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

We have made simultaneous measurements of membrane potential and wall tension in rat 200 microns mesenteric arteries. 2. The resting membrane potential was -59.2 +/- 0.4 mV and stable (218 measurements, fifty-two vessels). 3. With maximal exogenous noradrenaline stimulation (10 microM) the membrane depolarized to about -34 mV. During the onset of tension development oscillations (period about 6 sec) in both tension and membrane potential were often seen; the membrane potential changes led the tension changes by about 1.2 sec. 4. In the presence of increased K+ (e.g. 40 mM), vessels had an increased noradrenaline sensitivity, and here noradrenaline stimulation produced little change in membrane potential. 5. With maximal K+ stimulation (85 mM), in the presence of phentolamine (1 microM), the membrane depolarized to about -17 mV, the tension being about 70% of the maximal noradrenaline response. 6. In the presence of phentolamine (1 microM), noradrenaline caused hyperpolarization without tension development. The hyperpolarization was inhibited by propranolol and mimicked by isoprenaline. 7. The results suggest that in these small vessels membrane potential variations are not essential to, but have an important modulating influence on, the tension response to exogenous noradrenaline.