Effect of angiotensin II, ATP, and ionophore A23187 on potassium efflux in adrenal glomerulosa cells

Angiotensin II stimulus on perifused bovine adrenal glomerulosa cells elicited an increase in 86Rb efflux from cells previously equilibrated with the radioisotope. When 45Ca fluxes were measured under similar conditions, it was observed that Ca and Rb effluxes occurred within the first 30 s of the addition of the hormone and were independent of the presence of external Ca. The 86Rb efflux due to angotensin II was inhibited by quinine and apamin. The hypothesis that the angiotensin II response is a consequence of an increase in the K permeability of the glomerulosa cell membrane triggered by an increase in cytosolic Ca is supported by the finding that the divalent cation ionophore A23187 also initiated 86Rb or K loss (as measured by an external K electrode). This increased K conductance was also seen with 10-4 M ATP. Quinine and apamin greatly reduced the effect of ATP or A23187 on 86Rb or K release in adrenal glomerulosa cells. The results suggest that Ca-dependent K channels or carri

Angiotensin II causes a dual effect on potassium permeability in adrenal glomerulosa cells

In previous studies it was shown that angiotensin II causes a Ca-dependent increase in the K permeability of bovine adrenal glomerulosa cells [Am. J. Physiol. 250 (Endocrinol. Metab. 13): E125-E130, 1986]. Here we show that angiotensin II causes a significant and prolonged reduction in the 86Rb release immediately after the transient rise in 86Rb efflux. This inhibition was dose related. Apamin (100 nM) and tetraethylammonium (10 mM) completely abolished the initial transient rise in 86Rb efflux without affecting the latter sustained phase of reduced radioisotope release. On the contrary, the effect of angiotensin II on the second phase was absent when Ca was removed from the perifusion medium or replaced with Sr, but the effect on the early transient phase of 86Rb efflux was maintained in the absence of external Ca. An additional finding was the increased coefficient rate of 86Rb efflux that occurred when the cells were depolarized with 12 mM K. However, this effect was not observed

Role of the renin-angiotensin system in the biosynthesis of aldosterone

Acute infusions of angiotensin II or dog renin into hypophysectomized nephrectomized dogs has no effect on the conversion of corticosterone to aldosterone. This conversion was measured in an isolated mitochondrial fraction obtained from glands excised immediately after the infusion was over.In dogs injected for 4 days with homologous renin, the conversion of corticosterone to aldosterone was significantly increased. This increase resembles that seen in dogs fed with a low sodium diet, which also increases renin secretion. In dogs hypophysectomized the day before starting the renin injections, there was also a significant increase on the conversion of corticosterone to aldosterone.These data suggest that the increased conversion of corticosterone to aldosterone in the sodium deficient animals, is regulated by the renin-angiotensin system. The data also suggests that there is a double effect of angiotensin in the aldosterone biosynthetic pathway: one in “acute” conditions, increasing th

Contrasting effects of sn-1,2-dioctanoyl glycerol as compared to other protein kinase C activators in adrenal glomerulosa cells

Angiotensin II acts on adrenal glomerulosa cells to induce the phospholipase C-mediated generation of inositol trisphosphate and sn-1,2-diacyglycerol as the major products of inositol phospholipid breakdown. This last product is known to activate protein kinase C, but its role in the action of angiotensin II on steroidogenesis has not been defined. We report herein that, in bovine adrenal glomerulosa cells, protein kinase C activators, such as phorbol 12,13-dibutyrate, 12-O-tetradecanoylphorbol-13-acetate, mezerein and sn 1,2 oleoyl acetoylglycerol, each failed to increase steroidogenesis. These results contrast with our recent report on the enhancement of aldosterone output by sn-1,2-dioctanoylglycerol (DiC8) [J. Steroid Biochem. 35 (1990) 19-33]. In addition, the difference between DiC8 and the other protein kinase activators was also observed in the pattern of 86Rb efflux from preloaded glomerulosa cells; only DiC8 mimicked the effect of angiotensin II on ion fluxes. Furthermore, s

Further studies on the relationship between potassium and sodium levels and adrenocortical activity

Steroid production in vitro by dog adrenal cortical slices was measured in the presence of varying concentrations of sodium and potassium ions. Increasing concentrations of potassium produced a signincant increase in the intracellular potassium content and in the rate of synthesis of aldosterone. However, the potassium effect on aldosterone secretion may also occur without changes in tissue potassium content. Ouabain significantly diminished intracellular potassium content, but inhibited aldosterone production only at the high dose of 2.5 × 10-3 M in the presence of an elevated external potassium level. Physiological changes in sodium concentration can modify aldosterone production. The effect was observed with changes as small as 10 mEq/liter sodium. Changes in external potassium and sodium levels modulate aldosterone as well as corticosterone, but not cortisol production. No changes in the intracellular content of potassium were detectable in angiotensin-stimulated tissue. Neverthel

An unusual pattern of Na+ and K+ movements across the horse erythrocyte membrane

Marked differences in the activities of three monovalent cation transport systems in horse versus human erythrocytes are reported. Whereas horse erythrocytes exhibit a 6-fold higher sodium-lithium countertransport, the unidirectional flux of potassium through the sodium pump is 3-4-times slower and the sodium-potassium cotransport system cannot be detected. In spite of this, horse and human cells are able to maintain similar Na+ and K+ gradients. © 1986