Rabbit aorta: electrical properties and agonist-induced depolarization.

The resting membrane potential of the smooth muscle cells of strips of rabbit aorta varied between -50 to -60 mV. No spontaneous spike discharges were observed. The membrane of the myocytes showed a marked outward rectifying property. The rabbit aorta had cable properties with a space constant (lambda) of 1.54 +/- 0.04 mm. Parallel with a progressive mechanical tension development, noradrenaline and the alpha 1-agonist methoxamine depolarized the membrane in a concentration-dependent manner up to -40 mV. Stimulation of aortic alpha 1-adrenoceptors by noradrenaline reduced the steepness of the current-voltage relationship and diminished the space constant from 1.54 to 0.8 mm, indicating a decrease in membrane resistance. No action potentials were evoked by noradrenaline. The alpha 2-agonist, B-HT 920, produced only a slight contraction and virtually no change in membrane potential. As compared to noradrenaline or methoxamine, angiotensin II was a partial agonist to induce contraction, with an intrinsic activity of 0.6-0.7. The octapeptide depolarized the membrane of the myocytes in a concentration-dependent manner and to a maximal extent similar to that observed for alpha 1-adrenoceptor stimulation. No action potentials appeared with angiotensin II. In contrast to earlier reports, depolarization did occur in the rabbit aorta in response to noradrenaline. The demonstration of depolarization raises the possibility that contraction of this blood vessel occurs through electromechanical and not or not solely through pharmacomechanical coupling when receptors for two important endogenous vasoconstrictors, noradrenaline and angiotensin II, are stimulated.