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Titolo:
Relative deficiency of nitric oxide-dependent vasodilation in salt-hypertensive Dahl rats: the possible role of superoxide anions
Autore:
Zicha, J; Dobesova, Z; Kunes, J;
Indirizzi:
Acad Sci Czech Republ, Inst Physiol, CZ-14220 Prague 4, Czech Republic Acad Sci Czech Republ Prague Czech Republic 4 0 Prague 4, Czech Republic Ctr Expt Res Cardiovasc Dis, Prague, Czech Republic Ctr Expt Res Cardiovasc Dis Prague Czech Republic rague, Czech Republic
Titolo Testata:
JOURNAL OF HYPERTENSION
fascicolo: 2, volume: 19, anno: 2001,
pagine: 247 - 254
SICI:
0263-6352(200102)19:2<247:RDONOV>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-PRESSURE; SENSITIVE RATS; ENDOTHELIAL DYSFUNCTION; SYNTHASE; INHIBITION; HYPERCHOLESTEROLEMIA; NOREPINEPHRINE; RESISTANT; RELEASE; STRESS;
Keywords:
blood pressure; salt hypertension; Dahl rats; superoxide anions; sympathetic nervous system; renin-angiotensin system; nitric oxide; plasma lipids; tempol;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Zicha, J Acad Sci Czech Republ, Inst Physiol, Videnska 1083, CZ-14220 Prague 4, Czech Republic Acad Sci Czech Republ Videnska 1083 Prague Czech Republic 4 blic
Citazione:
J. Zicha et al., "Relative deficiency of nitric oxide-dependent vasodilation in salt-hypertensive Dahl rats: the possible role of superoxide anions", J HYPERTENS, 19(2), 2001, pp. 247-254

Abstract

Objective The contribution of major vasoactive systems (renin-angiotensin system, sympathetic nervous system and nitric oxide) to blood pressure maintenance and the possible involvement of superoxide anions in the reduced efficiency of nitric oxide (NO)-dependent vasodilation to counterbalance sympathetic vasoconstriction were studied in salt-hypertensive Dahl rats. Design and methods We used Dahl salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) female rats kept on a low-salt (0.3% NaCl) or high-salt diet (8% NaCl) for 6 weeks since weaning. Mean arterial pressure (MAP) was measured inconscious animals subjected to acute consecutive blockade of the renin-angiotensin system (RAS) [captopril, 10 mg/kg intravenously (i.v,)], the sympathetic nervous system (SNS) (pentolinium, 5 mg/kg i.v.) and NO synthase (NW-nitro-L-arginine methyl ester (L-NAME), 30 mg/kg i.v.), Before the consecutive blockade of vasoactive systems one-half of the animals in each experimental group was pre-treated with a stable membrane-permeable mimetic of superoxide dismutase (tempol, 25 mg/kg i.v.) which functions as a superoxide scavenger. Results Compared to normotensive SR/Jr animals, salt-hypertensive SS/Jr rats were characterized by an enhanced blood pressure (BP) fail after ganglionic blockade (-104 +/- 8 versus -62 +/- 5 mm Hg, P < 0.001) and by higher residual blood pressure recorded after the blockade of both RAS and SNS (70 /- 3 versus 43 +/- 3 mmHg, P < 0.01), but there was only a borderline elevation of their BP response to acute NO synthase inhibition (67 +/- 6 versus49 +/- 4 mmHg, P< 0.05), The acute tempol pre-treatment elicited the most pronounced reduction of basal BP (-13 +/- 1 mmHg, P < 0.001) in the salt-hypertensive SS/Jr group in which the BP rise after L-NAME administration wasaugmented by about 50%. On the contrary, tempol pre-treatment did not affect norepinephrine- or angiotensin II-dependent vasoconstriction. Conclusions The NO system is not able to counterbalance effectively the hyperactivity of the sympathetic nervous system in salt-hypertensive Dahl rats. The predominance of sympathetic vasoconstriction over NO-dependent vasodilation could be explained partially by enhanced NO inactivation due to augmented superoxide anion formation in hypertensive animals. (C) 2001 Lippincott Williams & Wilkins.

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Documento generato il 01/12/20 alle ore 21:44:03