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<sub>i</sub> recovery from acute acidosis on Na/H exchange and anion exchange pathways was demonstrated using pharmacological inhibitors. Additionally, removal of HCO<sub>3</sub> suggested the anion pathway involved was Na-dependent HCO<sub>3</sub> transport. Removal of extracellular calcium, or pharmacological inhibition of voltage-dependent calcium channels, prevented the tension development in response to NH<sub>4</sub>Cl pre-pulse in an Na-free medium, but did not affect pH<sub>i</sub>. Intracellular acidosis resulting from elevation of the P<sub>CO2</sub>resulted in initial vasoconstriction followed by profound vasodilatation of arteries pre-contracted with noradrenaline (NA). The response to alkalosis induced by NH<sub>4</sub>C1 or by lowering the Pco<sub>2</sub> ted to initial dilatation followed by potentiation of NA-induced tension.