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Title of Journal: Am J Hypertens

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Abbravation: American Journal of Hypertension

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Narnia

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DOI

10.1007/bf01161529

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0895-7061

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P156 Nitric oxide synthase inhibition mediated a

Authors: Feng MingGuo Navar LGabriel
Publish Date: 2004/05/01
Volume: 17, Issue: S1, Pages: 90A-91A
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Abstract

MingGuo Feng LGabriel Navar P156 Nitric oxide synthase inhibition mediated afferent and efferent arteriolar vasoconstriction involves Ltype calcium channel activation American Journal of Hypertension Volume 17 Issue S1 May 2004 Pages 90A–91A https//doiorg/101016/jamjhyper200403231Ltype Ca2+ channels are expressed in renal microvasculature but There is less functional evidence regarding the role of L and Ttype channels in regulating the NOS inhibition mediated vasoconstriction of afferent and efferent arterioles Recently NO have been implicated to affect voltagegated Ca2+ channel activity To test the hypothesis that Ltype Ca2+ channel may mediate afferent and efferent arteriole vasoconstriction following inhibition of nitric oxide synthase NOS ideomicroscopic measurements of vascular dimensions were performed on the isolated bloodperfused juxtamedullary nephron preparation from SpragueDawley rats Single afferent or efferent arterioles were superfused with solutions containing a NOS inhibitor LNNA or a Ltype Ca2+ channel blocker diltiazem or a Ttype Ca2+ channel blocker pimozide LNNA 100μM significantly decreased afferent and efferent arteriolar diameter by 196±30 from 186±05 to 149±04 μm p001 and 151±21 from 190±04 to 161±06 μm p001 respectively However LNNA induced vasoconstriction was markedly inhibited by administration of 10μM diltiazem affrent and efferent arterioles with diameters increasing by 363±64 p001 and 265±78 p001 respectively In addition adding 10μM pimozide after diltiazem did not significantly augment the dilation of afferent and efferent arteriolar diameter These results provide further evidence that NO may affect voltagegated Ca2+ channels activity in afferent and efferent arterioles The vasoconstriction elicited by NOS inhibition was blocked by diltiazem suggesting that the vasoconstriction involved activation of Ltype Ca2+ channel in afferent and efferent arterioles Ltype Ca2+ channel may act cooperatively with Ttype channels to mediate Ca2+ entry responsible for NOS inhibition mediated efferent and afferent arteriole vasoconstriction Ltype Ca2+ channel blockers may be of value in counteract endothelial dysfunction associated with hypertension and associated cardiovascular disorders

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