The aim of this study is to elucidate the long term effect Of captopril treatment on the endothelial func-tion to release nitric Oxide （NO） in spontaneOusly hypertensive rats （SHR）. The properties of endotheliumwere determined with a model of hindquarter perfusion in response to al adrenergic agonist

phenylephrine

at the age of 40 weeks of SHR which was administrated with captopril （100 mg/kg/day） from lntrauterineand withdrawn at 16 weeks of age. Furthermore

in the presence of N-nitro-L-arginine methyl ester（LNAME）

or L-arginine

the responses to phenylephrine were studied. From the curve of perfusion pres-sure

the minimal

maximal perfusiOn pressure （PPmin

PPmax） and the maximal slOpe （slope）

as well asthe 5O% of effective concentratiOn （EC

） were obtained. The data show that in captopril treated SHR

PPmin

PPmax and slope were markedly lower

but EC50 higher than those of untreated SHR. The curveinduced by phenylephrine was significantly right shift compared with that of untreated SHR. Like WKY

the intensive reactivity to phenylephrine in the presence of LNAME was much lower than that of untreatedSHR. ln the presence of L-arginine

however

the right shift of curves was seen only in captopril treatedSHR and WKY rats

but not in control SHR. In conclusipn

endothelium does involve in the respnse ofresistant vessel to phenylephrine. The mechanism of enhanced reactivity In untreated SHR may be

at leastin part

due to the diminished capacity of producing No frpm endpthelium

and the effect pf sustained hy-potension of early captopril treatment might be relevant to the improved ability of endOthelium.