Small vessel membrane potential, sympathetic input, and electrogenic pump rate in SHR.

Comparative measurements of transmembrane potential (Em) were made in situ in vascular smooth muscle cells (VSM) of mesenteric small principal arteries and veins with innervation and circulation intact. Vessels were in an externalized, topically suffused jejunal loop in 4- to 5-wk-old (initial hypertension) and 12- to 15-wk-old (established hypertension) anesthetized, spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive control rats. Comparable in vitro measurements of Em were also made in VSM of isolated intact small mesenteric vessel segments (from the 12- to 15-wk-old animals) maintained at their in situ lengths and suffused with physiological salt solution (PSS). During suffusion in situ with control PSS, VSM of both small veins and arteries in older (but not younger)SHR were less polarized than in WKY. Local chemical sympathetic denervation in situ (with 6-hydroxydopamine) hyperpolarized VSM of both vessel types in older (but not younger) SHR to the same Em levels measured in situ in respective WKY vessels. After local denervation, VSM of small arteries (but not veins) of both SHR and WKY remained less polarized in situ than in vitro, suggesting the presence of one or more circulating factors with a specific depolarizing action on the arterial side in both animal types. In vitro, VSM of both small arteries and veins from WKY but not SHR were depolarized immediately by 10(-3) M ouabain. In contrast, reduction of the PSS suffusate temperature to 16 degrees C caused a significantly greater depolarization in VSM of SHR vessels.(ABSTRACT TRUNCATED AT 250 WORDS)