Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
INCREASED VASCULAR RESPONSIVENESS TO ALPHA(2)-ADRENERGIC STIMULATION DURING NOS INHIBITION-INDUCED HYPERTENSION
Autore:
KANAGY NL;
Indirizzi:
UNIV NEW MEXICO,DEPT PHYSIOL & CELL BIOL,237 BASIC MED SCI BLDG ALBUQUERQUE NM 87131 UNIV NEW MEXICO,SCH MED,DEPT PHYSIOL ALBUQUERQUE NM 87131
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 6, volume: 42, anno: 1997,
pagine: 2756 - 2764
SICI:
0363-6135(1997)42:6<2756:IVRTAS>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADRENERGIC-RECEPTOR SUBTYPES; NITRO-L-ARGININE; ALPHA-ADRENOCEPTORS; SMOOTH-MUSCLE; BLOOD-VESSELS; RAT AORTA; OXIDE; CALCIUM; ALPHA-2-ADRENOCEPTORS; NOREPINEPHRINE;
Keywords:
NITRIC OXIDE; NITRIC OXIDE SYNTHASE; ALPHA(2)-ADRENOCEPTORS; UK-14304; VASCULAR SMOOTH MUSCLE;
Tipo documento:
Article
Natura:
Periodico
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
N.L. Kanagy, "INCREASED VASCULAR RESPONSIVENESS TO ALPHA(2)-ADRENERGIC STIMULATION DURING NOS INHIBITION-INDUCED HYPERTENSION", American journal of physiology. Heart and circulatory physiology, 42(6), 1997, pp. 2756-2764

Abstract

Increased vascular resistance during systemic nitric oxide synthase (NOS) inhibition is dependent on adrenergic vasoconstriction. This study tested the hypothesis that increased vascular sensitivity to adrenergic agonists contributes to this vasoconstriction. Superior mesentericarteries and thoracic aortae from male Sprague-Dawley rats drinking water containing N-omega-nitro-L-arginine (L-NNA; 14 days, 60 mg.kg(-1).day(-1)) and control rats were cut into helical strips, and endothelium was removed for contractile experiments. L-NNA arteries were more sensitive to UK-14304 (alpha(2)-adrenergic agonist) and norepinephrine (NE), whereas responses to phenylephrine (PE) were not different [concentration causing 50% maximal response (EC50), L-NNA vs. control: UK-14304, 0.071 vs. 0.71 mu mol/l; NE, 1.15 vs. 9.95 nmol/l]. Yohimbine, an alpha(2)-selective antagonist, caused a concentration-dependent inhibition of contraction to NE only in L-NNA arteries (EC50 = 6.3 vs. 1.6nmol/l at 1 nmol/l yohimbine), whereas prazosin shifted NE curves similarly in arteries from both groups. Yohimbine (10 nmol/l) inhibited contractions to UK-14304 (EC50 = 59 mu mol/l vs. 17 mu mol/l) but not contractions to PE, whereas prazosin inhibited both. These data indicate that L-NNA-induced hypertension leads to increased sensitivity of prazosin-sensitive alpha(2)-adrenoceptors, an upregulation that could cause the increased vasoconstrictor response to NE in this model of hypertension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 16:28:36