AJP - Renal Physiology, Vol 247, Issue 4 680-F685, Copyright © 1984 by American Physiological Society
Alpha 2-adrenoceptors and sodium reabsorption in the isolated perfused rat kidney
D. D. Smyth, S. Umemura and W. A. Pettinger
Alpha 2-Adrenoceptors are known to inhibit adenylate cyclase in a number of
tissues, but their function in the kidney is unknown. Adenylate cyclase and
sodium excretion were stimulated with furosemide (30 microM) in the rat
kidney perfused with Krebs-Henseleit solution (albumin 6.5 g/100 ml, 36
degrees C). beta-Adrenoceptors and alpha 1-adrenoceptors were blocked by
propranolol (100 nM) and prazosin (30 nM) in the perfusate. Urinary cAMP
and sodium excretion increased with furosemide. Activation of alpha
2-adrenoceptors with epinephrine (28 nM) caused no change in perfusion
pressure or flow but decreased urinary cAMP and sodium excretion. These
effects of epinephrine were reversed by the alpha 2-selective adrenoceptor
blocking agent yohimbine (300 nM). Thus, in the setting of
furosemide-stimulated sodium excretion and an associated elevation of
adenylate cyclase, alpha 2-adrenoceptor stimulation resulted in sodium
retention and inhibition of adenylate cyclase. By this receptor mechanism
the sympathoadrenal system may contribute to retention of sodium.
