Smyth D D, Umemura S, Pettinger W A
Am J Physiol. 1984 Oct;247(4 Pt 2):F680-5. doi: 10.1152/ajprenal.1984.247.4.F680.
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.
已知α2-肾上腺素能受体可抑制多种组织中的腺苷酸环化酶，但其在肾脏中的功能尚不清楚。在用克雷布斯-亨泽莱特溶液（白蛋白6.5 g/100 ml，36℃）灌注的大鼠肾脏中，用呋塞米（30μM）刺激腺苷酸环化酶和钠排泄。灌注液中的β-肾上腺素能受体和α1-肾上腺素能受体被普萘洛尔（100 nM）和哌唑嗪（30 nM）阻断。呋塞米使尿中cAMP和钠排泄增加。用肾上腺素（28 nM）激活α2-肾上腺素能受体不会引起灌注压力或流量的变化，但会降低尿中cAMP和钠排泄。肾上腺素的这些作用被α2选择性肾上腺素能受体阻断剂育亨宾（300 nM）逆转。因此，在呋塞米刺激钠排泄及相关的腺苷酸环化酶升高的情况下，α2-肾上腺素能受体刺激导致钠潴留并抑制腺苷酸环化酶。通过这种受体机制，交感肾上腺系统可能有助于钠的潴留。
