Role of membrane potential in the response of rat small mesenteric arteries to exogenous noradrenaline stimulation.

Abstract

Simultaneous measurements of membrane potential and wall tension were made in 200 .mu.m mesenteric arteries. The resting membrane potential was -59.2 .+-. 0.4 mV and stable (218 measurements, 52 vessels). With maximal exogenous noradrenaline [norepinephrine, NE] stimulation (10 .mu.M) the membrane depolarized to about -34 mV. During the onset of tension development oscillations (about 6 s) in both tension and membrane potential were often seen; the membrane potential changes led the tension changes by .apprx. 1.2 s. In the presence of increased K+ (e.g., 40 mM), vessels had an increased NE sensitivity, and here NE stimulation produced little change in membrane potential. With maximal K+ stimulation (85 mM), in the presence of phentolamine (1 .mu.M), the membrane depolarized to about -17 mV, the tension being .apprx. 70% of the maximal NE response. In the presence of phentolamine (1 .mu.M), NE caused hyperpolarization without tension development. The hyperpolarization was inhibited by propranolol and mimicked by isoprenaline. Apparently, in these small vessels, membrane potential variations are not essential to but have an important modulating influence on the tension response to exogenous NE.