1. Sodium, potassium-dependent adenosine triphosphatase (ATPase) of the renal tubule is known to be dependent on both gluco- and mineralo-corticoids. Recent evidence suggests that corticosteroids may modulate ATPase activity at extrarenal sites. The myocardium contains glucocorticoid receptors to which mineralocorticoids can also bind. Thus, the possibility that myocardial ATPase is corticosteroid dependent was examined in the Wistar-Kyoto (WKY) normotensive rat and also in the spontaneously hypertensive (SH) rat, a strain previously shown to exhibit reduced myocardial ATPase activity. 2. WKY and SH rats (in groups of 10) were either sham operated or adrenalectomized and placed on 1% NaCl solution as drinking water. Adrenalectomized rats subsequently received daily intraperitoneal injections of either vehicle (1% NaCl, 0.5 ml), aldosterone (30 μg/kg) or dexamethasone (60 μg/kg). Renal cortical and myocardial ATPase activities were determined 21 days later in all groups. 3. Adrenalectomized WKY rats had reduced myocardial ATPase activity (5.15 ± 0.88 vs 8.18 ± 0.93 μmol of phosphate h −1 mg −1 of protein in controls; P < 0.01). This observed decrease in ATPase in adrenalectomized rats could be at least partly prevented by selective aldosterone or dexamethasone replacement. Parallel changes were observed with renal cortical ATPase. 4. SH rat myocardial ATPase was lower than in WKY rats ( P <0.05, 5.88 ± 0.99 μmol of phosphate h −1 mg −1 of protein) and was unaffected by adrenalectomy (5.47 ± 0.68 μmol of phosphate h −1 mg −1 of protein) whether accompanied by aldosterone (6.08 ± 0.68 μmol of phosphate h −1 mg −1 of protein) or dexamethasone (6.47 ± 0.84 μmol of phosphate h −1 mg −1 of protein) therapy or not. Renal cortical ATPase, however, exhibited corticosteroid dependency in the SH rats that resembled the pattern observed in WKY rats. 5. It is suggested that the lower ATPase activity observed in SH rats after the evolution of hypertension may result from decreased sensitivity to endogenous corticosteroids.
1. The effects of dietary sodium intake on plasma 18-hydroxycorticosterone (18-OHB) responses to physiological stimuli and recumbent 24-h-plasma 18-OHB levels have been examined in nine normal male subjects. 2. Basal supine levels of 18-OHB during a 40 mmol of sodium intake period (62.5 ± 6.0 ng/dl) were considerably greater ( P < 0.0001) than the levels during a 200 mmol of sodium intake period (9.8 ± 1.2 ng/dl). Further incremental and percentage changes of 18-OHB in response to graded dose infusions of angiotensin II and adrenocorticotropic hormone (ACTH) were greater during the 40 mmol of sodium intake period. 3. Although the mean 24 h levels of plasma 18-OHB during the 40 mmol of sodium intake period (43.9 ± 4.0 ng/dl) were greater ( P < 0.001) than those during the 200 mmol of sodium intake period (9.4 ± 1.2 ng/dl), the circadian rhythm of 18-OHB secretion was similar under the two extremes of sodium intake. 4. Factors which increase angiotensin II levels, such as sodium restriction, isometric exercise and angiotensin infusion, selectively increase 18-OHB and aldosterone, suggesting that angiotensin II increases 18-OHB and aldosterone secretion, in part, by modulation of the 18-hydroxylation reaction involved in conversion of corticosterone into 18-OHB.