventricular masslbody weight
ratio,wallllumen ratio of branch III mesenteric and renalartery were determined. The perfusion
pressure re-sponse to ai adrenergic agonist (phenylephrine) of resis-tance blood vessels in a
hindquarter model in the pre-ence of Nw -nitro-1-arginine-methyl ester (LNAME) orLarginine were
examined.
Untreated SHR (n = 16)and untreated WKY (n= 17) served as controls. Bothdoses of
captopril treatment completely prevented hyper-trophy of vascular vessels to some extent
comparable tothat of the untreated WKY. But their SBP was still sig-nificantly higher than that of
the untreated WKY. Thecurves of perfusion pressure responding to incrementaldoses of
phenylephrine shifted rightward in the captopriltreatment groups in a dose dependent manner.
Thecurves of high dose group were almost identical to thoseof WKY , markedly different from
that of the untreatedSHR. Captopril decreased the over enhanced vasocon-strictor effect of
LNAME in SHR. The attenuated vaso-constrictor effect by L-arginine was greatly augmentedby
captopril, suggesting that captopril improves thefunction of resistance of vessels by mediating
endothelialcells. Captopril-induced alteration in vascular structureand function may be
separated from its hypotensive ef-fect. Clinically, continuing administration of captoprilmay be
beneficial to the improvement of the vascularsystem in those blood pressure unresponsive
patients.