Relationships between pHi and tension in isolated rat mesenteric resistance arteries

Investigations into the relationship between pHi and tension were carried out in rat mesenteric resistance arteries. Acute acidosis, induced by ammonium chloride pre-pulse, led to variable and transient tension development, but simultaneous removal of extracellular sodium led to a sustained rise in tension associated with maintained intracellular acidification. Dependence of tension and pHi recovery from acute acidosis on Na/H exchange and anion exchange pathways was demonstrated using pharmacological inhibitors. Additionally, removal of HCO3 suggested the anion pathway involved was Na-dependent HCO3 transport. Removal of extracellular calcium, or pharmacological inhibition of voltage-dependent calcium channels, prevented the tension development in response to NH4Cl pre-pulse in an Na-free medium, but did not affect pHi. Intracellular acidosis resulting from elevation of the PCO2 resulted in initial vasoconstriction followed by profound vasodilatation of arteries pre-contracted with noradrenaline (NA). The response to alkalosis induced by NH4Cl or by lowering the PCO2 led to initial dilatation followed by potentiation of NA-induced tension.