MYOGENIC ACTIVATION AND CALCIUM SENSITIVITY OF CANNULATED RAT MESENTERIC SMALL ARTERIES

Pressure-induced activation of vascular smooth muscle may involve elec tromechanical as well as nonelectromechanical coupling mechanisms. We compared calcium-tone relations of cannulated rat mesenteric small art eries during pressure-induced activation, depolarization (16 to 46 mmo l/L K+), and alpha(1)-adrenergic stimulation (1 mu mol/L phenylephrine ). The intracellular calcium concentration was expressed as the fura-2 ratio, normalized to the maximal and minimal ratios. In order to comp are activation levels at various pressures, tone was expressed as the ratio of active wall tension to the maximal active tension, The passiv e and maximal active pressure-diameter relations needed for the calcul ation of tone were determined in a separate set of experiments, using isometric loading of cannulated vessels. Pressure steps from 20 to 60 and then to 100 mm Hg caused a modest rise of calcium. Nifedipine (1 m u mol/L) blocked both the calcium rise and the resulting myogenic resp onses. Electromechanical coupling could not fully account for the myog enic response: the calcium sensitivity, defined as the slope of the ca lcium-tone relation, was five times higher during pressure-induced act ivation compared with potassium stimulation and twice as high as the s ensitivity during alpha(1)-adrenergic stimulation. We therefore conclu de that the myogenic response involves a small but necessary rise in c alcium due to influx through L-type calcium channels, as well as a non electromechanical coupling mechanism that greatly enhances the calcium sensitivity of the contractile machinery.