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Neuronal nitric oxide synthase: its role and regulation in macula densa cells

Kovács, Gergely ; Komlósi, Péter ; Fuson, Amanda ; Peti-Peterdi, János ; Rosivall, László ; Bell, P Darwin

Journal of the American Society of Nephrology : JASN, October 2003, Vol.14(10), pp.2475-83 [Peer Reviewed Journal]

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  • Title:
    Neuronal nitric oxide synthase: its role and regulation in macula densa cells
  • Author: Kovács, Gergely ; Komlósi, Péter ; Fuson, Amanda ; Peti-Peterdi, János ; Rosivall, László ; Bell, P Darwin
  • Description: Macula densa (MD) cells detect changes in distal tubular sodium chloride concentration ([NaCl](L)), at least in part, through an apical Na:2Cl:K co-transporter. This co-transporter may be a site for regulation of tubuloglomerular feedback (TGF), and recently angiotensin II (Ang II) was shown to regulate the MD Na:2Cl:K co-transporter. In addition, nitric oxide (NO) produced via neuronal NO synthase (nNOS) in MD cells attenuates MD-TGF signaling. This study investigated [NaCl](L)-dependent MD-NO production, the regulation of co-transporter activity by NO, and the possible interaction of NO with Ang II. MD cell Na(+) concentration ([Na(+)](i)) and NO production were measured using sodium-binding benzofuran isophthalate and 4-amino-5-methylamino-2',7'-difluorescein diacetate, respectively, using fluorescence microscopy. Na:2Cl:K co-transport activity was assessed as the initial rate of increase in [Na(+)](i) when [NaCl](L) was elevated from 25 to 150 mM. 10(-4) M 7-nitroindazole, a specific nNOS blocker, significantly increased by twofold the initial rate of rise in [Na(+)](i) when [NaCl](L) was increased from 25 to 150 mM, indicating co-transporter stimulation. There was no evidence for an interaction between the stimulatory effect of Ang II and the inhibitory effect of NO on co-transport activity, and, furthermore, Ang II failed to alter MD-NO production. NO production was sensitive to [NaCl](L) but increased only when [NaCl](L) was elevated from 60 to 150 mM. These studies indicate that MD-NO directly inhibits Na:2Cl:K co-transport and that NO and Ang II independently alter co-transporter activity. In addition, generation of MD-NO seems to occur only at markedly elevated [NaCl](L), suggesting that NO may serve as a buffer against high rates of MD cell transport and excessive TGF-mediated vasoconstriction.
  • Is Part Of: Journal of the American Society of Nephrology : JASN, October 2003, Vol.14(10), pp.2475-83
  • Identifier: ISSN: 1046-6673 ; PMID: 14514725 Version:1
  • Subjects: Juxtaglomerular Apparatus -- Enzymology ; Loop of Henle -- Enzymology ; Nitric Oxide Synthase -- Metabolism
  • Language: English

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