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Titolo:
COMPARISON OF THE EFFECTS OF NADOLOL AND BISOPROLOL ON NORADRENALINE-EVOKED VENOCONSTRICTION IN MAN IN-VIVO
Autore:
ABDELMAWLA AH; LANGLEY RW; SZABADI E; BRADSHAW CM;
Indirizzi:
QUEENS MED CTR,DEPT PSYCHIAT,FLOOR A,S BLOCK NOTTINGHAM NG7 2UH ENGLAND QUEENS MED CTR,DEPT PSYCHIAT NOTTINGHAM NG7 2UH ENGLAND
Titolo Testata:
British journal of clinical pharmacology
fascicolo: 3, volume: 45, anno: 1998,
pagine: 271 - 276
SICI:
0306-5251(1998)45:3<271:COTEON>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERNAL MAMMARY ARTERY; SAPHENOUS-VEIN; HAND VEINS; ADRENERGIC RESPONSIVENESS; ADRENOCEPTOR; RELAXATION; NEBIVOLOL; BLOCKADE;
Keywords:
NADOLOL; BISOPROLOL; NORADRENALINE; DORSAL HAND VEIN; BETA-ADRENOCEPTORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
A.H. Abdelmawla et al., "COMPARISON OF THE EFFECTS OF NADOLOL AND BISOPROLOL ON NORADRENALINE-EVOKED VENOCONSTRICTION IN MAN IN-VIVO", British journal of clinical pharmacology, 45(3), 1998, pp. 271-276

Abstract

Aims In an attempt to explore the possible involvement of venodilatorbeta-adrenoceptors in the constrictor response of the human dorsal hand vein to noradrenaline, we examined the ability of nadolol, a non-selective beta(1)/beta(2)-adrenoceptor antagonist, and bisoprolol a selective beta(1)-adrenoceptor antagonist, to potentiate the response. Methods Twelve healthy male volunteers participated in three weekly sessions. In each session nadolol (40 mg), bisoprolol (5 mg) or placebo wasingested, and (-) noradrenaline acid tartrate (0.33-33.33 ng min(-1))was infused locally into the dorsal hand vein 2 h after the ingestionof the drugs. Changes in vein diameter were monitored with the dorsalhand vein compliance technique. Subjects were allocated to treatmentsand sessions according to a double-blind balanced cross-over design. Systolic and diastolic blood pressure, and heart rate were also measured. Results Noradrenaline produced dose-dependent venoconstriction which was antagonized by bisoprolol but remained unaffected by nadolol (ANOVA with repeated measures: F(2,22) = 5.07, P < 0.025; Dunnett's test: placebo vs nadolol; t = 0.35, df = 22, k = 3, NS; placebo vs bisoprolol; t = 2.83, df = 22, k = 3, P < 0.01). Mean (+/- s.e. mean) log ED(50)s (ng min(-1)) were 0.44 +/- 0.15 (placebo), 0.73 +/- 0.11 (bisoprolol) and 0.50 +/- 0.21 (nadolol); mean (95% CI) differences were 0.29 (-0.005, 0.58) for placebo vs bisoprolol and 0.06 (-0.35, 0.46) for placebo vs nadolol. Both active drugs significantly (compared with placebo, P < 0.05) decreased (mean change from pretreatment +/- s.e. mean) heart rate (bisoprolol -16.08 +/- 2.01; nadolol -11.67 +/- 2.06) and systolic blood pressure (bisoprolol -15.0 +/- 0.80; nadolol -9.47 +/- 0.18). Conclusions The failure of nadolol and bisoprolol to potentiate noradrenaline-evoked venoconstriction argues against the involvement of masked venodilator beta-adrenoceptors in the response. The mechanismunderlying the antagonism of noradrenaline-evoked venoconstriction bybisoprolol remains to be elucidated.

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Documento generato il 30/03/20 alle ore 00:52:50