Hypocalcaemic disorders, hypoparathyroidism, and pseudohypoparathyroidism

2011 ◽  
pp. 675-686 ◽  
Author(s):  
Rajesh V. Thakker
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Parathyroid Hormone ◽  
Calcium Ion ◽  
Extracellular Calcium ◽  
Ion Concentration ◽  
Common Causes ◽  
Abnormal Metabolism ◽  
Serum Pth ◽  
Calcium Ion Concentration

Extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) on kidney and bone (Fig. 4.5.1). The intact peptide is secreted by the parathyroid glands at a rate that is appropriate to and dependent upon the prevailing extracellular calcium ion concentration. The causes of hypocalcaemia (Box 4.5.1) can be classified according to whether serum PTH concentrations are low (that is hypoparathyroid disorders) or high (that is disorders associated with secondary hyperparathyroidism) (1–6). The most common causes of hypocalcaemia are hypoparathyroidism, a deficiency or abnormal metabolism of vitamin D, acute or chronic renal failure, and hypomagnesaemia. This chapter will initially review the clinical features and management of hypocalcaemia, and then discuss the specific hypocalcaemic disorders.

Effect of calcium on neurohumoral stimulation of feline colonic smooth muscle

1982 ◽  
Vol 243 (2) ◽  
pp. G134-G140
Author(s):  
W. J. Snape
Keyword(s):  
Smooth Muscle ◽  
Spike Activity ◽  
Calcium Ion ◽  
Calcium Concentration ◽  
Extracellular Calcium ◽  
Ion Concentration ◽  
Myoelectric Activity ◽  
Ionic Calcium ◽  
Calcium Ion Concentration ◽  
Stimulation Of

The purpose of this study was to compare the effect of altering the extracellular calcium ion concentration on bethanechol or octapeptide of cholecystokinin (OP-CCK) stimulation of the isolated transverse colon of the cat. Myoelectric activity was recorded with monopolar glass-pore electrodes. Bethanechol (10(-6) M) stimulated an increase in the number of slow waves with superimposed spike potentials to 85.5 +/- 5.3% (P less than 0.001) compared with the basal spike activity (8.9 +/- 1.4%). OP-CCK (4 x 10(-9)) also increased spike activity (80.7 +/- 3.8%, P less than 0.001), which was not inhibited by atropine, phentolamine, or propranolol. Addition of 0.0 mM calcium solution to the colonic smooth muscle abolished both slow-wave and spike activity, which returned after replacing 0.25 mM calcium in the solution. Bethanechol stimulated a greater increase in spike activity as the concentration of calcium was increased. OP-CCK stimulation of colonic spike activity was more sensitive to the extracellular calcium concentration than bethanechol stimulation. Verapamil had a minimal effect on bethanechol stimulation of colonic spike activity, but it inhibited the OP-CCK stimulation. These studies suggest that 1) OP-CCK appears to stimulate colonic smooth muscle directly and 2) OP-CCK requires the presence of a greater amount of extracellular ionic calcium in order to stimulate colonic spike activity compared with bethanechol.

Disorders of plasma calcium

2018 ◽  
Author(s):  
Aron Chakera ◽  
William G. Herrington ◽  
Christopher A. O’Callaghant
Keyword(s):  
Vitamin D ◽  
Normal Serum ◽  
Ion Concentration ◽  
Normal Range ◽  
Physiological Regulation ◽  
Dihydroxyvitamin D ◽  
Diagnostic Approaches ◽  
Serum Pth ◽  
Calcium Ion Concentration ◽  
Pth Level

The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.

scholarly journals Effects of calcium-modulating hormones on thiazide receptor density.

1996 ◽  
Vol 7 (7) ◽  
pp. 1052-1057 ◽  
Author(s):  
P Blakely ◽  
D A Vaughn ◽  
D D Fanestil
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Ion ◽  
Excretion Rate ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Urinary Calcium Excretion ◽  
Ion Concentration ◽  
Calcium Excretion ◽  
Calcitropic Hormones ◽  
Calcium Ion Concentration

Thiazide diuretic drugs act in the distal convoluted tubule (DCT) to inhibit a Na+Cl- cotransporter and enhance reabsorption of luminal calcium. The density of receptors for thiazides in the rat DCT is known to be increased by adrenocortical steroids, furosemide, and bendroflumethiazide, but decreased by ischemia. Because the DCT is a physiologic site of action by calcitonin and parathyroid hormone, this study examined the effects of these calcitropic hormones in thyroparathyroidectomized Sprague-Dawley rats on (1) the density of the rat thiazide receptor (TZR), as quantitated by binding of (3H)metolazone to renal membranes, and (2) urinary electrolyte excretion rate. Salmon calcitonin (sCT) (20 to 100 ng/h) (1) increased the density of the renal TZR twofold, an effect that is maximal by 6 h after sCT administration, and (2) decreased urinary calcium excretion rate. Adequate dietary calcium must be provided for the effects of sCT to be observed. Regression analysis demonstrated that renal TZR density correlated negatively with total urinary calcium excretion rate but not with plasma calcium ion concentration. In addition, neither rat calcitonin (rCT), at doses that cause hypocalcemia, nor parathyroid hormone, at doses that cause hypercalcemia, produce direct effects on TZR density in the DCT of the thyroparathyroidectomized rat. Our findings indicate that upregulation of TZR by sCT, which occurs independently of plasma calcium-ion concentration, is likely via a calcitonin-like receptor other than that for rat calcitonin itself.

