Bisoprolol attenuates noradrenaline‐ and phenylephrine‐evoked venoconstriction in man in vivo

Abdelmawla, A. H.; Langley, R. W.; Szabadi, E.; Bradshaw, C. M.

doi:10.1046/j.1365-2125.1997.00624.x

Cited by 4 publications

(3 citation statements)

References 8 publications

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“…A study confirmed that atenolol does not improve vascular compliance [39], and that atenolol is relatively ineffective in lowering central aortic systolic pressure [14], [18]–[22]. Third, it was reported that bisoprolol failed to potentiate the constrictor response to noradrenaline, and that it antagonized the constrictor responses both to noradrenaline and the selective α1-adrenoceptor agonist, PE [40], [41]. In addition, another study in rats showed that bisoprolol treatment lowered the production of the vasoconstrictive endothelin-1 (ET-1) and thromboxane [42].…”

Section: Discussionmentioning

confidence: 87%

A Randomized Controlled Study on the Effects of Bisoprolol and Atenolol on Sympathetic Nervous Activity and Central Aortic Pressure in Patients with Essential Hypertension

Zhou

Wang

et al. 2013

PLoS ONE

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Objectiveβ-blockers (BBs) with different pharmacological properties may have heterogeneous effects on sympathetic nervous activity (SNA) and central aortic pressure (CAP), which are independent cardiovascular factors for hypertension. Hence, we analyzed the effects of bisoprolol and atenolol on SNA and CAP in hypertensive patients.MethodsThis was a prospective, randomized, controlled study in 109 never-treated hypertensive subjects randomized to bisoprolol (5 mg) or atenolol (50 mg) for 4–8 weeks. SNA, baroreflex sensitivity (BRS) and heart rate (HR) variability (HRV) were measured using power spectral analysis using a Finometer. CAP and related parameters were determined using the SphygmoCor device (pulse wave analysis).ResultsBoth drugs were similarly effective in reducing brachial BP. However, central systolic BP (−14±10 mm Hg vs −6±9 mm Hg; P<0.001) and aortic pulse pressure (−3±10 mm Hg vs +3±8 mm Hg; P<0.001) decreased more significantly with bisoprolol than with atenolol. The augmentation index at a HR of 75 bpm (AIxatHR75) was significantly decreased (29%±11% to 25%±12%; P = 0.026) in the bisoprolol group only. Furthermore, the change in BRS in the bisoprolol group (3.99±4.19 ms/mmHg) was higher than in the atenolol group (2.66±3.78 ms/mmHg), although not statistically significant (P>0.05). BRS was stable when RHR was controlled (RHR≤65 bpm), and the two treatments had similar effects on the low frequency/high frequency (HF) ratio and on HF.ConclusionBBs seem to have different effects on arterial distensibility and compliance in hypertensive subjects. Compared with atenolol, bisoprolol may have a better effect on CAP.Trial RegistrationClinicalTrials.gov NCT01762436

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Section: Discussionmentioning

confidence: 87%

A Randomized Controlled Study on the Effects of Bisoprolol and Atenolol on Sympathetic Nervous Activity and Central Aortic Pressure in Patients with Essential Hypertension

Zhou

Wang

et al. 2013

PLoS ONE

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“…It should be noted, however, that bisoprolol may have additional pharmacological properties, which may have masked the antagonism of the responses to isoprenaline. Indeed, in a separate study, we observed that bisoprolol could antagonize both noradrenaline‐and phenylephrine‐evoked venoconstriction in a dose dependent manner [9]. As there is evidence that the venoconstrictor responses to noradrenaline and phenylephrine are mediated by α 1 ‐ and α 2 ‐adrenoceptors [3], and bisoprolol has no affinity for these receptors [6, 7], the antagonism of the constrictor responses by bisoprolol is likely to reflect functional rather than competitive antagonism due to a possible venodilator effect of the drug [9].…”

Section: Discussionmentioning

confidence: 99%

“…More recently, we have reinvestigated the question of the probable involvement of masked b 1 -adrenoceptors in the venoconstrictor response to noradrenaline by using bisoprolol, a highly selective b 1 -adrenoceptor antagonist lacking in intrinsic sympathomimetic activity [6±8]. We found that bisoprolol failed to potentiate the constrictor response to noradrenaline, and that it antagonized the constrictor responses both to noradrenaline and the selective a 1 -adrenoceptor agonist phenylephrine [9,10].…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effects of nadolol and bisoprolol on the isoprenaline‐evoked dilatation of the dorsal hand vein in man

