Aldosterone and Pressor Responses to Angiotensin II in Primary Hyperparathyroidism

Fallo, Francesco; Rocco, Stefano; Pagotto, Uberto; Zangari, M.; Luisetto, Giovanni; Musaio, F.; Mantero, Franco

doi:10.1055/s-2007-1009262

Cited by 6 publications

(6 citation statements)

References 6 publications

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“…Clinically, aldosterone and renin concentrations have been reported to be higher in patients with primary hyperparathyroidism and to fall following parathyroidectomy (61,267), and both aldosterone (240) and renin (214) levels appear to rise in response to PTH infusion. In patients with PA, PTH infusion was associated with an exaggeration in the rise of plasma aldosterone during ANG II infusion, suggesting that PTH sensitizes the adrenal to stimulation by ANG II (137). There is also evidence to suggest that aldosterone may induce PTH secretion.…”

Section: Parathyroid Hormonementioning

confidence: 99%

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Stowasser

Gordon

2016

Physiological Reviews

128

134

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In the 60 years that have passed since the discovery of the mineralocorticoid hormone aldosterone, much has been learned about its synthesis (both adrenal and extraadrenal), regulation (by renin-angiotensin II, potassium, adrenocorticotrophin, and other factors), and effects (on both epithelial and nonepithelial tissues). Once thought to be rare, primary aldosteronism (PA, in which aldosterone secretion by the adrenal is excessive and autonomous of its principal regulator, angiotensin II) is now known to be the most common specifically treatable and potentially curable form of hypertension, with most patients lacking the clinical feature of hypokalemia, the presence of which was previously considered to be necessary to warrant further efforts towards confirming a diagnosis of PA. This, and the appreciation that aldosterone excess leads to adverse cardiovascular, renal, central nervous, and psychological effects, that are at least partly independent of its effects on blood pressure, have had a profound influence on raising clinical and research interest in PA. Such research on patients with PA has, in turn, furthered knowledge regarding aldosterone synthesis, regulation, and effects. This review summarizes current progress in our understanding of the physiology of aldosterone, and towards defining the causes (including genetic bases), epidemiology, outcomes, and clinical approaches to diagnostic workup (including screening, diagnostic confirmation, and subtype differentiation) and treatment of PA.

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Section: Parathyroid Hormonementioning

confidence: 99%

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Stowasser

Gordon

2016

Physiological Reviews

128

134

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“…In a controlled interventional study of 5 subjects with PHPT, angiotensin II infusion resulted in an enhanced aldosterone response compared with matched controls [19], and in a study of healthy volunteers, PTH infusion led to increased levels of urinary tetrahydroaldosterone [72]. These studies emphasize an action at the level of adrenocortical aldosterone synthesis, where there is in vitro evidence of PTH receptor expression [16*, 20] and of a stimulatory effect of intracellular calcium [73] and PTH [74] on adrenal aldosterone-producing cells, providing a plausible direct effect of the calcium system on aldosterone (Figure 1D).…”

Section: Calcium- Pth- and Vitamin D-mediated Control Of The Raasmentioning

confidence: 99%

Interactions between adrenal-regulatory and calcium-regulatory hormones in human health

Brown

Vaidya

2014

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

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Purpose of Review To summarize evidence characterizing the interactions between adrenal- and calcium-regulating hormones, and the relevance of these interactions to human cardiovascular and skeletal health. Recent Findings Human studies support the regulation of parathyroid hormone (PTH) by the renin-angiotensin-aldosterone system (RAAS): angiotensin II may stimulate PTH secretion via an acute and direct mechanism, whereas aldosterone may exert a chronic stimulation of PTH secretion. Studies in primary aldosteronism, congestive heart failure, and chronic kidney disease have identified associations between hyperaldosteronism, hyperparathyroidism, and bone loss, which appear to improve when inhibiting the RAAS. Conversely, elevated PTH and insufficient vitamin D status have been associated with adverse cardiovascular outcomes, which may be mediated by the RAAS. Studies of primary hyperparathyroidism implicate PTH-mediated stimulation of the RAAS, and recent evidence shows that the vitamin D-vitamin D receptor (VDR) complex may negatively regulate renin expression and RAAS activity. Ongoing human interventional studies are evaluating the influence of RAAS inhibition on PTH and the influence of VDR agonists on RAAS activity. Summary While previously considered independent endocrine systems, emerging evidence supports a complex web of interactions between adrenal and calcium-regulating hormones, with implications for human cardiovascular and skeletal health.

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“…In vitro studies describe similar stimulation of renin by PTH (81, 82), suggesting that PTH may enhance the activity of the RAAS via multiple methods. Patients with primary hyperparathyroidism (P-HPT) have been shown to demonstrate a heightened aldosterone secretory response to an infusion of angiotensin II(83), and in at least three well-documented reports, patients with P-HPT have developed concomitant primary aldosteronism(66, 68, 84). In some of these cases surgical parathyroidectomy resulted in cure of the aldosteronism, providing tantalizing evidence as to cause and effect(84).…”

Section: Introductionmentioning

confidence: 99%

The renin–angiotensin–aldosterone system and calcium-regulatory hormones

2015

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There is increasing evidence of a clinically relevant interplay between the renin-angiotensin-aldosterone system and calcium regulatory systems. Classically, the former is considered a key regulator of sodium and volume homeostasis while the latter is most often associated with skeletal health. However, emerging evidence suggests an overlap in regulatory control. Hyperaldosteronism and hyperparathyroidism represent pathophysiologic conditions that may contribute to or perpetuate each other; aldosterone regulates parathyroid hormone and associates with adverse skeletal complications, and parathyroid hormone regulates aldosterone and associates with adverse cardiovascular complications. As dysregulation in both systems is linked to poor cardiovascular and skeletal health, it is increasingly important to fully characterize how they interact in order to more precisely understand their impact on human health and potential therapies to modulate these interactions. This review describes the known clinical interactions between these two systems including observational and interventional studies. Specifically, we review studies describing the inhibition of renin activity by calcium and vitamin D, and a potentially bidirectional and stimulatory relationship between aldosterone and parathyroid hormone. Deciphering these relationships might clarify variability in outcomes research, inform the design of future intervention studies, and provide insight into the results of prior and on-going intervention studies. However, before these opportunities can be addressed, more effort must be placed on shifting observational data to the proof of concept phase. This will require reallocation of resources to conduct interventional studies and secure the necessary talent.

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Aldosterone and Pressor Responses to Angiotensin II in Primary Hyperparathyroidism

Cited by 6 publications

References 6 publications

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney

Interactions between adrenal-regulatory and calcium-regulatory hormones in human health

The renin–angiotensin–aldosterone system and calcium-regulatory hormones

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