Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Ca2+ channel subtypes and pharmacology in the kidney Hayashi K; Wakino S; Sugano N; Ozawa Y; Homma K; Saruta TCirc Res 2007[Feb]; 100 (3): 342-53A large body of evidence has accrued indicating that voltage-gated Ca(2+) channel subtypes, including L-, T-, N-, and P/Q-type, are present within renal vascular and tubular tissues, and the blockade of these Ca(2+) channels produces diverse actions on renal microcirculation. Because nifedipine acts exclusively on L-type Ca(2+) channels, the observation that nifedipine predominantly dilates afferent arterioles implicates intrarenal heterogeneity in the distribution of L-type Ca(2+) channels and suggests that it potentially causes glomerular hypertension. In contrast, recently developed Ca(2+) channel blockers (CCBs), including mibefradil and efonidipine, exert blocking action on L-type and T-type Ca(2+) channels and elicit vasodilation of afferent and efferent arterioles, which suggests the presence of T-type Ca(2+) channels in both arterioles and the distinct impact on intraglomerular pressure. Recently, aldosterone has been established as an aggravating factor in kidney disease, and T-type Ca(2+) channels mediate aldosterone release as well as its effect on renal efferent arteriolar tone. Furthermore, T-type CCBs are reported to exert inhibitory action on inflammatory process and renin secretion. Similarly, N-type Ca(2+) channels are present in nerve terminals, and the inhibition of neurotransmitter release by N-type CCBs (eg, cilnidipine) elicits dilation of afferent and efferent arterioles and reduces glomerular pressure. Collectively, the kidney is endowed with a variety of Ca(2+) channel subtypes, and the inhibition of these channels by their specific CCBs leads to variable impact on renal microcirculation. Furthermore, multifaceted activity of CCBs on T- and N-type Ca(2+) channels may offer additive benefits through nonhemodynamic mechanisms in the progression of chronic kidney disease.|Aldosterone/physiology[MESH]|Animals[MESH]|Antihypertensive Agents/adverse effects/classification/pharmacology/therapeutic use[MESH]|Arterioles/drug effects/physiology[MESH]|Blood Pressure/drug effects[MESH]|Calcium Channel Blockers/adverse effects/*pharmacology/therapeutic use[MESH]|Calcium Channels, L-Type/chemistry/drug effects/physiology[MESH]|Calcium Channels, N-Type/chemistry/drug effects/physiology[MESH]|Calcium Channels, T-Type/chemistry/drug effects/physiology[MESH]|Calcium Channels/chemistry/classification/drug effects/*physiology[MESH]|Calcium Signaling/drug effects/physiology[MESH]|Cardiovascular Diseases/drug therapy/physiopathology[MESH]|Diabetes Mellitus/physiopathology[MESH]|Disease Progression[MESH]|Humans[MESH]|Hydronephrosis/physiopathology[MESH]|Hypertension/drug therapy/physiopathology[MESH]|Kidney Diseases/*drug therapy/metabolism[MESH]|Kidney/blood supply/*drug effects/physiology[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Microcirculation/drug effects/physiology[MESH]|Models, Biological[MESH]|Neurotransmitter Agents/metabolism[MESH]|Protein Subunits[MESH]|Rats[MESH]|Renal Circulation/drug effects/physiology[MESH]|Renin-Angiotensin System/physiology[MESH]|Renin/metabolism[MESH]|Vasodilation/drug effects[MESH] |
