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Titolo:
Impaired renal vascular endothelial function in vitro in experimental hypercholesterolemia
Autore:
Stulak, JM; Lerman, A; Caccitolo, JA; Wilson, SH; Romero, JC; Schaff, HV; Porcel, MR; Lerman, LO;
Indirizzi:
Mayo Clin & Mayo Fdn, Dept Internal Med, Div Hypertens, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 tens, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Surg, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 Surg, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Internal Med, Div Cardiovasc Dis, Rochester, MN55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 c Dis, Rochester, MN55905 USA Mayo Clin & Mayo Fdn, Dept Physiol & Biophys, Rochester, MN 55905 USA MayoClin & Mayo Fdn Rochester MN USA 55905 phys, Rochester, MN 55905 USA
Titolo Testata:
ATHEROSCLEROSIS
fascicolo: 1, volume: 154, anno: 2001,
pagine: 195 - 201
SICI:
0021-9150(200101)154:1<195:IRVEFI>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE PATHWAY; L-ARGININE; RESPONSES; ARTERIES; RATS; INHIBITION; RABBITS; FAILURE; INTACT;
Keywords:
hypercholesterolemia; kidney; renal artery; endothelium; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Lerman, LO Mayo Clin & Mayo Fdn, Dept Internal Med, Div Hypertens, 200 1stSt SW, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn 200 1st St SW Rochester MN USA 55905 5 USA
Citazione:
J.M. Stulak et al., "Impaired renal vascular endothelial function in vitro in experimental hypercholesterolemia", ATHEROSCLER, 154(1), 2001, pp. 195-201

Abstract

Hypercholesterolemia (HC) induces alterations in systemic vascular reactivity, which can manifest as an attenuated endothelium-dependent relaxation, partly consequent to an impairment in nitric oxide (NO) activity. To determine whether experimental HC has a similar effect on renal vascular function, renal artery segments obtained from pigs fed a HC (n = 5) or normal (n = 5) diet were studied in vitro. Endothelium-dependent relaxation was examined using increasing concentrations of acetylcholine (Ach), calcium ionophoreA23187, and Ach following pre-incubation with N-G-monomethyl-L-arginine orL-arginine (L-ARG). The NO-donor diethylamine (DEA) was used to examine smooth muscle relaxation response and cyclic GMP generation in endothelium-denuded vessels. The expression of endothelial NO synthase (eNOS) in the renal arteries was examined using Western blotting. Endothelium-dependent relaxation to Ach was significantly attenuated in the HC group compared to normal (53.3 +/- 9.1 vs. 98.8 +/- 3.7%, P < 0.005), but normalized after pre-incubation with L-ARG (82.3 <plus/minus> 13.8%, P = 0.21). Receptor-independent endothelium-dependent relaxation to A23187 was also significantly bluntedin HC (75.2 +/- 10.5 vs. 115.5 +/- 4.2%, P < 0.017). Smooth muscle relaxation and cyclic GMP generation in response to DEA were greater in denuded HCvessels, while relaxation of intact vessels to nitroprusside was unaltered. In the HC vessels eNOS was almost undetectable. In conclusion, experimental HC attenuates in vitro endothelium-dependent relaxation of the porcine renal artery, possibly due to low bioavailability of NO. These vascular alterations in HC could play a role in the pathogenesis of renal disease or hypertension, supporting a role for HC as a risk factor for renovascular disease. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 00:28:17