2011
DOI: 10.1016/j.regpep.2011.06.002
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PTH-receptors regulate norepinephrine release in human heart and kidney

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Cited by 24 publications
(17 citation statements)
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“…These include direct effects on cardiomyocytes, endothelial and smooth-muscle cells,111,135 stimulation of endothelial expression of atherosclerotic, inflammatory, and growth136 factors, reduction of endothelial osteoprotegerin (OPG) secretion (a vascular-protective factor that controls vascular calcification),137 increase in sympathetic nerve activity (by facilitating norepinephrine release),138 increase in circulating ionized calcium (because of release from bone and decreased renal excretion), decreased expression of the calcium-sensing receptor,139 stimulation of renin, angiotensin II, and aldosterone synthesis,140147 indirect effects of PTH-induced hyperphoshatemia148 and hyperlipidemia,149 and decreased insulin sensitivity 117. Furthermore, the effects of hyperparathyroidism may be amplified by vitamin D insufficiency, as vitamin D is known to contribute directly or indirectly to the (patho) physiological functions mentioned above, such as renin–angiotensin–aldosterone system (RAAS) activation, insulin resistance, and systemic and vascular inflammations 150.…”
Section: Discussionmentioning
confidence: 99%
“…These include direct effects on cardiomyocytes, endothelial and smooth-muscle cells,111,135 stimulation of endothelial expression of atherosclerotic, inflammatory, and growth136 factors, reduction of endothelial osteoprotegerin (OPG) secretion (a vascular-protective factor that controls vascular calcification),137 increase in sympathetic nerve activity (by facilitating norepinephrine release),138 increase in circulating ionized calcium (because of release from bone and decreased renal excretion), decreased expression of the calcium-sensing receptor,139 stimulation of renin, angiotensin II, and aldosterone synthesis,140147 indirect effects of PTH-induced hyperphoshatemia148 and hyperlipidemia,149 and decreased insulin sensitivity 117. Furthermore, the effects of hyperparathyroidism may be amplified by vitamin D insufficiency, as vitamin D is known to contribute directly or indirectly to the (patho) physiological functions mentioned above, such as renin–angiotensin–aldosterone system (RAAS) activation, insulin resistance, and systemic and vascular inflammations 150.…”
Section: Discussionmentioning
confidence: 99%
“…A biological mechanism for this association has not been definitively demonstrated to date. In vitro, both cardiac and renal tissues increase norepinephrine release when the PTH1R receptor is activated, suggesting a possible sympathomimetic mechanism (Potthoff et al, 2011), although our patient had no clinical or biochemical indicators of a generalized increase in sympathomimetic activity.…”
Section: Discussionmentioning
confidence: 59%
“…Moreover, catecholamines, cortisol, and insulin were reported to cause a slight, short‐term elevation of PTH blood levels in patients with normal parathyroids as well . We suggest that the different magnitude of PTH elevation in reaction to general anesthesia and endotracheal intubation in the 2 different groups (patients with primary HPT vs patients with normal parathyroids) is because of an altered or impaired response to stress modulators in patients with primary HPT . The extra sensitivity to stress in patients with primary HPT is reflected by the association of primary HPT with cardiac disease .…”
Section: Discussionmentioning
confidence: 83%