Regulation of angiotensin II receptors in the rat adrenal cortex by dietary electrolytes.

Abstract

A B S T R A C T The binding affinity and concentration of specific angiotensin II receptor sites of rat adrenal cortical cells and homogenates were determined after 1 and 6 wk of altered sodium and potassium intake. Sodium deprivation caused marked increases in plasma renin, blood angiotensin II, and plasma aldosterone, and was accompanied by a significant increase (+ 74%) in the number of specific angiotensin II receptor sites per adrenal cortical cell. High potassium intake was followed by increased serum potassium and markedly elevated plasma aldosterone, with subnormal levels of renin and angiotensin II and a 170% increase in the number of angiotensin II receptors per cell after 1 wk. Sodium loading and potassium deprivation were followed by the opposite effect upon adrenal receptors, with reduction of the angiotensin II-binding capacity. None of the dietary electrolyte changes were accompanied by an increase in receptor affinity above the control value of 2 nM'. A decrease in receptor affinity was noted after 6 wk of either low sodium or low potassium intake, when the renin and angiotensin II levels were increased by 104-129%.The adrenals of normal rats infused acutely with synthetic angiotensin II, or anesthetized with ether or sodium pentobarbital, which markedly increased plasma renin activity, contained fewer angiotensin receptors. These reductions in binding site concentration were not accompanied by changes in affinity and were attributed to occupancy by angiotensin II.These studies have demonstrated that chronic changes in sodium or potassium balance and acute changes in blood angiotensin II levels can exert modulating effects upon the adrenal content and/or affinity of specific receptor sites for angiotensin II.

Subpressor infusions of angiotensin II alter glomerular binding, prostaglandin E2, and cyclic AMP production.

“…A progressive decrease in the number of ANG II receptors on hepatocytes was correlated with increasing adenosine 5'-diphosphate (ADP) ribosylation of M with pertussis toxin and loss of ANG II inhibition of cAMP production. 33 A similar relationship between opiate agonist receptor number and ADP-ribosylated Ni has been demonstrated with cultured Ng-108-15 cells. 41 The opposite was observed in the present study, in which enhanced binding was correlated with greater inhibition of cAMP production.…”

“…In hepatocytes, it has been demonstrated that the inhibitory guanine nucleotide-binding regulatory protein of adenylate cyclase (Ni) mediates the inhibitory effect of ANG II on adenylate cyclase. 33 In vivo, however, ANG II regulation of cAMP production mediated through Ni has not been previously shown. 33 Inhibition of cAMP production may be an important contributor to the amplification of the contractile response of the whole glomerulus beyond what can be explained by an increase in the number and affinity of ANG II binding sites.…”

“…33 In vivo, however, ANG II regulation of cAMP production mediated through Ni has not been previously shown. 33 Inhibition of cAMP production may be an important contributor to the amplification of the contractile response of the whole glomerulus beyond what can be explained by an increase in the number and affinity of ANG II binding sites. In several models of acute renal injury in which intrarenal ANG II is increased slightly, the enhanced ability of ANG II to decrease cAMP may be an important modulator of function.…”

The Renin-Angiotensin System

“…Nephrectomy or administration of angiotensin antagonists block the aldosterone secretory response in dogs subjected to dietary sodium deprivation (Davis, Ayers & Carpenter, 1961;Davis & Freeman, 1976;Stephens et al, 1977). Plasma aldosterone levels for any level of angiotensin II are higher during sodium depletion than during direct infusion of the octapeptide (Boyd et al, 1972); this may be due to an increase in the number of specific angiotensin II receptors on the adrenal glomerulosa cell (Douglas & Catt, 1976 (Haber et al, 1975;Samuels et al, 1976).…”

Abnormal regulation of adrenal angiotensin II receptors in spontaneously hypertensive rats.

“…The level of Ang II in plasma appears to regulate adrenal receptor number. Increasing the angiotensin level, either by sodium restriction or by continuous low-dose infusion by means of a minipump, 8 " 10 -20 ' 23 increases the number of adrenal receptors, while reducing the plasma level (sodiumloading or inhibiting angiotensin converting enzyme) 8 -' 02423 reduces angiotensin receptors. In our experiments, however, there were no significant differences between the PRA or plasma Ang II level of SHR and WKY on either high or low salt intake.…”