Abstract
Summary
Lithium administration blocks the antidiuretic effect of arginine vasopres-sin (AVP). In order to determine whether or not Li+ administration also blocks the natriuretic effect of AVP, we administered AVP at 50 mU/kg/min (“high dose”) or 50 mU/kg/hr (“low dose”) to normal and Li+treated dogs. AVP administration at both doses resulted in a significant increase in urine flow and sodium excretion in both normal and Li+-treated dogs. In addition, AVP administration resulted in a dramatic increase in plasma phosphate concentration. Studies were therefore performed in thyro-parathyroidectomized (TPTX) dogs in order to determine whether an increase in parathyroid hormone (PTH) release could account for the natriuretic effect of AVP. AVP administration to TPTX dogs also resulted in the same increase in sodium excretion and plasma phosphate concentration as in normal dogs. The hyperphosphatemia of AVP was unrelated to the vasoconstrictor-pressor effect of the hormone since it was present when blood pressure was prevented from rising by sodium nitroprusside administration. These data suggest a difference in the mechanism of action whereby AVP elicits its natriuretic and antidiuretic effects. The hyperphosphatemic effect of AVP administration is described for the first time.
Dr. Arruda is a Research Associate at the Veterans Administration West Side Hospital in Chicago, Illinois. This research was supported in part by the following grants: Veterans Administration Central Office Grant No. 7083-04, Veterans Administration Basic Institutional Support Grant No. 3324-01, Veterans Administration Research Associate Grant No. 052-01, and National Institutes of Health Grant No. AM 18399.
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