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Titolo:
Physiological and genomic consequences of intermittent hypoxia - Selected contribution: Altered vascular reactivity in arterioles of chronic intermittent hypoxic rats
Autore:
Tahawi, Z; Orolinova, N; Joshua, IG; Bader, M; Fletcher, EC;
Indirizzi:
Univ Louisville, Dept Med, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 ept Med, Louisville, KY 40292 USA Univ Louisville, Dept Resp Dis, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 esp Dis, Louisville, KY 40292 USA Univ Louisville, Dept Physiol Biophys, Louisville, KY 40292 USA Univ Louisville Louisville KY USA 40292 Biophys, Louisville, KY 40292 USA Humboldt Univ, Max Delbruck Ctr Mol Med, D-13092 Berlin, Germany Humboldt Univ Berlin Germany D-13092 tr Mol Med, D-13092 Berlin, Germany
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 5, volume: 90, anno: 2001,
pagine: 2007 - 2013
SICI:
8750-7587(200105)90:5<2007:PAGCOI>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
OBSTRUCTIVE SLEEP-APNEA; NITRIC-OXIDE SYNTHASE; BLOOD-PRESSURE; EPISODIC HYPOXIA; L-ARGININE; HYPERTENSION; ENDOTHELIN-1; ELEVATION; MODEL; CELL;
Keywords:
systemic hypertension; sleep apnea; vasoconstriction; endothelial microvasculature; endothelial nitric oxide synthase mRNA; vasodilation; vascular tone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Fletcher, EC Univ Louisville, Sch Med, Div Resp Crit Care & Environm Med, Ambulatory Care Bldg,Rm A3L01,530 S Jackson St, Louisville, KY 40222 USA Univ Louisville Ambulatory Care Bldg,Rm A3L01,530 S Jackson St Louisville KY USA 40222
Citazione:
Z. Tahawi et al., "Physiological and genomic consequences of intermittent hypoxia - Selected contribution: Altered vascular reactivity in arterioles of chronic intermittent hypoxic rats", J APP PHYSL, 90(5), 2001, pp. 2007-2013

Abstract

Recurrent episodic hypoxia (EH) is a feature of sleep apnea that may be responsible for some chronic cardiovascular sequelae such as systemic hypertension. Chronic EH (8 h/day for 35 days) causes elevation of diurnal resting(unstimulated) mean arterial blood pressure (MAP) in the rat. We used in vivo video microscopy to examine arteriolar reactivity in the cremaster muscle of male Sprague-Dawley rats subjected to 35 days of EH. Cremaster muscles of EH (n = 6) and control (n = 6) rats were exposed to varying doses of norepinephrine (NE) (10(-10) to 10(-5) M), ACh (10(-9) to 10(-5) M), and endothelin-1 (10(-12) to 10(-8) M). In a separate experiment, EH (n = 5) and control (n = 6) rats were given one dose of a nitric oxide synthase (NOS) inhibitor N-G-nitro-L-arginine methyl ester (L-NAME; 10(-5) M). We also examined endothelial NOS mRNA from the kidneys of EH-stimulated and control (unstimulated) rats. Telemetry-monitored EH rats showed a 16-mmHg increase in MAP over 35 days, whereas control rats showed no change. The response to NE and endothelin-1 were similar for EH and control rats. ACh vasodilatation of arterioles in EH rats was significantly attenuated compared with that of controls. The degree of vasoconstriction in response to blockade of the nitric oxide system by L-NAME was significantly less (83% of baseline diameterwith L-NAME) for arterioles of EH rats compared with that for controls (61% of baseline diameter), implying lower basal resting nitric oxide release in the EH rats. Whole kidney mRNA endothelial NOS levels were not differentbetween groups. These data support the hypothesis that chronic elevation of blood pressure associated with EH involves increased peripheral resistance from decreased basal release or production of nitric oxide after 35 days of EH.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/21 alle ore 03:03:04