Systemic Activation of the Calcium Sensing Receptor Produces Acute Effects on Vascular Tone and Circulatory Function in Uremic and Normal Rats: Focus on Central versus Peripheral Control of Vascular Tone and Blood Pressure by Cinacalcet

Lithium is a mood stabiliser widely used in the treatment and prophylaxis of mania, bipolar disorders and recurrent depression. Treatment with lithium can give rise to various endocrine and metabolic abnormalities, including thyroid dysfunction, nephrogenic diabetes insipidus and hypercalcaemia. Lithium may induce hypercalcaemia through both acute and chronic effects. The initial acute effects are potentially reversible and occur as a result of lithium's action on the calcium-sensing receptor pathway and glycogen synthase kinase 3, giving rise to a biochemical picture similar to that seen in familial hypocalciuric hypercalcaemia. In the long term, chronic lithium therapy leads to permanent changes within the parathyroid glands by either unmasking hyperparathyroidism in patients with a subclinical parathyroid adenoma or possibly by initiating multiglandular hyperparathyroidism. The latter biochemical picture is identical to that of primary hyperparathyroidism. Lithium-associated hyperparathyroidism, especially in patients on chronic lithium therapy, is associated with increased morbidity. Hence, regular monitoring of calcium levels in patients on lithium therapy is of paramount importance as early recognition of lithium-associated hyperparathyroidism can improve outcomes. This review focuses on the definition, pathophysiology, presentation, investigations and management of lithium-associated hyperparathyroidism.

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Possible participation of extracellular calcium-sensing receptor in blood pressure regulation in rats

Brain Research ◽

10.1016/j.brainres.2010.10.013 ◽

2011 ◽

Vol 1367 ◽

pp. 181-187 ◽

Cited By ~ 4

Author(s):

Mikako Kobayashi-Torii ◽

Yoshiko Takahashi ◽

Jinko Sunanaga ◽

Megumi Fujita ◽

Eun-Young Lee ◽

...

Keyword(s):

Blood Pressure ◽

Blood Pressure Regulation ◽

Extracellular Calcium ◽

Pressure Regulation ◽

Calcium Sensing Receptor ◽

Calcium Sensing

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Novel Role of the Calcium-Sensing Receptor in Blood Pressure Modulation

Hypertension ◽

10.1161/hypertensionaha.108.117689 ◽

2008 ◽

Vol 52 (6) ◽

pp. 994-1000 ◽

Cited By ~ 24

Author(s):

Sanela Smajilovic ◽

Jacob Tfelt-Hansen

Keyword(s):

Blood Pressure ◽

Calcium Sensing Receptor ◽

Calcium Sensing ◽

Pressure Modulation

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Hypertensive effect of calcilytic NPS 2143 administration in rats

Journal of Endocrinology ◽

10.1677/joe.1.06924 ◽

2006 ◽

Vol 191 (1) ◽

pp. 189-195 ◽

Cited By ~ 22

Author(s):

Apolonia Rybczynska ◽

Artur Lehmann ◽

Anna Jurska-Jasko ◽

Konrad Boblewski ◽

Czeslawa Orlewska ◽

...

Keyword(s):

Blood Pressure ◽

Group Performance ◽

Parathyroid Glands ◽

Control Group ◽

Calcium Sensing Receptor ◽

Spontaneously Hypertensive ◽

Calcium Sensing ◽

Arterial Blood ◽

Male Wistar Rats ◽

The Difference

Secretion of parathormone (PTH), the main parathyroid hormone, which is under the control of the calcium sensing receptor, might be inhibited by calcimimetics and stimulated by calcilytics. Parathyroid glands also secrete parathyroid hypertensive factor. Recently, it was shown that calcimimetic NPS R-568 induced decreased blood pressure in spontaneously hypertensive rats (SHR) in the presence of parathyroid glands. Therefore, the aim of this study was to determine whether administration of the calcilytic NPS 2143 provoked an increase of mean arterial blood pressure (MAP) in normotensive rats. We used male Wistar rats anaesthetized with thiopental. Clearance experiments were performed and the effect of bolus, 1 mg/kg body weight i.v. of NPS 2143 on MAP in the presence and absence of thyroparathyroidectomy (TPTX) was monitored continuously. Calcilytic properties of NPS 2143 were confirmed directly by a significant (P < 0.05) increase of plasma PTH concentration, and indirectly by a rise of plasma Ca2+ concentration and urinary fractional phosphate excretion (FE Pi). NPS 2143 administration markedly (P < 0.05) increased MAP, calculated as the difference ( Δ ) in MAP between sequential measurements and the time of bolus injection of calcilytic. The observed increase of blood pressure in the NPS 2143 group was also significant (P < 0.05) compared with the control group. Performance of TPTX prevented the hypertensive effect of NPS 2143. We conclude that NPS 2143 is responsible for increased blood pressure in rats in the presence of parathyroid glands.

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