Medical College of Wisconsin
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Short-term angiotensin converting enzyme inhibition reduces basal tone and dilator reactivity in skeletal muscle arterioles. Am J Hypertens 2000 Apr;13(4 Pt 1):389-95

Date

05/23/2000

Pubmed ID

10821341

DOI

10.1016/s0895-7061(99)00204-6

Scopus ID

2-s2.0-0034122846 (requires institutional sign-in at Scopus site)   8 Citations

Abstract

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.

Author List

Frisbee JC, Lombard JH

Author

Julian Lombard PhD, MS Emeritus Professor in the Physiology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Acetylcholine
Angiotensin-Converting Enzyme Inhibitors
Animals
Arterioles
Blood Pressure
Body Weight
Captopril
Male
Microcirculation
Muscle, Skeletal
Muscle, Smooth, Vascular
Nitroprusside
Rats
Rats, Sprague-Dawley
Vasodilation
Vasodilator Agents