Role of Intracellular Calcium in the Regulation of Renal Hemodynamics
Intracellular calcium contributes to renal hemodynamic regulatory mechanisms in multiple ways. Calcium channel blockers elicit a selective vasodilation of preglomerular arterioles leading to increases in renal blood flow (RBF), glomerular filtration rate (GFR), and glomerular pressure, with marked attenuation of autoregulatory capability. The effects of these agents seem to be restricted to the component of renal vascular resistance responsible for autoregulation and contrast with other agents which vasodilate the kidney at arterial pressures below, as well as within, the auto-regulatory range. This component of renal vascular resistance that is not influenced by calcium entry blockade can be altered by angiotensin converting enzyme inhibition. Studies at the microvascular level have demonstrated that the effects of angiotensin II on afferent arterioles are dependent upon calcium entry whereas the vasoconstrictor actions on efferent arterioles are not influenced by calcium channel blockade. The macula densa cells responsible for mediating tubular glomerular feedback (TGF) appears to utilize a different type of intracellular calcium mechanism for transmission of feedback signals. Increases in the intralumenal solute concentration at the macula densa elicit feedback signals to constrict the afferent arterioles and reduce glomerular pressure. These effects can be artificially induced by the intralumenal addition of calcium ionophores; however, intralumenal addition of calcium channel blockers or variation in intralumenal calcium concentration do not interfere with signal transmission. In contrast, agents that interfere with intracellular calcium mobilization can block TGF responses. Thus, intracellular mobilization of cytosolic calcium within the macula densa cells leads to transmission of TGF signals to the vascular cells. At the afferent arteriolar effector site, transmembrane calcium flux appears to serve as the dominant mechanism for regulating intracellular calcium, since TGF-mediated vasoconstrictor responses are abolished by calcium channel blockade. The efferent arterioles may be less responsive to TGF signals because of their relative insensitivity to agents that alter transmembrane calcium flux.
KeywordsAttenuation Manganese Angiotensin Peri Acetylcholine
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