Relationships between pHi and Tension in Isolated Rat Mesenteric Resistance Arteries

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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 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 PCO2resulted 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.

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