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—α1 -Adrenoceptor (α1 -AR) stimulation increases sarcolemmal Na+ -H+ exchanger (NHE) activity. The present study was designed to determine the role(s) of α1 -AR subtype(s) in mediating this response. As an index of NHE activity, acid efflux rates (J H s) were determined in single rat ventricular myocytes loaded with the pH-sensitive fluoroprobe carboxy-seminaphthorhodafluor-1 after 2 consecutive intracellular acid pulses in bicarbonate-free medium.J H at pHi 6.90 did not change significantly during the second pulse relative to the first in control cells but increased in a dose-dependent manner when the second pulse occurred in the presence of phenylephrine (nonselective α1 -AR agonist) or A61603 (α1A -AR–selective agonist), with EC50 values of 1.24 μmol/L and 3.6 nmol/L, respectively (both agonists given together with 1 μmol/L atenolol). Stimulation of NHE activity by 10 μmol/L phenylephrine was inhibited in a dose-dependent manner by the competitive antagonists prazosin, WB4101, and 5-methylurapidil, with IC50 values of 12, 32, and 149 nmol/L, respectively. Analyses of the relative EC50 and IC50 values obtained (andK i values estimated from the antagonist IC50 s) in relation to the relative potencies of these agents at native rat α1 -AR subtypes and their relative affinities for recombinant rat α1 -ARs suggest that α1 -adrenergic stimulation of sarcolemmal NHE activity is likely to be mediated selectively by the α1A -AR.

α 1 -Adrenergic Stimulation of Sarcolemmal Na + -H + Exchanger Activity in Rat Ventricular Myocytes

α ₁ -Adrenergic Stimulation of Sarcolemmal Na ⁺ -H ⁺ Exchanger Activity in Rat Ventricular Myocytes