Steady-state effects of arginine vasopressin on force and pHi of isolated mesenteric resistance arteries from rats.

Control of intracellular pH (pHi) in rat intact resistance arteries has been assessed during activation with arginine vasopressin (AVP) or depolarization with a high potassium concentration. Isometric force of isolated arteries was measured simultaneously with pHi using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Under control conditions, pHi was unchanged during AVP-induced force development but fell during potassium activation. After inhibition of Na(+)-HCO3- cotransport, AVP-induced force development was associated with a fall in pHi. After inhibition of Na(+)-H+ exchange pHi was unchanged during activation with AVP. In the absence of bicarbonate, inhibition of Na(+)-H+ exchange caused an exaggerated fall in pHi during activation with AVP. When AVP was added to depolarized vessels, a further force development and an increase in pHi was seen. This increase in pHi was not affected by amiloride but disappeared after inhibition of Na(+)-HCO3- cotransport by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid or sodium-free conditions. These data suggest that AVP, but not depolarization, changes the characteristics of the Na(+)-HCO3- exchange and the Na(+)-H+ exchange so that these transport systems extrude the acid load associated with the force development more efficiently. We suggest that the importance of the effect of vasoconstrictor hormones on the characteristics of acid extrusion from vascular smooth muscle cells (VSMC) in situ lies in their ability to maintain pHi at resting levels during the metabolic load associated with contraction in the tonically active VSMC.