Plasma renin activity related to sodium balance, renal function and urinary vasopressin in the newborn infant.

Plasma renin activity was determined in 25 healthy, full-term, newborn infants aged 1 day to 9 weeks. High values were found, the mean level at 1-2 days of life (24.8 +/- 8.4 ng/ml/hr, SE) being significantly higher than the mean levels at 7-9 days (5.8 +/- 1.5) and at 4-9 weeks (8.1 +/- 1.3) (P less than 0.05). No correlation was found between plasma renin activity and systolic blood pressure, hematocrit, creatinine clearance, serum sodium, or serum potassium. Plasma renin activity (log values) was inversely correlated with sodium intake (r = -0.58) or with urinary sodium (r = -0.44), and positively with urinary osmolality (r = 0.67). The correlations reached higher coefficients if only infants aged less than or equal to 9 days were considered. In addition, vasopressin was measured by radioimmunoassay in the urine. The daily excretion was lower in newborn infants (9.4 +/- 1.6 ng/m2/day, SE, at 1-2 days of postnatal life) than in healthy children (37.1 +/- 5.6), and was significantly correlated with creatinine clearance (r = 0.69), but not with urinary osmolality

Long-term effects of ACTH combined with angiotensin II on steroidogenesis and adrenal zona glomerulosa morphology in the rat.

To test the hypothesis that the trophic action of angiotensin II on the adrenal zona glomerulosa may allow a sustained stimulation of aldosterone by ACTH by preventing the morphological changes of the zona glomerulosa cells into zona fasciculata-like elements we investigated the effects in rats of a 6-day treatment with ACTH (100 micrograms/kg/day) alone or combined with angiotensin II (300 ng/kg/day) on corticosterone and aldosterone production and adrenal morphology. The responsiveness of both steroids to an acute ACTH dose was also studied on the last day of long-term treatment. Morphologic data showed that prolonged ACTH treatment stimulated the growth of zona glomerulosa cells, though it transformed the tubulo-lamellar cristae of mitochondria into a homogeneous population of vesicles. Angiotensin II furthered the trophic effects of ACTH but prevented the mitochondrial transformation. Despite its ability to conserve the well differentiated aspect of the zona glomerulosa cells, the administration of angiotensin II was unable to prevent the fall in the secretion of aldosterone caused by chronic ACTH treatment and its subsequent unresponsiveness to ACTH stimulation