Hyperparathyroidism and the Calcium Paradox of Aldosteronism

Chhokar, Vikram S.; Sun, Yao; Bhattacharya, Syamal K.; Ahokas, Robert A.; Myers, Linda K.; Xing, Zhiqiang; Smith, Richard A.; Gerling, Ivan; Weber, Karl T.

doi:10.1161/01.cir.0000155621.10213.06

Cited by 188 publications

(213 citation statements)

References 66 publications

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“…Moreover, when infused into normotensive rats, aldosterone caused an increase in PTH, which was attributed to the decrease in serum [Ca 2+ ] due to the hypercalciuria that accompanies the escape phenomenon. 11 These observations suggest a bidirectional relationship between the adrenocortical zona glomerulosa and the parathyroid gland (Figure 1). Hence, secondary hyperparathyroidism can contribute to the maintenance of a relative degree of hyperaldosteronism, and therefore to increased BP under these common conditions.…”

Section: P Rimary Hyperparathyroidism (Ppth) Ismentioning

confidence: 91%

Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage?

Rossi

2010

Hypertens Res

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P rimary hyperparathyroidism (PPTH) isgenerally thought to be a common endocrine disorder. However, it represents an uncommon endocrine cause of arterial hypertension, with a likely prevalence among hypertensive patients of less than 0.01%-an imprecise estimate because of the lack of prospective studies.However, between 56% and 80% of the patients with PPTH have high blood pressure (BP) and display hypertension-related target organ damage. On the basis of large studies from Scandinavia, a high rate of cardiovascular complications and mortality that has been consistently observed in PPTH patients compared with patients with essential hypertension without PPTH; this can be related to an excess organ damage in PPTH patients. 1 Despite these findings, the mechanisms by which PPTH is associated with hypertension and increased cardiovascular risk remain poorly understood and somewhat intriguing. In fact, parathyroid hormone (PTH) exerts a vasodilatory effect in different models 2,3 and induces an endothelium-dependent vasodilatory effect through increased nitric oxide production, 4,5 both of which are effects that would be expected to decrease, rather than increase, BP. However, PPTH has also been associated with endothelial dysfunction, which is usually due to reduced nitric oxide bioactivity, and represents a hallmark of high BP and many other conditions that are associated with increased cardiovascular risk. In contrast with this finding, increased levels of markers that are downstream of nitric oxide signaling, which were normalized after parathyroidectomy, have also been documented in PPTH patients. 6 Therefore, it has been proposed that increased nitric oxide bioactivity is a compensatory mechanism that counteracts the pressor effects of PTH-induced increases in intracellular calcium. 6 In this issue of the journal, Rosa et al. 7 report on their investigation of PPTH patients based on measurements of pulse wave velocity (PWV) before and after surgical treatment of PPTH; PWV is an index of aortic stiffness and hypertension-related target organ damage, which is recommended by the current guidelines of the ESC/ESH as part of the standard evaluation of hypertensive patients because it conveys information that is useful for risk stratification purposes. Interestingly, they found that PWV was higher in PPTH patients than in essential hypertensive patients, which suggests that excess PTH changes the mechanical properties of the arterial walls. However, this important finding is not consistent with the results of another recent study from Israel: compared with control subjects who were matched for age, gender and CV risk factors, neither the patients with full-blown (hypercalcemic) PPTH nor those with mild (normocalcemic) PPTH showed increased arterial stiffness, as assessed by several indices, including the PWV. 8 Although these inconsistencies could reflect either a selection bias, involving differences in ethnicity, overall cardiovascular risk profile, stage of PPTH disease in the patients and/or different selectio...

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Section: P Rimary Hyperparathyroidism (Ppth) Ismentioning

confidence: 91%

Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage?

Rossi

2010

Hypertens Res

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“…These results are of particular importance when considering the crucial role of PTH for the diagnosis and treatment of bone and mineral disorders [2] and the accumulating data on PTH and cardiovascular risk [3][4][5]. With our letter we seek to guide the attention towards previous data suggesting that the renin-angiotensinaldosterone system (RAAS) may also have a significant impact on PTH levels [5][6][7][8][9]. Towards this, we and others have shown that high aldosterone levels are associated with high PTH levels [5][6][7][8][9].…”

mentioning

confidence: 94%

“…Clinical data suggest that treatment of either disease is effective in normalising the levels of both hormones [6,8,9,14,15]. We therefore believe that the awareness of an interplay between PTH and aldosterone could, for selected cases, be clinically relevant for diagnostic considerations of patients with elevated levels of any of these two hormones.…”

mentioning

confidence: 94%

“…With our letter we seek to guide the attention towards previous data suggesting that the renin-angiotensinaldosterone system (RAAS) may also have a significant impact on PTH levels [5][6][7][8][9]. Towards this, we and others have shown that high aldosterone levels are associated with high PTH levels [5][6][7][8][9]. In experimental studies it has been demonstrated that aldosterone excess increases renal and fecal loss of calcium [8][9][10].…”

mentioning

confidence: 98%

“…In experimental studies it has been demonstrated that aldosterone excess increases renal and fecal loss of calcium [8][9][10]. This in turn results in secondary hyperparathyroidism which could be effectively treated by mineralocorticoid receptor (MR) blocking therapy in rats [8,9].…”

mentioning

confidence: 99%

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Aldosterone and Parathyroid Hormone: A Complex and Clinically Relevant Relationship

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Mineralocorticoid Receptor Antagonists in the Management of Heart Failure and Resistant Hypertension

et al. 2016

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Hyperparathyroidism and the Calcium Paradox of Aldosteronism

Abstract: Background-Aldosteronism may account for oxi/nitrosative stress, a proinflammatory phenotype, and wasting in congestive heart failure. We hypothesized that aldosterone/1% NaCl treatment (ALDOST) in rats enhances

Cited by 188 publications

References 66 publications

Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage?

Hyperparathyroidism, arterial hypertension and aortic stiffness: a possible bidirectional link between the adrenal cortex and the parathyroid glands that causes vascular damage?

Aldosterone and Parathyroid Hormone: A Complex and Clinically Relevant Relationship

Mineralocorticoid Receptor Antagonists in the Management of Heart Failure and Resistant Hypertension

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