BOTH LOW-SODIUM AND HIGH POTASSIUM INTAKE INCREASE THE LEVEL OF ADRENAL ANGIOTENSIN-II RECEPTOR-TYPE-1, BUT NOT THAT OF ADRENOCORTICOTROPINRECEPTOR

Angiotensin-II (AII), a component of the renin-angiotensin system, is the major factor that regulates the formation of aldosterone in the ad renal cortex tons glomerulosa (ZG). The activity of this system is inc reased by an increase in potassium intake or a decrease in sodium inta ke. Using immunoblotting analysis, we determined whether these ions af fect the expression of type 1 All receptors (AT(1)) and compared the r esults thus obtained with the AT(1) receptor mRNA levels. We also stud ied the interrelation among AII, AT(1) receptors, cytochrome P450 aldo sterone synthase (P450(c18)), and plasma aldosterone levels in rats fe d a normal diet or a low sodium or high potassium diet with or without captopril, an inhibitor of angiotensin-converting enzyme, for 7 days. The effects of ions on the level of ACTH receptor mRNA were also anal yzed. We found that a low sodium intake increased plasma aldosterone l evels from 5.5 to 236 ng/dl and led to 2.3- and 3.7-fold increases in the levels of adrenal ZG AT(1) receptor protein and AT(1) receptor mRN A, whereas a 11.8-fold increase was found in the level of P450(c18) mR NA. Captopril almost completely reversed these effects. We have shown that a high potassium intake increased plasma aldosterone levels to 25 .9 ng/dl and also led to 1.84- and 1.95-fold increases in the level of ZG AT(1) receptor protein and AT(1) receptor mRNA, whereas the ZG P45 0(c18) mRNA level was increased 3.5-fold. The plasma aldosterone level of animals fed a high diet of potassium and captopril was still highe r than that in control animals at 16.6 ng/dl, and the levels of ZG AT( 1) receptor and P450(c18) mRNAs were only slighly less than those of t he high potassium groups, indicating that captopril did not efficientl y block aldosterone formation under these conditions. ACTH receptor mR NA levels remained unaffected by either low sodium or high potassium i ntake. Collectively, these results indicate that the increased aldoste rone secretion induced by low sodium or high potassium intake involves concomittent increases in AT(1) receptor and P450(c18) mRNAs, which a re effectively translated into their respective proteins, and that the expression of both proteins is mediated in part by AII.