Sympathetic supraspinal control of venous membrane potential in spontaneous hypertension in vivo

Abstract

To clarify the mechanisms controlling mesenteric venous membrane potential (Em) in spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY), Em was measured in vivo with flexibly mounted glass microelectrodes. Venous diameters were also measured. Em under control conditions were significantly less in SHR. .alpha.-Adrenergic blockade with phenoxybenzamine (PBZ) significantly dilated and hyperpolarized SHR small veins but failed to alter the membrane potential of WKY small veins. After blockade with PBZ, membrane potentials were similar in both strains. Propranolol suffusion failed to alter the SHR membrane potential but depolarized WKY small veins. During blockade with PBZ, propranolol depolarized venous membranes equally in both strains. Membrane potentials after spinal section were similar in both strains and equal to the Em during total adrenergic blockade. In SHR, the relatively depolarized Em derives apparently from altered .alpha.-adrenergic input. In SHR, .alpha.-adrenergic input appears to exert its depolarizing effect, at least in part, by interfering with the expression of endogenous, .beta.-adrenergic hyperpolarization. The .beta.-adrenergic influence, like the .alpha.-adrenergic input in SHR, is dependent on intact supraspinal pathways.