Relationships between pH _i and Tension in Isolated Rat Mesenteric Resistance Arteries

Abstract

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 pH_i 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 pH_i. Intracellular acidosis resulting from elevation of the P_CO2resulted in initial vasoconstriction followed by profound vasodilatation of arteries pre-contracted with noradrenaline (NA). The response to alkalosis induced by NH₄C1 or by lowering the Pco₂ ted to initial dilatation followed by potentiation of NA-induced tension.