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Titolo:
BENZAMIL BLOCKADE OF BRAIN NA-INDUCED HYPERTENSION IN RATS( CHANNELS AVERTS NA+)
Autore:
NISHIMURA M; OHTSUKA K; NANBU A; TAKAHASHI H; YOSHIMURA M;
Indirizzi:
KYOTO PREFECTURAL UNIV MED,DEPT CLIN & LAB MED,KAMIKYO KU,465 KAJII-CHO KYOTO 602 JAPAN KANSAI MED UNIV,DEPT CLIN SCI & LAB MED MORIGUCHI OSAKA 570 JAPAN
Titolo Testata:
American journal of physiology. Regulatory, integrative and comparative physiology
fascicolo: 3, volume: 43, anno: 1998,
pagine: 635 - 644
SICI:
0363-6119(1998)43:3<635:BBOBNH>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBROSPINAL-FLUID SODIUM; BLOOD-PRESSURE; ANGIOTENSIN-II; CARDIOVASCULAR-RESPONSE; ARTERIAL-PRESSURE; HYPERTONIC NACL; SALT; VASOPRESSIN; MECHANISMS; ANTAGONIST;
Keywords:
AMILORIDE-SENSITIVE SODIUM ION CHANNELS; DEOXYCORTICOSTERONE ACETATE-SALT; STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RAT; AORTIC LIGATION; SYMPATHETIC NERVOUS SYSTEM; ARGININE VASOPRESSIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
M. Nishimura et al., "BENZAMIL BLOCKADE OF BRAIN NA-INDUCED HYPERTENSION IN RATS( CHANNELS AVERTS NA+)", American journal of physiology. Regulatory, integrative and comparative physiology, 43(3), 1998, pp. 635-644

Abstract

To determine the possible involvement of brain amiloride-sensitive Na channels in Na+-induced hypertension, we investigated the effects ofbenzamil hydrochloride, a specific blocker of these Na+ channels, on the acute presser mechanisms of intracerebroventricular infusion of hypertonic NaCl and the continuous presser mechanisms of Na+-induced chronic hypertension, such as deoxycorticosterone acetate-salt hypertensive or stroke-prone spontaneous hypertensive rats, and of non-Na+-induced hypertension, such as renovascular hypertensive rats. Intracerebroventricular preinjection with benzamil (1 or 10 nmol/kg) abolished the increase in mean arterial pressure, heart rate, abdominal sympathetic discharge, and plasma vasopressin concentration induced by an acute increase in cerebrospinal Na+ concentrations at intracerebroventricular infusion of 1.5 M hypertonic NaCl. Continuous intracerebroventricular infusion of benzamil (1 or 10 nmol.kg(-1).day(-1)) for 7 days attenuated Na+-induced chronic hypertension in both deoxycorticosterone acetate-salt and stroke-prone spontaneous hypertensive rats, accompanied by reduction of urinary excretion of vasopressin and norepinephrine but not in renovascular hypertensive rats. Intravenous infusion of benzamil(10 nmol.kg(-1).day(-1)) for 7 days affected neither arterial pressure nor urinary excretion of vasopressin and norepinephrine in either model of hypertension. Benzamil-blockable brain amiloride-sensitive Na+ channels are expected to function as one of the Na+ receptors in the brain and to be involved in the presser mechanism of Na+-induced hypertension.

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Documento generato il 23/11/20 alle ore 21:45:22