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Titolo:
beta-Adrenoceptor and nNOS-derived NO interactions modulate hypoglycemic pial arteriolar dilation in rats
Autore:
Santizo, RA; Koenig, HM; Pelligrino, DA;
Indirizzi:
Univ Illinois, Neuroanesthesia Res Lab, Chicago, IL 60607 USA Univ Illinois Chicago IL USA 60607 sthesia Res Lab, Chicago, IL 60607 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 2, volume: 280, anno: 2001,
pagine: H562 - H568
SICI:
0363-6135(200102)280:2<H562:BANNIM>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; CEREBRAL BLOOD-FLOW; INSULIN-INDUCED HYPOGLYCEMIA; PARAVENTRICULAR NUCLEUS; LOCUS-COERULEUS; AWAKE GOATS; BRAIN-STEM; IN-VIVO; HYPERCAPNIA; RECEPTORS;
Keywords:
7-nitroindazole; ARR-17477; brain; propranolol; tetrodotoxin; vasodilation; nitric oxide; neuronal nitric oxide synthase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Pelligrino, DA Univ Illinois, Neuroanesthesia Res Lab, MBRB M-C 513,900 S Ashland Ave, Chicago, IL 60607 USA Univ Illinois MBRB M-C 513,900 S AshlandAve Chicago IL USA 60607
Citazione:
R.A. Santizo et al., "beta-Adrenoceptor and nNOS-derived NO interactions modulate hypoglycemic pial arteriolar dilation in rats", AM J P-HEAR, 280(2), 2001, pp. H562-H568

Abstract

We examined the relative contributions from nitric oxide (NO) and catecholaminergic pathways in promoting cerebral arteriolar dilation during hypoglycemia (plasma glucose congruent to 1.4 mM). To that end, we monitored the effects of beta -adrenoceptor (beta -AR) blockade with propranolol (Pro, 1.5mg/kg iv), neuronal nitric oxide synthase (nNOS) inhibition with 7-nitroindazole (7-NI, 40 mg/kg ip) or ARR-17477 (300 muM, via topical application),or combined intravenous Pro + 7-NI or ARR-17477 on pial arteriolar diameter changes in anesthetized rats subjected to insulin-induced hypoglycemia. Additional experiments, employing topically applied TTX (1 muM), addressed the possibility that the pial arteriolar response to hypoglycemia required neuronal transmission. Separately, Pro and 7-NI elicited modest but statistically insignificant 10-20% reductions in the normal similar to 40% increasein arteriolar diameter accompanying hypoglycemia. However, combined Pro-7-NI was accompanied by a >80% reduction in the hypoglycemia-induced dilation. On the other hand, the combination of intravenous Pro and topical ARR-17477 did not affect the hypoglycemia response. In the presence of TTX, the pial arteriolar response to hypoglycemia was lost completely. These results suggest that 1) beta -ARs and nNOS-derived NO interact in contributing to hypoglycemia-induced pial arteriolar dilation; 2) the interaction does not occur in the vicinity of the arteriole; and 3) the vasodilating signal is transmitted via a neuronal pathway.

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Documento generato il 02/06/20 alle ore 21:42:53