scholarly journals Blood Calcium Levels in Immature Rats: Influence of Extracellular Calcium Concentration on Myocardial Calcium Handling

2012 ◽  
Vol 61 (4) ◽  
pp. 399-405 ◽  
Author(s):  
Rosana A. Bassani ◽  
Rovilson Gilioli ◽  
Eliz^|^acirc;ngela S. Oliveira ◽  
Nelci F. Hoehr
2018 ◽  
Vol 315 (4) ◽  
pp. F834-F843 ◽  
Author(s):  
D. Steppan ◽  
L. Pan ◽  
K. W. Gross ◽  
A. Kurtz

The secretion of the protease renin from renal juxtaglomerular cells is enhanced by subnormal extracellular calcium concentrations. The mechanisms underlying this atypical effect of calcium have not yet been unraveled. We therefore aimed to characterize the effect of extracellular calcium concentration on calcium handling of juxtaglomerular cells and on renin secretion in more detail. For this purpose, we used a combination of experiments with isolated perfused mouse kidneys and direct calcium measurements in renin-secreting cells in situ. We found that lowering of the extracellular calcium concentration led to a sustained elevation of renin secretion. Electron-microscopical analysis of renin-secreting cells exposed to subnormal extracellular calcium concentrations revealed big omega-shaped structures resulting from the intracellular fusion and subsequent emptying of renin storage vesicles. The calcium concentration dependencies as well as the kinetics of changes were rather similar for renin secretion and for renovascular resistance. Since vascular resistance is fundamentally influenced by myosin light chain kinase (MLCK), myosin light chain phosphatase (MLCP), and Rho-associated protein kinase (Rho-K) activities, we examined the effects of MLCK-, MLCP-, and Rho-K inhibitors on renin secretion. Only MLCK inhibition stimulated renin secretion. Conversely, inhibition of MCLP activity lowered perfusate flow and strongly inhibited renin secretion, which could not be reversed by lowering of the extracellular calcium concentration. Renin-secreting cells and smooth muscle cells of afferent arterioles showed immunoreactivity of MLCK. These findings suggest that the inhibitory effect of calcium on renin secretion could be explained by phosphorylation-dependent processes under control of the MLCK.


Endocrine ◽  
2021 ◽  
Vol 71 (3) ◽  
pp. 611-617
Author(s):  
Judit Tőke ◽  
Gábor Czirják ◽  
Péter Enyedi ◽  
Miklós Tóth

AbstractThe calcium-sensing receptor (CaSR) provides the major mechanism for the detection of extracellular calcium concentration in several cell types, via the induction of G-protein-coupled signalling. Accordingly, CaSR plays a pivotal role in calcium homeostasis, and the CaSR gene defects are related to diseases characterized by serum calcium level changes. Activating mutations of the CaSR gene cause enhanced sensitivity to extracellular calcium concentration resulting in autosomal dominant hypocalcemia or Bartter-syndrome type V. Inactivating CaSR gene mutations lead to resistance to extracellular calcium. In these cases, familial hypocalciuric hypercalcaemia (FHH1) or neonatal severe hyperparathyroidism (NSHPT) can develop. FHH2 and FHH3 are associated with mutations of genes of partner proteins of calcium signal transduction. The common polymorphisms of the CaSR gene have been reported not to affect the calcium homeostasis itself; however, they may be associated with the increased risk of malignancies.


1978 ◽  
Vol 33 (7-8) ◽  
pp. 574-579 ◽  
Author(s):  
H. Stieve ◽  
M. Bruns

Abstract The membrane potential in the dark and the saturated response height of the ventral nerve photoreceptor of Limulus was measured by an intracellular electrode while the external concentration of calcium, magnesium and sodium ions was varied. Decreasing the extracellular calcium concentration from 10-2 mol/l causes a calcium-dependent lowering of the dark membrane potential and at very low concentrations (<10-8 mol/l a reversal to ca. +5 to +11 mV, if the external magnesium concentration is also low. Also, the light response diminishes with decreasing extracellular calcium concentration and disappears at a concentration of 10-9 mol/l. External magnesium can substitute for certain properties of extracellular calcium. Lowering the extracellular sodium concentration from 543 mmol/l to 30 - 50 mmol/1 reduces the dark membrane potential and the light responses at normal calcium concentration, whereas at low calcium concentration it causes a substantial rise of both. Interpretation: The results are in accordance with our working hypothesis that a strong reduction of the external calcium (and magnesium) concentration causes a calcium concentration dependent opening of “ light channels” in the dark. Additional lowering the extracellular sodium concentration counteracts this effect; opening and closing of light channels is controlled by negative binding sites on the cell membrane for which calcium and sodium ions compete with an antagonistic action.


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