Dissociation of membrane potential and hormone secretion in bovine parathyroid cells

1983 ◽  
Vol 245 (1) ◽  
pp. E102-E105
Author(s):  
J. J. Morrissey ◽  
S. Klahr
Keyword(s):  
Parathyroid Hormone ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Calcium Ion ◽  
Cell Function ◽  
Hormone Secretion ◽  
Ion Concentration ◽  
Parathyroid Cell ◽  
High Potassium ◽  
Calcium Ion Concentration

An increase in the calcium ion concentration of the medium from 0.5 to 2.0 mM is associated with a 65% decrease in the secretion of parathyroid hormone from dispersed parathyroid cells. This maneuver also depolarized the cell membrane from -55 to -21 mV as measured by the distribution of [3H]tetraphenylphosphonium ion between cells and medium. An increase in the potassium ion concentration of the medium to 50 mM caused a 67% increase in hormone secretion at 0.5 mM calcium and depolarized the cell to -31 mV. The high potassium did not significantly change hormone secretion or the membrane potential at 2.0 mM calcium. Chlorpromazine inhibited hormone secretion by 40% and depolarized the cell to -30 mV at 0.5 mM calcium in the medium. Chlorpromazine did not change hormone secretion or membrane potential in cells incubated at 2.0 mM calcium. These results suggest that depolarization of the cell by calcium cannot account by itself for the inhibition of hormone secretion and chlorpromazine mimics the effect of an increase in calcium on parathyroid cell function.

scholarly journals Extracellular Calcium Ion Concentration Regulates Chondrocyte Elastic Modulus and Adhesion Behavior

2021 ◽  
Vol 22 (18) ◽  
pp. 10034
Author(s):  
Xingyu Shen ◽  
Liqiu Hu ◽  
Zhen Li ◽  
Liyun Wang ◽  
Xiangchao Pang ◽  
...  
Keyword(s):  
Elastic Modulus ◽  
Calcium Ion ◽  
Baseline Level ◽  
Adhesion Force ◽  
Extracellular Calcium ◽  
Ion Concentration ◽  
Cell Stiffness ◽  
Peak Point ◽  
Subsequent Decrease ◽  
Calcium Ion Concentration

Extracellular calcium ion concentration levels increase in human osteoarthritic (OA) joints and contribute to OA pathogenesis. Given the fact that OA is a mechanical problem, the effect of the extracellular calcium level ([Ca2+]) on the mechanical behavior of primary human OA chondrocytes remains to be elucidated. Here, we measured the elastic modulus and cell–ECM adhesion forces of human primary chondrocytes with atomic force microscopy (AFM) at different extracellular calcium ion concentration ([Ca2+]) levels. With the [Ca2+] level increasing from the normal baseline level, the elastic modulus of chondrocytes showed a trend of an increase and a subsequent decrease at the level of [Ca2+], reaching 2.75 mM. The maximum increment of the elastic modulus of chondrocytes is a 37% increase at the peak point. The maximum unbinding force of cell-ECM adhesion increased by up to 72% at the peak point relative to the baseline level. qPCR and immunofluorescence also indicated that dose-dependent changes in the expression of myosin and integrin β1 due to the elevated [Ca2+] may be responsible for the variations in cell stiffness and cell-ECM adhesion. Scratch assay showed that the chondrocyte migration ability was modulated by cell stiffness and cell-ECM adhesion: as chondrocyte’s elastic modulus and cell-ECM adhesion force increased, the migration speed of chondrocytes decreased. Taken together, our results showed that [Ca2+] could regulate chondrocytes stiffness and cell-ECM adhesion, and consequently, influence cell migration, which is critical in cartilage repair.

Desulfated Hirugen (Hirudin 54-65) Induces Endothelium-Dependent Relaxation of Porcine Pulmonary Arteries

1994 ◽  
Vol 72 (02) ◽  
pp. 318-321 ◽  
Author(s):  
Erika Glusa
Keyword(s):  
Calcium Ion ◽  
Anticoagulant Activity ◽  
Pulmonary Arteries ◽  
Extracellular Calcium ◽  
Ion Concentration ◽  
Pronounced Increase ◽  
Relaxant Effect ◽  
Calcium Ion Concentration ◽  
Endothelium Dependent Relaxation ◽  
Dependent Mechanism

SummaryDesulfated hirugen (hirudin 54-65) at concentrations from 0.1 to 2 μM was found to relax PGF2α-precontracted ring segments of porcine pulmonary arteries with intact endothelium. The relaxation was associated with a pronounced increase in cGMP in the vessels. This endothelium-dependent relaxant effect depended on the extracellular calcium ion concentration and was probably due to the release of endothelium-derived NO as indicated by its susceptibility to blockade of the NO synthesis by NG-nitro-L-arginine. In the presence of indomethacin (3 μM) the maximum hirugen effect was significantly diminished by about 25%. In contrast, neither the sulfated hirugen nor recombinant desulfato hirudin at equimolar concentrations exerted endothelium-dependent relaxation. Hence, the relaxant effect did not correspond to the anticoagulant activity. Desulfated hirugen can be assigned to the group of well-known peptides causing vasodilatation via an endothelium-dependent mechanism.

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