Beck N P, Kaneko T, Zor U, Field J B, Davis B B
J Clin Invest. 1971 Dec;50(12):2461-5. doi: 10.1172/JCI106746.
Vasopressin increased adenyl cyclase activity in homogenates of both inner and outer renal medulla of the rat. It also increased the concentration of cyclic 3',5'-adenosine monophosphate (AMP) in slices of both inner and outer medulla but not in renal cortex. In the inner medulla, a concentration of prostaglandin E(1) (PGE(1)), which was ineffective by itself significantly reduced the stimulation of adenyl cyclase activity and cyclic AMP concentration induced by vasopressin. These results are consistent with the hypothesis that PGE(1) can compete with vasopressin for adenyl cyclase-binding sites. However, the findings in the outer medulla suggest the situation is more complex. Although 10(-8) M PGE(1) had no effect by itself and inhibited the vasopressin-induced elevation of cyclic AMP, larger amounts of PGE(1) increased both adenyl cyclase activity and cyclic AMP levels. The maximum effect on the latter parameter was at least 6 times as great as that of maximum amounts of vasopressin.
血管加压素可增加大鼠肾内髓质和外髓质匀浆中的腺苷酸环化酶活性。它还可提高内髓质和外髓质切片中环磷酸腺苷(cAMP)的浓度,但对肾皮质无此作用。在内髓质中,单独使用无效的前列腺素E1(PGE1)浓度可显著降低血管加压素诱导的腺苷酸环化酶活性刺激和cAMP浓度升高。这些结果与PGE1可与血管加压素竞争腺苷酸环化酶结合位点的假说一致。然而,外髓质的研究结果表明情况更为复杂。虽然10^(-8)M的PGE1单独使用无作用且可抑制血管加压素诱导的cAMP升高,但大量的PGE1可增加腺苷酸环化酶活性和cAMP水平。对后一参数的最大作用至少是最大量血管加压素作用的6倍。