Abstract
The CaSR regulates Ca 2+ -mediated release of parathyroid hormone (PTH) from parathyroid cells by sensing small changes in serum Ca 2+ concentration. The receptor is also involved in the regulation of cell Ca 2+ levels independent of PTH secretion. The renin-angiotensin-aldosterone system (RAAS) plays vital roles in the development of hypertension, which is associated with vascular and renal dysfunction, and treatment is difficult because the mechanisms are not fully understood. Studies show that adequate Ca 2+ intake (1.0 to 1.5 g/day) is critical for optimal BP regulation and randomized controlled trials have revealed significant reductions in hypertension risk and BP levels in humans. In the kidney, the CaSR is expressed along the nephron and plays an important role, with the Na + /Ca 2+ exchanger (NCX), in the regulation of tubular Ca 2+ , Na + and water reabsorption. In the present study, we analyzed the effects of mutation, sex hormones and high salt diets on the expression of the CaSR, its downstream signaling complements and proteins in the RAAS in both female and male salt-sensitive (SS) rats. Our data indicate that CaSR gene mutation and high salt diets modulate the expression of the CaSR, GRK2, PKCα, NCX1 and RAAS proteins in the kidney of SS female rats than male rats. And also showed statistically significant difference in electrolytes as shown in the data below. Thus, CaSR signaling is linked to RAAS to control hypertension.
Published Version
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