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.
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - 1988|
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