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The pressor response to angiotensin II (A II) has been shown to be enhanced, and aldosterone production to be attenuated following administration of indomethacin (Ind), a cyclooxygenase inhibitor, pretreatment. Since PGI2 has been proposed to be a potent vasodepressor prostaglandins, with steroidogenic action, the present study was undertaken to evaluate the regulatory role of PGI2 in the blood pressure and aldosterone responses to A II. Ind was administered to suppress the production of endogenous prostaglandins (30 mg/kg. im. Ind-group) and PGI2 was given after Ind pretreatment (2 ng/kg/min. iv. Ind + PGI2 group) to conscious male rabbits (2.5 approximately 3.5 kg). Baseline blood pressure readings were similar in three groups (control, Ind-, and Ind + PGI2-group). The increment of blood pressure by A II infusion were significantly enhanced in the Ind-group (12.6 +/- 1.3 mmHg) compared with the control-group (8.6 +/- 1.5 mmHg). This enhancement was diminished by PGI2 infusion (7.0 +/- 2.3 mmHg). PGI2 infusion alone does not influence blood pressure in the dose of 0.5 approximately 4.0 ng/kg/min. Aldosterone response to A II was significantly attenuated in the Ind-group (1.5 +/- 1.2 ng/dl) compared with the control-group (7.5 +/- 3.1 ng/dl), but was restored in the Ind + PGI2-group (4.5 +/- 1.3 ng/dl). It is suggested that circulating PGI2 may play a role in the regulation of blood pressure by modulating the pressor response and the aldosterone response to A II.

The Role of Prostacyclin (PGI<SUB>2</SUB>) in the Regulation of Blood Pressure and Aldosterone Response to Angiotensin II