Why the study?
Do different dihydropyridine calcium channel blockers have diverse effects on glomerular hemodynamics in spontaneously hypertensive rats?
Do different dihydropyridine calcium channel blockers have diverse effects on glomerular hemodynamics in spontaneously hypertensive rats?
Different dihydropyridine calcium channel blockers exert diverse effects on glomerular hemodynamics, likely due to distinct pharmacological actions on the renal microvasculature.
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DHP subclass differences on glomerular pressure in hypertensive rats are hypothesis-generating; human studies required before any clinical consideration.
Effects of dihydropyridine (DHP) Ca2+ channel blocker (CaB) on glomerular hemodynamics are controversial. We examined the effects of two DHP derivatives, benidipine hydrochloride (BDP) and nifedipine (NDP), on glomerular hemodynamics by an in vivo micropuncture method by using spontaneously hypertensive rats (SHRs). Systemic bolus infusion of BDP (4 microg/kg) or NDP (250 microg/kg) elicited comparable decreases in mean arterial blood pressure (MAP). The proximal stop-flow pressure (Psf), an indicator of glomerular capillary pressure, revealed significant decreases in BDP but nonsignificant increases in NDP. To minimize the influence of MAP or other systemic events, we monitored Psf during perinephron infusion of CaB and observed significant increases in Psf during 10(-3) M NDP perfusion and nonsignificant changes with 10(-3) M BDP. Moreover, the stability of Psf during alteration of renal perfusion pressure was significantly impaired in the nephron treated with topical NDP. These findings support the notion that CaB has diverse effects on glomerular hemodynamics, and such effects may in part be the result of different pharmacologic actions on the renal microvasculature.
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Kawata et al. (1997) studied this question.
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