Influence of extracellular pH, sodium propionate and trimethylamine on excitation-contraction coupling in the rat tail artery.
1. The effects of extracellular or intracellular pH changes on agonist- or depolarization-induced contractions of the rat tail artery were investigated. 2. Vessels were perfused initially (25 min) with physiological salt solution (PSS) at a pressure of 30 mmHg. Perfusion was then continued with calcium-free PSS containing either 3.0 micromol/L noradrenaline (NA) or 100 mmol/L K+, which had been made either acidotic or alkalotic. Contractile responses to graded concentrations of calcium were assessed. 3. A reduction in the intracellular or extracellular pH was induced by the addition of a weak acid (30 mmol/L sodium propionate) or reduction of the concentration of HCO3- in the PSS, respectively; an elevation of the intracellular or extracellular pH was produced by the addition of a weak base (10 mmol/L trimethylamine) or by increasing HCO3-, respectively. The PSS was bubbled with 5% CO2/95% O2. 4. Lowered intracellular pH did not alter NA- or K+-stimulated contractions. During lowered extracellular pH, contractile responsiveness and peak response were significantly reduced in K+-stimulated arteries, but were not affected in NA-stimulated arteries. 5. Elevated intracellular pH did not alter NA-induced contraction, but reduced the sensitivity to K+-stimulated contractions. Elevated extracellular pH had little effect on the magnitude of K+-induced contractions, but slightly enhanced (although not significantly) NA-induced contractions. 6. It is concluded that reduced contractile responses to K+ during extracellular acidosis are due to the modulation of potential-operated calcium channels (POC). Alkalotic vasodilatation is mediated by intracellular events and is POC-modulated, whereas alkalotic vasoconstriction appears to be due to extracellular events and is modulated by receptor-operated calcium channels (ROC).