1. Aldosterone responsiveness to ACTH was compared in eleven patients with angiotensin-unresponsive (AII-U) aldosterone-producing adenomas (APA), 16 with AII-responsive (AII-R) APA and 19 with bilateral adrenal hyperplasia (BAH). 2. After overnight recumbency, aldosterone levels were highest in AII-U APA and lowest in BAH. Following 2 h of upright posture, however, levels were similar among the three groups. 3. During ACTH infusion, aldosterone levels in AII-U and AII-R APA were similar, and higher than those in BAH. Because of the higher basal level, the percentage rise in aldosterone was lower in AII-U APA compared with the other groups, as was the ratio of per cent aldosterone rise to per cent cortisol rise. 4. Slightly but significantly reduced plasma cortisol levels observed in the AII-R APA group may reflect secretion by AII-R APA of a cortisol-like substance that is capable of suppressing ACTH and thus adrenal cortisol production. 5. The tendency of aldosterone to follow the diurnal rhythm of ACTH in AII-U APA may thus represent an unmasking of the normal ability of ACTH to regulate aldosterone, secondary to the loss of AII responsiveness, rather than an enhancement of ACTH effect.
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http://dx.doi.org/10.1111/j.1440-1681.1995.tb02044.x | DOI Listing |
Mol Cell Endocrinol
June 1999
Department of Medicine, National Taiwan University Hospital, Taipei, ROC.
Aldosterone secretion in most patients with aldosterone-producing adenomas (APAs) is typically unresponsive to angiotensin II stimulation (AII-unresponsive, AII-U). In some patients, however, plasma aldosterone increases in response to AII stimulation (AII-responsive, AII-R). This differential aldosterone responsiveness could be related to the levels of type 1 AII receptors (AT1R) in the APA.
View Article and Find Full Text PDFClin Exp Pharmacol Physiol
November 1996
Hypertension Unit, Greenslopes Hospital, Brisbane, Queensland, Australia.
1. In familial hyperaldosteronism type I (FH-I), expression of an adrenocorticotropic hormone (ACTH)-dependent hybrid 11 beta-hydroxylase/aldosterone synthase gene causes excessive 'hybrid steroid' (18-hydroxy- and 18-oxo-cortisol) production. In order to study the mechanism of elevated 'hybrid steroid' levels in angiotensin-unresponsive (AII-U) aldosterone-producing adenoma (APA), we compared responses of 24 h urinary 18-oxo-cortisol, aldosterone and cortisol to dexamethasone (0.
View Article and Find Full Text PDFClin Exp Pharmacol Physiol
November 1996
Hypertension Unit, Greenslopes Hospital, Brisbane, Queensland, Australia.
1. Aldosterone-producing adenomas (APA) of the adrenal gland may be responsive or un-responsive to the renin-angiotensin system. 2.
View Article and Find Full Text PDFJ Endocrinol Invest
July 1997
Hypertension Unit, Greenslopes Hospital, Brisbane, Australia.
The basic clinical pathophysiology of primary aldosteronism (PAL) was described by Conn in terms of autonomous production of aldosterone, secondary suppression of renin and development of hypertension with hypokalaemic alkalosis. Conn recognised a normokalaemic form of the syndrome and suggested that it might masquerade as essential hypertension and be not uncommon. This was hotly disputed at the time, and normokalaemic PAL considered rare until recently, and, as a consequence, overlooked.
View Article and Find Full Text PDFClin Exp Pharmacol Physiol
March 1996
Hypertension Unit, Greenslopes Hospital, Brisbane, Queensland, Australia.
1. Angiotensin-responsive aldosterone-producing adenomas (AII-R-APA) have increased expression of renin mRNA compared with angiotensin-unresponsive aldosterone-producing adenomas (AII-U-APA) or normal adrenals. 2.
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