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Aldosterone production by isolated adrenal glomerulosa cells from the rat was estimated in the presence of varying concentrations of sodium ion. The reduction of sodium concentration by 5–20 mmol/l, with or without osmotic changes, did not influence the rate of aldosterone production. Aldosterone response to angiotensin II was not modified by varying the sodium concentration.
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SUMMARY
Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.
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SUMMARY
The mechanism of diuretic-induced hyperaldosteronism was examined in dexamethasone-pretreated rats. The diuretic drug frusemide brought about a rapid increase in plasma renin activity and aldosterone concentration in serum. Half an hour after the administration of frusemide the mean concentration of aldosterone was 25 times higher than in vehicle-treated control animals. Administration of SQ 20,881, an inhibitor of angiotensin converting enzyme, prevented the adrenal response to frusemide. The response of aldosterone was completely blocked by indomethacin. This drug reduced renin release and probably also inhibited the effect on the adrenal glands of angiotensin, released in response to frusemide. Our results indicate that the effects of diuretics on the adrenal glomerulosa cells are mediated by the renin–angiotensin system also in the rat. Hyperaldosteronism is dependent on the maintenance of prostaglandin synthesis. ACTH has no essential role in this response.
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SUMMARY
Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration.
Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.
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An important way of examining adrenocortical function is the analysis of adrenal venous blood. In the rat, owing to the small dimensions, direct cannulation of the adrenal vein is not suitable for routine work. Vogt (1954) overcame this obstacle by collecting adrenal venous blood from the left renal vein. However, ligation of the renal pedicle disturbs physiological conditions, and if the kidney plays any role in aldosterone regulation, Vogt's method cannot be considered suitable for experiments on aldosterone secretion.
In order to avoid the disturbance of the renal circulation during the collection of adrenal venous blood, the following method has been developed. After ligation of the renal end of the left adrenal vein, the vessel is opened carefully (but not transsected!). Adrenal venous blood flows without resistance through the aperture into the abdominal cavity. In order to prevent intravascular clotting the animal is heparinized. A reduction in the rate of
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The role of prostaglandins in the control of aldosterone production was studied in isolated rat glomerulosa cells. Exogenous prostaglandin E2 in concentrations above 10−9 mol/l increased the production rate of aldosterone; this effect was attenuated by the competitive antagonist, 7-oxa-13-prostynoic acid. Prostaglandin F2α (10−9–10−5 mol/l) failed to influence the production rate of aldosterone. The aldosterone-stimulating effect of the prostaglandin precursor, arachidonic acid (5 × 10−4 mol/l), could not be blocked by inhibitors of prostaglandin synthesis. Basal production rate of aldosterone was not significantly influenced by non-steroidal anti-inflammatory drugs. Glomerulosa cells were stimulated by angiotensin II; this effect was not potentiated by arachidonic acid and was reduced only slightly by indomethacin. The cells were also stimulated by corticotrophin and potassium ions. The effect of these substances was not potentiated by arachidonic acid and was not inhibited by non-steroidal anti-inflammatory drugs. These results do not confirm the presumption that intra-adrenal prostaglandins play an essential role in the control of aldosterone secretion. Some effects of arachidonic acid and its antagonist, eicosatetraynoic acid, on aldosterone production are considered to be independent of changes in prostaglandin synthesis.
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Department of Physiology, Semmelweis Medical University, H-1444 Budapest 8, Hungary
(Received 23 December 1975)
The role of the renin-angiotensin system (RAS) in the control of aldosterone secretion in the rat has been a subject for disagreement for more than a decade (cf. Müller, 1971). Recent investigations of the effect of synthetic angiotensin II on isolated glomerulosa cells (Haning, Tait & Tait, 1970; Brecher, Tabacchi, Pyun & Chobanian, 1973; Williams, McDonnell, Raux & Hollenberg, 1974; Mendelsohn, Mackie & Mee, 1975) failed again to give concordant results concerning even the efficiency of the octapeptide.
Information on the physiological function of the RAS may be obtained by experiments studying the response of aldosterone secretion rate to an evoked increase in endogenous renin activity. A situation where the RAS may be expected to play a mediator role in aldosterone regulation is the reduction of renal perfusion pressure. The effect of this manoeuvre on aldosterone
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Department of Physiology, Semmelweis University Medical School, 1444 Budapest 8, POB 259, Hungary
(Received 30 November 1976)
Prostaglandins (PG) of the A-type selectively stimulate the aldosterone secretion rate in man (Fichman, Littenburg, Brooker & Horton, 1972) and aldosterone production rate in the rat (Spät & Józan, 1975). Since PGA escapes inactivation by pulmonary tissue (McGiff, Terragno, Strand, Lee, Lonigro & Ng, 1969), this compound or an active metabolite of it may function as a hormone in the circulation. In view of its zonal specificity and its action in the early stage of aldosterone biosynthesis (Spät & Józan, 1975) as well as the increased plasma level of immunoreactive PGA during sodium depletion (Lee, 1973; Zusman, Forman, Schneider, Caldwell, Speroff & Mulrow, 1973), a mediating function may be postulated for PGA in acute fluid depletion-induced hyperaldosteronism. To test this possibility we examined the effect of diuretic treatment on peripheral aldosterone concentration with
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The present experiments were designed to study the effect of extracellular hyponatraemia on aldosterone secretion. Hyperaldosteronism was induced by peritoneal dialysis with 5% glucose solution in dexamethasone-pretreated rats. In the narrow physiological range of 135–142 mmol/l, as well as in the whole range of the study (122–142 mmol/l), the plasma concentration of sodium showed a close negative correlation with the serum concentration of aldosterone (r = −0·71 and −0·83, respectively). Plasma renin activity increased after peritoneal dialysis; however, no close correlation was observed either between sodium concentration and plasma renin activity or plasma renin activity and serum aldosterone concentration within the dialysed group. The ratio of serum concentration of aldosterone to plasma renin activity showed no considerable change between 132 and 142 mmol/l but rose steeply below 132 mmol sodium/l suggesting that a factor(s) other than angiotensin may also contribute to the induction of hyperaldosteronism.
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ABSTRACT
Initial 45Ca uptake was measured in isolated rat glomerulosa cells. A small reduction in membrane potential produced by increasing the K+ concentration from 2 to 3·6 mmol/l stimulated 45Ca uptake by about 35%, while a bigger depolarization induced by 18·5 mmol K+/l increased the uptake by about 100%. Since Ca2+ influx was already activated at a calculated membrane potential below −70 mV, and was found to be sensitive to the dihydropyridine antagonist nifedipine (1 μmol/l), but insensitive to nickel ions (100 μmol/l), it does not meet the criteria established for T- or L-type voltage-dependent Ca2+ channels. Exposure of glomerulosa cells to angiotensin II (AII) for 10 min also enhanced the rate of 45Ca influx. The effect of AII was not sensitive to 1 μmol nifedipine/l, but was strongly inhibited by 5-(N-4-chlorobenzyl)-N-(2′,4′-dimethyl)benzamil (CBDMB, 30 μmol/l), an inhibitor of the Na+/Ca2+ antiporter. These observations suggest that during the sustained phase of stimulation with AII, a CBDMB-sensitive mechanism, rather than dihydropyridine-sensitive calcium channels, is involved in Ca2+ uptake in rat glomerulosa cells. The bulk Ca2+ influx did not correlate with aldosterone production; however, the maintained activity of different Ca2+ entry mechanisms seems to be essential for AII-induced aldosterone production.
Journal of Endocrinology (1989) 122, 361–370
