The Influence of Potassium on the Renal Vasculature and the Adrenal Gland, and Their Responsiveness to Angiotensin II in Normal Man

Hollenberg, Norman K.; Williams, Gordon H.; Burger, B; Hooshmand, I.

doi:10.1042/cs0490527

Cited by 56 publications

(29 citation statements)

References 17 publications

(33 reference statements)

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confidence: 99%

“…Ang II and extracellular K are potent independent regulators of aldosterone production, yet the strength of these agonists in the physiological setting depends on their combined activities and their synergy (11)(12)(13)(14). Small elevations in plasma potassium within the physiological range increase the sensitivity of ZG cells to stimulation by Ang II (13,15). In this setting, both K and Ang II mediate membrane depolarization of ZG cells (14,16) to enhance the opening of Ang II-modulated, low-voltage-activated, Ca channels (Cav3.2) whose activity underlies the in vivo control of aldosterone production (17,18).…”

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TASK channel deletion in mice causes primary hyperaldosteronism

Davies

Hu²,

Guagliardo³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.Has correction 2008-9-9

167

157

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When inappropriate for salt status, the mineralocorticoid aldosterone induces cardiac and renal injury. Autonomous overproduction of aldosterone from the adrenal zona glomerulosa (ZG) is also the most frequent cause of secondary hypertension. Yet, the etiology of nontumorigenic primary hyperaldosteronism caused by bilateral idiopathic hyperaldosteronism remains unknown. Here, we show that genetic deletion of TWIK-related acid-sensitive K (TASK)-1 and TASK-3 channels removes an important background K current that results in a marked depolarization of ZG cell membrane potential. Although TASK channel deletion mice (TASK −/− ) adjust urinary Na excretion and aldosterone production to match Na intake, they produce more aldosterone than control mice across the range of Na intake. Overproduction of aldosterone is not the result of enhanced activity of the renin–angiotensin system because circulating renin concentrations remain either unchanged or lower than those of control mice at each level of Na intake. In addition, TASK −/− mice fail to suppress aldosterone production in response to dietary Na loading. Autonomous aldosterone production is also demonstrated by the failure of an angiotensin type 1 receptor blocker, candesartan, to normalize aldosterone production to control levels in TASK −/− mice. Thus, TASK −/− channel knockout mice exhibit the hallmarks of primary hyperaldosteronism. Our studies establish an animal model of nontumorigenic primary hyperaldosteronism and identify TASK channels as a possible therapeutic target for primary hyperaldosteronism.

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confidence: 99%

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confidence: 99%

TASK channel deletion in mice causes primary hyperaldosteronism

Davies

Hu²,

Guagliardo³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.Has correction 2008-9-9

167

157

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“…Potassium chloride (0.52 meq/ml of normal saline) was infused at a rate of 1 meq/min for 15 min. Blood samples were drawn at -60, -30, -15, -5, and 0 min before potassium infusion, and 5,10,15,30,45 The plasma aldosterone concentration was measured by radioimmunoassay (14), plasma 11-hydroxycorticosteroids by the competitive protein binding method of Murphy (15), and plasma renin activity (PRA)l by the method of Haber et al (16). The plasma potassium concentration was measured using the ion selective electrode procedure of the Astra-8 by Beckman Instrument Co.…”

Section: Methodsmentioning

confidence: 99%

“…Sodium depletion increases aldosterone secretion to a greater extent when subjects are potassium replete than when potassium deplete (2,4,9). Both in vivo and in vitro, potassium augments stimulation by angiotensin II and by ACTH (10)(11)(12). To what extent, if any, this synergism of potassium with other stimuli represents enhancement of potassium's stimulatory capacity by the other stimuli is unknown.…”

Section: As Does Infusion Of Potassiummentioning

confidence: 99%

Role of angiotensin II in potassium-mediated stimulation of aldosterone secretion in the dog.

