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• W2085010355 abstract "S83 INTRODUCTION: Vasorelaxation is directly correlated with hyperpolarization of vascular smooth muscle (VSM) [1]. Previously we observed that isoflurane (ISO) hyperpolarizes VSM and this involves withdrawal of sympathetic tone as well as direct effects at the level of calcium-dependent (KCa) and adenosine triphosphate sensitive (KATP) potassium (K) channels [2]. The purpose of these experiments was to study intrinsic (neurally independent) mechanisms of ISO-mediated VSM hyperpolarization in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) controls as a possible explanation for the hemodynamic instability characteristic of anesthetics in chronic hypertension [3]. METHODS: We measured VSM transmembrane potentials (Em) in situ in externalized small mesenteric arteries and veins of pentobarbital-anesthetized SHR and WKY to indirectly assess contractile state. We recorded the effect of 0.6 mM locally superfused ISO (1.0 MAC) on VSM Em in the presence and absence of the following inhibitors of mechanisms of VSM relaxation: 10-7 M iberiotoxin (IBX), the specific inhibitor of VSM KCa channels; 10-6 M glybenclamide (GLY), the specific inhibitor of VSM KATP channels; 50 [micro sign]M G-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of endothelially derived nitric oxide (NO) synthesis; and 15 [micro sign]M, H-[1,2,4] oxadiazolo [4,3,-alpha] quinoxalin-1one (ODQ), a specific inhibitor of intracellular cyclic guanosine 3[prime],5[prime] monophosphate (cGMP) synthesis. All vessel preparations were sympathetically denervated by superfusion with 6-hydroxydopamine prior to initial measurement of Em. RESULTS: For each vessel type superfused ISO hyperpolarized and all of the inhibitors depolarized VSM equally in SHR versus WKY. Further, both K channel inhibitors abolished the superfused ISO-induced hyperpolarization in both SHR and WKY. However, the inhibitors of the NO-cGMP pathway had no effect on this response. Mean +/- SD arterial VSM Em's are reported in Table 1 (below) while unreported venous data are similar. ODQ data for inhibitor were not reported because the vasoconstriction was excessive and precluded consistent VSM Em measurements.Table 1CONCLUSIONS: These data suggest that superfused ISO-mediated hyperpolarization (and relaxation) of denervated VSM (without systemic hypotension) is not stretch-dependent but involves increased or maintained activation of membrane-bound KCa and KATP channels. Further, such ISO-mediated hyperpolarization appears to be independent of the NO and cGMP-pathways. The similarity of such effects between SHR and WKY indicates that altered VSM K channel function or activity cannot (alone) account for altered circulatory responses to anesthetics in hypertensives using the SHR-WKY model and that the major difference appears to be proximal to the VSM membrane (e.g. the level of sympathetic control)." @default.
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• W2085010355 date "1999-02-01" @default.
• W2085010355 modified "2023-09-25" @default.
• W2085010355 title "MECHANISMS OF ISOFLURANE-MEDIATED HYPERPOLARIZATION OF VASCULAR SMOOTH MUSCLE FROM HYPERTENSIVE AND NORMO-TENSIVE RATS" @default.
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• W2085010355 doi "https://doi.org/10.1097/00000539-199902001-00083" @default.
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