Alpha 2-adrenoceptors and sodium reabsorption in the isolated perfused rat kidney.
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.
D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D000242:Cyclic AMP / Q000652:urine; D004837:Epinephrine / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D066298:In Vitro Techniques; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010477:Perfusion / Q000295:instrumentation; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D012079:Renal Circulation / Q000187:drug effects; D012964:Sodium / Q000378:metabolism*; D015016:Yohimbine / Q000494:pharmacology
D011942:Receptors, Adrenergic, alpha; D015016:Yohimbine; D005665:Furosemide; D012964:Sodium; D000242:Cyclic AMP; D000262:Adenylyl Cyclases; D011188:Potassium; D004837:Epinephrine