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Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age- and sex-matched controls (p less than 0.02). PGF 2 alpha--excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p less than 0.001), while the increase in PGF 2 alpha-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167% +/- 11, SEM) than in the normotensive (386% +/- 46) group (p less than 0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.

Reabsorption of osmotically free water (TmcH2O) was studied in 10 patients after renal transplantation. A rising or constant free water reabsorption was observed under hydropenia and increasing tubular solute load. These findings suggest that in the transplanted kidney the functioning nephrons respond in a normal way to plasma ADH-activity. The excretion of plasma-hypotonic urine reflects decreased antidiuretic activity as in overhydration rather than tubular unresponsiveness to ADH. The excretion of plasma-hypertonic urine indicates tubular reabsorption of osmotically free water due to ADH, and this in general rules out overhydration. Daily estimation of urinary and plasma osmolality will be useful in judging the actual state of hydration after renal transplantation.