The Role of Corticosteroids in the Regulation of Myocardial Na, K-ATPase in Normotensive and Spontaneously Hypertensive Rats

Abstract

Sodium, potassium-dependent adenosine triphosphatase (ATPase) of the renal tubule is known to be dependent on both gluco- and mineralocorticoids. 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. 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 micrograms/kg) or dexamethasone (60 micrograms/kg). Renal cortical and myocardial ATPase activities were determined 21 days later in all groups. Adrenalectomized WKY rats had reduced myocardial ATPase activity (5.15 +/- 0.88 vs 8.18 +/- 0.93 mumol of phosphate h-1 mg-1 of protein in controls; P less than 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. SH rat myocardial ATPase was lower than in WKY rats (P less than 0.05, 5.88 +/- 0.99 mumol of phosphate h-1 mg-1 of protein) and was unaffected by adrenalectomy (5.47 +/- 0.68 mumol of phosphate h-1 mg-1 of protein) whether accompanied by aldosterone (6.08 +/- 0.68 mumol of phosphate h-1 mg-1 of protein) or dexamethasone (6.47 +/- 0.84 mumol of phosphate h-1 mg-1 of protein) therapy or not.(ABSTRACT TRUNCATED AT 250 WORDS)