Short-term angiotensin converting enzyme inhibition reduces basal tone and dilator reactivity in skeletal muscle arterioles.

Alterations in resting tone, maximum diameter, and dilator reactivity to acetylcholine (ACH) and sodium nitroprusside (SNP) were assessed in cremaster muscle microvessels of Sprague-Dawley rats receiving angiotensin converting enzyme (ACE) inhibition with captopril for 4 days and in untreated time-control rats. The transilluminated in situ cremaster muscle was superfused with physiologic salt solution (PSS) and viewed via television microscopy; arteriolar diameter was measured using a videomicrometer. Before agonist challenge, resting arteriolar diameter was significantly increased in captopril-treated rats. Although maximum arteriolar diameter (determined during superfusion of the cremaster muscle with Ca2+-free PSS containing 10(-4) mol/L adenosine) was not altered with ACE inhibition, the maximum possible arteriolar dilation was reduced in captopril-treated rats. Captopril administration reduced both ACH- and SNP-induced dilation of cremasteric arterioles compared with responses in control rats, although this was partially a function of the reduced capacity for dilation, primarily to SNP. These observations indicate that short-term ACE inhibition reduces both resting tone and agonist-induced dilator responses of skeletal muscle arterioles.