FORCE, MEMBRANE-POTENTIAL, AND [CA2- EFFECTS OF CHANGES IN PHI(]I DURING ACTIVATION OF RAT MESENTERIC SMALL ARTERIES WITH NOREPINEPHRINE, POTASSIUM, ALUMINUM FLUORIDE, AND PHORBOL ESTER )

In activated rat mesenteric small arteries, the effect of pH(i) on for ce, membrane potential, and free cytosolic calcium ([Ca2+]i) was asses sed. Arteries were mounted in a myograph for isometric force developme nt, and [Ca2+]i, pH(i), or membrane potential was measured simultaneou sly with force. During activation with norepinephrine, potassium, alum inum fluoride (AlF4-), and phorbol 12-myristate 13-acetate (PMA, a pho rbol ester), the vessels depolarized and [Ca2+]i increased, although t he ratio of force to [Ca2+]i was less during potassium activation than with the other types of activation. Changes in pH(i), with a constant pH(o) were induced with NH4Cl or by changing PCO2. In resting vessels , the effects of the changes in pH(i) on tension, membrane potential, and [Ca2+]i were negligible. In vessels activated with norepinephrine or AIF4-, alkalinization caused an acute decrease of tone, which could be explained by a decrease in [Ca2+]i Consequent to repolarization of the membrane. In vessels activated with potassium or PMA, the effects of alkalinization were smaller. This is consistent with acute alkalin ization, affecting steps proximal in the excitation-contraction coupli ng distal to activation of G proteins. Acidification caused a transien t increase in tone and [Ca2+]i, irrespective of the mode of stimulatio n, without affecting the membrane potential. Ryanodine did not abolish the transient increase in tone and [Ca2+]i. Thus, acute intracellular acidification may induce tone by release of an intracellular ryanodin e-insensitive calcium pool or by affecting transmembranal calcium flux although in a membrane potential-independent way.