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• W2147534811 abstract "Little is known about the effects of nitric oxide (NO) and the cyclic GMP (cGMP)/protein kinase G (PKG) system on Ca 2+ signaling in vascular smooth muscle cells (VSMC) of resistance vessels in general and afferent arterioles in particular. We tested the hypotheses that cGMP-, Ca 2+ -dependent big potassium channels (BK Ca 2+ ) buffer the Ca 2+ response to depolarization by high extracellular KCl and that NO inhibits adenosine diphosphoribose (ADPR) cyclase, thereby reducing the Ca 2+ -induced Ca 2+ release. We isolated rat afferent arterioles, utilizing the magnetized microsphere method, and measured cytosolic Ca 2+ concentration ([Ca 2+ ] i ) with fura-2, a preparation in which endothelial cells do not participate in [Ca 2+ ] i responses. KCl (50 mM)-induced depolarization causes an immediate increase in [Ca 2+ ] i of 151 nM. The blockers N ω -nitro-l-arginine methyl ester (of nitric oxide synthase), 1,2,4-oxodiazolo-[4,3- a]quinoxalin-1-one (ODQ, of guanylyl cyclase), KT-5823 (of PKG activation), and iberiotoxin (IBX, of BK Ca 2+ activity) do not alter the [Ca 2+ ] i response to KCl, suggesting no discernible endogenous NO production under basal conditions. The NO donor sodium nitroprusside (SNP) reduces the [Ca 2+ ] i response to 77 nM; IBX restores the response to control values. These data show that activation of BK Ca 2+ in the presence of NO/cGMP provides a brake on KCl-induced [Ca 2+ ] i responses. Experiments with the inhibitor of cyclic ADPR 8-bromo-cyclic ADPR (8-Br-cADPR) and SNP + downstream inhibitors of PKG and BK Ca 2+ suggest that NO inhibits ADPR cyclase in intact arterioles. When we pretreat afferent arterioles with 8-bromoguanosine 3′,5′-cyclic monophosphate (8-Br-cGMP; 10 μM), the response to KCl is 143 nM. However, in the presence of both IBX and 8-Br-cGMP, we observe a surprising doubling of the [Ca 2+ ] i response to KCl. In summary, we present evidence for effects of the NO/cGMP/PKG system to reduce [Ca 2+ ] i , via activation of BK Ca 2+ and possibly by inhibition of ADPR cyclase, and to increase [Ca 2+ ] i , by a mechanism(s) yet to be defined." @default.
• W2147534811 created "2016-06-24" @default.
• W2147534811 creator A5018346235 @default.
• W2147534811 creator A5061630338 @default.
• W2147534811 date "2010-01-01" @default.
• W2147534811 modified "2023-10-15" @default.
• W2147534811 title "Complex interactions of NO/cGMP/PKG systems on Ca²⁺signaling in afferent arteriolar vascular smooth muscle" @default.
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• W2147534811 doi "https://doi.org/10.1152/ajpheart.00485.2009" @default.
• W2147534811 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2806127" @default.
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