Effects of isoflurane on in situ vascular smooth muscle transmembrane potentials (EM) in small vessels of spontaneously hypertensive rats (SHR)

Volatile anesthetics are vasodilators that inhibit neural, endothehal, and VSM membrane control of vascular tone. In chronic hypertension they enhance hemodynamic instability and adverse clinical outcome. Little is known about (he relative importance of such inhibitory mechanisms in situ and possible differences between hypertensives and nonmotensives. Previously we observed a volatile anesthetic-mediated resting hyperpolanzation in in silu capacilance and resistance vessels that was similar in chronically hypertcnsive rats (SHR) and normotensive controls (WKY). The present study compared the effect of isoflurane (iso) on in situ Em's of VSM in mesenteric (resistance) arteries and (capacitance) veins of 11-14 week old SHR and WKY in the absence of sympathetic neural regulation. Em's were measured sequentially with glass microelectrodes in the same vessel be fore and after local chemical sympathectomy (LCS) (with 6-hydroxydopamine) and during and alter i MAL iso in the uenervalea vessels. LCS hyperpolarized boih vessel lypes in SHR and iso caused additional hyperpolarizatinn in denervated arteries from WKY and denervated veins from SHR (figure). This indicates that sympathetic regulation of VSM tone is enhanced in capacitance and resistance vessels of SHR. It also suggests that during iso in SHR. inhibition of sympathetic regulation accounts for nearly all of the reduction of VSM tone in capacitance vessels but for only part of such reduction in resistance vessels .