The relationship between renal prostaglandin (PG)I2 biosynthesis and renin release was examined in conscious dogs before and during renal artery constriction. Dogs were chronically instrumented with femoral vein, femoral artery and left renal vein catheters and an inflatable cuff and electromagnetic flow probe were positioned on the left renal artery. After 2 days, mean arterial blood pressure, heart rate, renal blood flow and renal secretion rates of renin and 6-keto-PGF1 alpha were determined before and 10 min after a reduction in renal blood flow. Plasma levels of 6-keto-PGF1 alpha, measured by a gas chromatographic-mass spectrometric assay, were used as an index of PGI2 synthesis. A 38% reduction in renal blood flow did not significantly alter mean arterial blood pressure, heart rate or arterial levels of plasma renin activity or 6-keto-PGF1 alpha. In contrast, renal artery constriction increased renal venous plasma levels of both renin activity and 6-keto-PGF1 alpha by 308% (P less than .002) and 132% (P less than .05), respectively. As a consequence, the renal secretion rate of renin was increased from 80 +/- 40 to 917 +/- 231 ng of angiotensin I . min-1 . hr-1 (P less than .02) and the renal secretion rate of 6-keto-PGF1 alpha was increased from -2.1 +/- 1.1 to 9.0 +/- 3.6 ng/min (P less than .05). In addition, there was a significant correlation between the renal secretion rates of renin and 6-keto-PGF1 alpha (r = 0.688; P less than .013; n = 12). These data indicate a close association between the renal biosynthesis and PGI2 and renin release and are consistent with the concept that PGI2 participates in the release of renin.