Vasopressin Stimulates Phosphatidylinositol Turnover and Aldosterone Synthesis in Rat Adrenal Glomerulosa Cells: Comparison with Angiotensin II*

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Abstract
Vasopressin (VP) action was identified in rat adrenal glomerulosa cells measuring the VP stimulation of phosphatidylinositol breakdown to inositol-1-phosphate (IP). The pKb value (negative log of EC50) for arginine VP (AVP) was 9.1 .+-. 0.4 (n = 6). The V2-selective agonist 1-deamino-8-D-arginine VP did not stimulate IP accumulation. Furthermore, the V1-selective antagonist [1-(.beta.-mercapto-.beta., .beta.-cyclopentamethylenepropionic acid) 2-(O-methyl) tyrosine]AVP (10-7 M) prevented the stimulation by VP. Thus, the VP receptors in adrenal glomerulosa cells appeared to be V1-type similar to those found in liver and vasculature and different from those in kidney. Angiotensin II (AII) also stimulated accumulation of IP but the maximum stimulation achieved was much greater than with VP. In the cases of AII, stimulation of phosphatidylinositol breakdown is thought to be the initiating event in the stimulation of aldosterone synthesis. In agreement with this, both VP and AII stimulated aldosterone synthesis, the maximum AII stimulation (6.5- .+-. 1.3-fold, n = 7) being much greater than the VP stimulation (1.7- .+-. 0.33-fold, n = 7).