Pratt¹

1982

J. Clin. Invest.

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A B S T R A C T Potassium is known to enhance the aldosterone-stimulating action of angiotensin II. Such a synergistic interaction of potassium with angiotensin II could represent an action by angiotensin II to potentiate potassium as a stimulus. To examine for this effect of angiotensin II on potassium, plasma aldosterone levels were measured before and after an infusion of potassium chloride (15 meq i.v.) into dogs without and with prevention of angiotensin II formation by captopril, an angiotensin converting-enzyme inhibitor. In addition, responses to potassium were measured in a group of dogs receiving angiotensin II plus captopril. After potassium infusion, control dogs showed an increase of 7.7±1.9 (SEM) ng/dl (P < 0.001) in the level of plasma aldosterone. In contrast, captopril-treated dogs showed no change in plasma aldosterone concentration in response to potassium. When angiotensin II was administered to captopril-treated dogs responsiveness to potassium administration was restored (plasma aldosterone concentration increased by 7.4±2.1 ng/dl, P < 0.002). ACTH stimulated aldosterone secretion despite captopril treatment (P < 0.001), however, ACTH produced a greater increase in the plasma aldosterone concentration in controls than in captopriltreated animals. It is evident from these results that stimulation of aldosterone secretion by potassium is considerably enhanced by angiotensin II. There appears to exist an important interdependence of these stimuli in the regulation of aldosterone secretion.

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“…A-11, angiotensin I1 ACTH, adrenocorticotrophin PRA, plasma renin activity Much has been learned about the direct mediators governing aldosterone secretion in adult humans and experimental animals ( 14,18). However, mechanisms regulating aldosterone secretion during fetal life are poorly understood.…”

Section: Abbreviationsmentioning

confidence: 99%

Factors Controlling Aldosterone Secretion during Hypoxemia in Fetal Lambs

et al. 1984

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SummaryFactors modulating the fetal aldosterone response to hypoxemia were studied in three groups of chronically catheterized fetal lambs between 131 and 143 days of gestation (term, 145 days). One group (control group) received an infusion of 5% dextrose in water; the second group (captopril-treated group) was given captopril, an inhibitor of angiotensin-converting enzyme; the third group (captopril plus dexamethasone-treated group) received dexamethasone in addition to captopril. In all groups of fetuses, hypoxemia was associated with a significant increase in plasma K+ concentration (+0.7 2 0.1 meqtliter). In control fetuses, changes in plasma aldosterone concentration during hypoxemia correlated closely with changes in plasma K+ concentration r = 0.79; P < 0.001) and with changes in plasma angiotensin I1 concentration ( r = 0.77; P < 0.001). In the captopril-treated fetuses, the rise in plasma aldosterone concentration during hypoxemia correlated closely with plasma K+ ( r = 0.79; P < 0.001) but not with plasma angiotensin I1 values ( r = 0.17). No significant correlation was found between percent changes in maternal aldosterone and percent changes in fetal aldosterone during hypoxemia and following recovery ( r = 0.36; P > 0.1) in captopriltreated fetuses. Administration of dexamethasone to fetuses receiving captopril completely inhibited the rise in plasma aldosterone associated with hypoxemia. Taken together, the present results suggest that the rise in plasma aldosterone during hypoxemia is not related to the level of activity of the renin-angiotensin system but depends probably on the increased secretion of adrenocorticotrophin by the fetus. It is also suggested that maternal placental transfer of aldosterone is not an important factor controlling the rise in fetal plasma aldosterone concentration during hypoxemia.Abbreviations A-11, angiotensin I1 ACTH, adrenocorticotrophin PRA, plasma renin activity Much has been learned about the direct mediators governing aldosterone secretion in adult humans and experimental animals ( 14, 18). However, mechanisms regulating aldosterone secretion during fetal life are poorly understood. Previous in vitro studies (3, 8,20,32,33) have shown that the fetal adrenal gland has the ability to synthesize and secrete aldosterone following stimulation by either A-I1 (33), ACTH (33), or increasing potassium concentration (32). More recently, we (2 1, 22) and others (27) demonstrated that in vivo elevation of plasma A-I1 concentration stimulates aldosterone secretion during the last trimester of gestation in fetal lambs but to a lesser degree than in adult ewes (22). However, in vivo attempts to stimulate aldosterone secretion by ACTH (1, 5 ) or potassium infusion (3 1) have been unsuccessful, suggesting a relative insensitivity of the fetal adrenal to these stimuli.On the other hand, we have found a close correlation between plasma aldosterone and plasma potassium concentrations iia nephrectomized fetuses submitted to blood volume depletion (21). Similar findings have also be...

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The Influence of Potassium on the Renal Vasculature and the Adrenal Gland, and Their Responsiveness to Angiotensin II in Normal Man

Cited by 56 publications

References 17 publications

TASK channel deletion in mice causes primary hyperaldosteronism

TASK channel deletion in mice causes primary hyperaldosteronism

Role of angiotensin II in potassium-mediated stimulation of aldosterone secretion in the dog.

Factors Controlling Aldosterone Secretion during Hypoxemia in Fetal Lambs

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