Suzuki S, Franco-Saenz R, Mulrow P J
Endocrinology. 1981 May;108(5):1654-7. doi: 10.1210/endo-108-5-1654.
Renal prostaglandins (PGs) have been considered to be important mediators of renin release. However, the mechanism and the site of action have not been clarified. To investigate the role of PGs in the control of isoproterenol-induced renin release, we studied the effect of two inhibitors of PG synthesis, indomethacin and meclofenamate, on the renin release stimulated by isoproterenol and dibutyryl cAMP. We used an in vitro superfusion system of rat renal cortical slices. Neither indomethacin nor meclofenamate affected basal renin release. Isoproterenol (8 x 10(-7) M) increased renin and PGE2 release which was blocked by indomethacin (10(-4) M) and meclofenamate (10(-4) M). Dibutyryl cAMP stimulated renin release significantly, and this effect was not blocked by indomethacin (10(-4) M). Moreover, dibutyryl cAMP did not stimulate PGE2 release. In view of the fact that we have previously shown that PG-stimulated renin release is not blocked by propranolol and is enhanced by phosphodiesterase inhibitors, our present experiments suggest that the site of action of PGs on renin release is located between the beta-adrenergic receptor and the generation of cAMP.
肾前列腺素（PGs）被认为是肾素释放的重要介质。然而，其作用机制和作用部位尚未明确。为了研究PGs在异丙肾上腺素诱导的肾素释放调控中的作用，我们研究了两种PG合成抑制剂吲哚美辛和甲氯芬那酸对异丙肾上腺素和二丁酰环磷腺苷（dibutyryl cAMP）刺激的肾素释放的影响。我们使用了大鼠肾皮质切片的体外灌注系统。吲哚美辛和甲氯芬那酸均不影响基础肾素释放。异丙肾上腺素（8×10⁻⁷ M）增加肾素和前列腺素E2（PGE2）释放，这被吲哚美辛（10⁻⁴ M）和甲氯芬那酸（10⁻⁴ M）阻断。二丁酰环磷腺苷显著刺激肾素释放，且该作用不被吲哚美辛（10⁻⁴ M）阻断。此外，二丁酰环磷腺苷不刺激PGE2释放。鉴于我们之前已表明PG刺激的肾素释放不被普萘洛尔阻断且被磷酸二酯酶抑制剂增强，我们目前的实验表明PGs对肾素释放的作用部位位于β-肾上腺素能受体和环磷腺苷生成之间。
