α₁-Adrenoceptor mediation of urinary bicarbonate excretion

The adrenoceptor mechanism that mediates the reduction of urinary sodium (U(Na)V̇) and bicarbonate (U(HCO₃)V̇) excretion during 1.0-Hz renal nerve stimulation (RNS) was evaluated in 21 anesthetized dogs. In each animal RNS decreased U(Na)V̇ and U(HCO₃)V̇ without changing mean arterial pressure, renal blood flow, or glomerular filtration rate. After these initial responses, dogs were administered phentolamine [2.0 μg · kg^-1 · min^-1 intrarenal artery (ira); n = 7], prazosin (0.7 μg · kg^-1 · min^-1 ira; n = 5), (±)-propranolol (2.0 μg · kg^-1 · min^-1 ira; n = 4), or atenolol (50 mg/kg iv; n = 5) and the renal responses to RNS were again tested. Both the antinatriuretic response and reduction of U(HCO₃)V̇ during RNS were abolished by α₁/α₂-adrenoceptor blockade with phentolamine and by α₁-adrenoceptor antagonism with prazosin. β-Adrenoceptor blockade with (±)-propranolol (β₁/β₂) or atenolol (β₁) did not alter either the decrease in U(Na)V̇ or U(HCO₃)V̇ after RNS. These results provide further evidence that, during low-frequency RNS, reduction of U(Na)V̇ is mediated in part by carbonic anhydrase-dependent bicarbonate reabsorption. These antinatriuretic responses and decreases in U(HCO₃)V̇ during 1.0-Hz RNS are mediated by adrenergic neurotransmitter stimulation of α₁-adrenoceptors.