Atrial Natriuretic Peptide during Mineralocorticoid Escape in the Human*

Zimmerman, Robert S.; Edwards, Brooks S.; Schwab, Thomas R.; Heublein, Denise M.; Burnett, John C.

doi:10.1210/jcem-64-3-624

Cited by 36 publications

(17 citation statements)

References 15 publications

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“…In the present study we did not observe an increase in ventricular BNP peptide and mRNA levels during DOCA treatment suggesting that ventricular BNP biosynthesis was not significantly stimulated. Absence of ventricular BNP activation may be explained by the insignificant change in arterial blood pressure, and therefore, of left ventricular wall tension, during mineralocorticoid escape (12)(13)(14). It was noted in the present work that the highest plasma and ventricular BNP and specific mRNA levels were observed in rats treated with DOCA together with 0.6 mg/h HS.…”

Section: Natriuretic Peptides In Mineralocorticoid Renal Escapementioning

confidence: 99%

“…ANF markedly increases renal sodium excretion and urinary volume despite an attendant decrease in systemic arterial pressure (17). Several reports have shown a preceding or coincidental rise in plasma ANF during mineralocorticoid escape, both in animals ( 15, [21][22][23][24] and in humans ( 12,13,25 ). Further, elevated plasma ANF has been found in patients with primary hyperaldosteronism in which congestive heart failure is not part of the syndrome (26).…”

Section: Introductionmentioning

confidence: 98%

“…The ability of the kidney to "escape" the continued sodium-retaining effects of mineralocorticoid excess has been the subject of extensive investigation, leading to several mechanistic explanations including increases in systemic arterial pressure (2), GFR (3), renal perfusion pressure (4), renal peritubular capillary and interstitial hydrostatic pressure (5), and renal prostaglandins and kinins (6,7), as well as decreases in the levels of angiotensin 11 (8), renal sympathetic nerve activity (9), and renomedullary papillary osmolality (10). However, a significant number of reports have failed to find complete support for many of the above mechanisms (6)(7)(8)(11)(12)(13)(14)(15)(16) and have, therefore, left open the question as to the existence of alternative or complementary mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Yokota

Bruneau²,

Bold³

et al. 1994

J. Clin. Invest.

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The mechanism underlying the mineralocorticoid escape phenomenon remains unknown. To assess the possible contribution of natriuretic peptides to mineralocorticoid escape, rats were injected with 5 mg deoxycorticosterone acetate for 3 d. Plasma atrial natriuretic factor (ANF) rose to twice basal levels and atrial ANF content decreased significantly by 24 h of treatment. This coincided with renal escape and with a significant increase in urinary cGMP excretion. Plasma ANF remained elevated and atrial ANF content continued to decline by 48 and 72 h while atrial ANF mRNA levels increased significantly only at 72 h. Plasma brain natriuretic peptide did not increase during escape although atrial brain natriuretic peptide mRNA levels increased significantly. Chronically administered HS-142-1 (HS), a specific antagonist of the guanylate cyclase-coupled natriuretic peptide receptors, significantly and dose-dependently impaired the escape phenomenon. The highest dose of HS completely suppressed the increase in urinary cGMP. Despite the continued suppression, partial escape was observed by the end of the observation period. HS alone influenced neither plasma nor tissue or urine parameters. These findings show that despite activation of atrial ANF, blockade of the guanylate cyclase-coupled natriuretic peptide receptors impairs the ability of the kidney to escape the Na+ retaining effect of excess mineralocorticoid in a dose-dependent fashion. Later-acting, unknown mechanisms eventually come into play to mediate the escape phenomenon through a guanylate cyclase-independent pathway. Therefore, ANF of cardiac origin appears to be a major factor initiating mineralocorticoid escape through a guanylate cyclase-dependent pathway. (J.

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Section: Natriuretic Peptides In Mineralocorticoid Renal Escapementioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Atrial natriuretic factor significantly contributes to the mineralocorticoid escape phenomenon. Evidence for a guanylate cyclase-mediated pathway.

Yokota

Bruneau²,

Bold³

et al. 1994

J. Clin. Invest.

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“…This transient hypervolemia, but also the direct effect of aldosterone, induce secretion of natriuretic factors such as ANH (19,20). Blood pressure remains high because of several factors, including increased peripheral vascular resistance, a direct hypertensive effect of aldosterone on the central nervous system (CNS), and increased vascular sensitivity to pressor drugs such as angiotensin and adrenalin.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone-producing adenoma without hypertension: a report of two cases

et al. 1999

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Normotensive primary hyperaldosteronism is exceedingly rare. We report two new cases of this syndrome in two middle-aged women, one of Asian origin. The presenting signs were tetany in one case and an adrenal mass in the other. Neither patient had hypertension, despite repeated measurements with a manual armlet. A typical biological profile of primary hyperaldosteronism was demonstrated in both patients, including hypokalemia with inappropriate kaliuresis, elevated resting plasma aldosterone, and undetectable plasma renin activity. The circadian rhythm of blood pressure was studied by ambulatory monitoring pre-and post-operatively. It confirmed the lack of hypertension, but the circadian rhythm of blood pressure was lost before surgery in one patient. Surgical removal of the histologically typical aldosterone-producing adenomas normalized the kalemia. The main finding in these two patients was spontaneously low blood pressure in the post-operative period. This suggests that excess aldosterone induced relative hypertension in these patients whose blood pressure was spontaneously very low. Genetic screening for dexamethasone-sensitive hyperaldosteronism was negative in both patients.

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“…Changes in plasma ANF have not been as impressive when excess mineralocorticoid states have been produced experimentally. In one study, plasma ANF was increased about 1.6-fold only on the day on which escape occurred [111]. In another study in hu mans, plasma ANF increased progressively over an 11-day period of fludrocortisone administration, peaking at about 2 times basal levels on day 11 [109].…”

Section: Evidence From Studies O F Chronic Alterations In Sodium Intamentioning

confidence: 94%