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ABSTRACT: Rationale
Calcium channel blockers (CCBs) exert their antihypertensive effect by reducing cardiac afterload but not preload, suggesting that Ca(2+) influx through L-type Ca(2+) channels (LTCC) mediates arterial but not venous tone.Objective
The object of this study was to resolve the mechanism of venous resistance to CCBs.Methods and results
We compared the sensitivity of depolarization (KCl)-induced constriction of rat small mesenteric arteries (MAs) and veins (MVs) to the dilator effect of CCBs. Initial findings confirmed that nifedipine progressively dilated depolarization-induced constrictions in MAs but not MVs. However, Western blots showed a similar expression of the alpha(1C) pore-forming subunit of the LTCC in both vessels. Patch-clamp studies revealed a si
SUBMITTER: Thakali KM
PROVIDER: S-EPMC2855128 | biostudies-literature | 2010 Mar
REPOSITORIES: biostudies-literature