Affiliation:
1. University of Texas Health Science Center, Department of Pharmacology, Division of Clinical Pharmacology, Dallas, Texas, U.S.A.
Abstract
1. Since prostaglandins appear to mediate adrenergically stimulated renin release, the effect of indomethacin was examined on insulin-induced renin and catecholamine release in conscious rats. Insulin (10 units/kg subcutaneously) increased plasma renin activity from 2.8 ± 0.5 to 9.0 ± 1.1 pmol h−1 ml−1 (P<0.001) while also increasing plasma adrenaline, noradrenaline and the urinary excretion of prostaglandin E2 and F2α. Plasma potassium and glucose were reduced by 16 and 54%respectively.
2. Indomethacin (14 μmol/kg subcutaneously) reduced the urinary excretion of prostaglandin E2 and F2α by 67 and 54%respectively, without altering the other parameters.
3. Indomethacin inhibited insulin-induced renin release by 67%(P<0.01) and blocked the insulin-induced increases in urinary postaglandin E2 and F2α. The insulin-induced changes in plasma catecholamines, potassium and glucose were unaltered by indomethacin.
4. These findings suggest that renal prostaglandins mediate this form of adrenergically stimulated renin release by acting at a site distal to the β-adrenoreceptor.
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22 articles.
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