Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
NO inhibits NaCl absorption by rat thick ascending limb through activationof cGMP-stimulated phosphodiesterase
Autore:
Ortiz, PA; Garvin, JL;
Indirizzi:
Henry Ford Hosp, Div Hypertens & Vasc Res, Detroit, MI 48202 USA Henry Ford Hosp Detroit MI USA 48202 ns & Vasc Res, Detroit, MI 48202 USA
Titolo Testata:
HYPERTENSION
fascicolo: 2, volume: 37, anno: 2001,
parte:, 2 supplemento:, S
pagine: 467 - 471
SICI:
0194-911X(200102)37:2<467:NINABR>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
OXIDE-INDUCED INHIBITION; NITRIC-OXIDE; COLLECTING DUCT; GUANYLATE-CYCLASE; PROTEIN-KINASE; SMOOTH-MUSCLE; TRANSPORT; MECHANISMS; CHLORIDE; DECREASE;
Keywords:
limb, thick, ascending; nitric oxide; cGMP; phosphodiesterases; transport, chloride;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Garvin, JL Henry Ford Hosp, Div Hypertens & Vasc Res, 2799 W Grand Blvd, Detroit, MI 48202 USA Henry Ford Hosp 2799 W Grand Blvd Detroit MI USA 482028202 USA
Citazione:
P.A. Ortiz e J.L. Garvin, "NO inhibits NaCl absorption by rat thick ascending limb through activationof cGMP-stimulated phosphodiesterase", HYPERTENSIO, 37(2), 2001, pp. 467-471

Abstract

In the isolated, perfused rat thick ascending limb (THAL), L-arginine (L-Arg) stimulates endogenous nitric oxide (NO) production, which inhibits NaClabsorption. However, the intracellular cascade responsible for the effectsof NO has not been studied. We hypothesized that endogenous NO inhibits THAL NaCl transport by increasing cGMP, which activates protein kinase G (PKG) and cGMP-stimulated phosphodiesterase (PDE II), which, in turn, decreasescAMP levels. THALs from rats were isolated and perfused, and net chloride flux (J(Cl-)) was measured. L-Arg was used to stimulate NO production. Adding L-Arg (0.5 mmol/L) to the bath decreased J(Cl-) from 154.4+/-9.9 to 101.9+/-14.1 pmol . mm(-1) . min(-1), a 35.2% decrease (n=6; P<0.05). In the presence of the soluble guanylate cyclase inhibitor LY-83583 (10 <mu>mol/L), adding L-Arg to the bath did not affect THAL J(Cl-) (143.7+/-28.1 versus 136.7+/-22.2 pmol . mm(-1) . min(-1); n=6). LY-83583 alone had no effect on J(Cl-). In the presence of the PDE II inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) 50 mu mol/L, L-Arg reduced J(Cl-) by only 13% (142.1+/-8.9versus 122.7+/-11.5 pmol . mm(-1) . min(-1); P<0.05; n=6). EHNA alone had no effect on THAL J(Cl-). In the presence of 10(-5) mol/L dibutyryl (db)-cAMP, L-Arg did not significantly reduce J(Cl-) (116.3+/-18.2 versus 102.6+/-15.6 pmol . mm(-1) . min(-1); n=6), db-cAMP (10(-5) mol/L) had no effect onTHAL J(Cl-). In the presence of the PKG inhibitor KT-5823 (2 <mu>mol/L), L-Arg lowered J(Cl-) from 142.6+/-14.1 to 85.9+/-8.3 pmol . mm(-1) . min(-1), a decrease of 35.6% (n=8; P<0.05). We conclude that (1) endogenous NO inhibits THAL J(Cl-) by stimulating soluble guanylate cyclase and increasing cGMP; (2) NO inhibits THAL J(Cl-) by stimulation of PDE II, which, in turn, decreases cAMP levels; and (3) PKG does not mediate NO-induced inhibition of THAL J(Cl-).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 01:44:35