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J. Arendshorst. NO and NO-independent mechanisms mediate ETB

Title: J. Arendshorst. NO and NO-independent mechanisms mediate ETB
Authors: Armin Just; Andrea J. M. Olson; John R. Falck; William J. Arendshorst; Am J Physiol; Regul Integr; Comp Physiol R–r
Contributors: The Pennsylvania State University CiteSeerX Archives
Source: http://omnibus.uni-freiburg.de/~aj57/Just_05_ETB-NO.pdf.
Publication Year: 2004
Collection: CiteSeerX
Description: Vascular endothelin (ET) type B (ETB) receptors exert dilator and constrictor actions in a complex interaction with ETA receptors. We aimed to clarify the presence and relative importance of nitric oxide (NO) and other mechanisms underlying the dilator effects of ETB receptors in rat kidneys. Complete inhibition of NO production with N-nitro-L-arginine methyl ester (L-NAME, 25 mg/kg iv) enhanced the renal vasoconstriction elicited by ET-1 injected into the renal artery from 15 to 30%. Additional infusion of the NO donor nitroprusside (NP) into the renal artery did not reverse this effect (29%) but effectively buffered ANG II-mediated vasoconstriction. Similarly, ET-1 responses were enhanced after a smaller intrarenal dose of L-NAME (22 vs.15%) and were unaffected by subsequent NP infusion (21%). These results indicate that the responsiveness to ET-1 is buffered by ETB receptor-stimulated phasic release of NO, rather than its static mean level. Infusion of the ETB receptor antag-
Document Type: text
File Description: application/pdf
Language: English
Relation: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.521.2503
Availability: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.521.2503; http://omnibus.uni-freiburg.de/~aj57/Just_05_ETB-NO.pdf
Rights: Metadata may be used without restrictions as long as the oai identifier remains attached to it.
Accession Number: edsbas.8EAC7FD4
Database: BASE