Abdelmawla

Langley

Szabadi

et al. 2001

Brit J Clinical Pharma

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Aims We attempted to explore the possible differential involvement of badrenoceptor subtypes in the dilator response of the human dorsal hand vein to isoprenaline by examining the ability of bisoprolol, a selective b 1 -adrenoceptor antagonist, and nadolol, a nonselective b 1 /b 2 -adrenoceptor antagonist, to antagonize the response. Methods Twelve healthy male volunteers participated in four weekly sessions. In the preliminary session a dose-response curve to the vasoconstrictor effect of phenylephrine was constructed and the dose producing 50±75% maximal response was determined for each individual. In each of the remaining three (treatment) sessions, nadolol (40 mg), bisoprolol (5 mg) or placebo was ingested, and isoprenaline hydrochloride (3.33±1000 ng min x1 ) was infused locally into the dorsal hand vein along with a constant dose of phenylephrine hydrochloride (to preconstrict the vein) 2 h after the ingestion of the drugs. Changes in vein diameter were monitored with the dorsal hand vein compliance technique. Subjects were allocated to treatment session according to a double-blind balanced cross-over design. Systolic and diastolic blood pressure, and heart rate were also measured. Results Isoprenaline produced dose-dependent venodilatation which was antagonized by nadolol but remained unaffected by bisoprolol (ANOVA with repeated measures: P<0.025; Dunnett's test: placebo vs nadolol, P<0.01; placebo vs bisoprolol, P=NS). Mean log ED 50 (ng min x1 ) was signi®cantly increased in the presence of nadolol and remained unchanged in the presence of bisoprolol (ANOVA, P<0.025; Dunnett's test: placebo vs nadolol, P<0.005; placebo vs bisoprolol, P=NS; differences between mean log ED 50 [95% CI]: placebo vs bisoprolol x0.11 [-0.38, 0.16

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Comparison of the effects of nadolol and bisoprolol on noradrenaline‐evoked venoconstriction in man in vivo

Abdelmawla

Langley

Szabadi

et al. 1998

Brit J Clinical Pharma

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AimsIn an attempt to explore the possible involvement of venodilator b-adrenoceptors in the constrictor response of the human dorsal hand vein to noradrenaline, we examined the ability of nadolol, a non-selective b 1 /b 2 -adrenoceptor antagonist, and bisoprolol a selective b 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 was ingested, and (-) noradrenaline acid tartrate (0.33-33.33 ng min −1 ) was infused locally into the dorsal hand vein 2 h after the ingestion of the drugs. Changes in vein diameter were monitored with the dorsal hand vein compliance technique. Subjects were allocated to treatments and 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, In the present study we compared the effects of is generally acknowledged that venodilator b-adrenoceptors are of the b 2 subtype, the possible involvement of b 1 -pharmacodynamically active small single oral doses [18] of the non-selective b 1 /b 2 -adrenoceptor antagonist, nadolol adrenoceptors has not been excluded [9][10][11][12].The physiological sympathomimetic amine noradrenaline and the selective b 1 -adrenoceptor antagonist, bisoprolol on noradrenaline-evoked venoconstriction in man, using the has affinity for both a-and b-adrenoceptors [9]. Although noradrenaline is a powerful constrictor of the human dorsal dorsal hand vein compliance technique. Our prediction was that if the venoconstrictor response to noradrenaline is hand vein [13][14], it is possible that the constrictor response is attenuated by the activation of masked venodilator attenuated by masked b 2 -adrenoceptors, but not by b 1 -adrenoceptors, nadolol would potentiate the response but b-adrenoceptors. The possible involvement of these masked receptors could be revealed by the use of b-adrenoceptor bisoprolol would be without any effect. On the other hand, if both b 2 -and b 1 -adrenoceptors are involved both antagonists would cause potentiation of the response.

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Bisoprolol attenuates noradrenaline‐ and phenylephrine‐evoked venoconstriction in man in vivo

Cited by 4 publications

References 8 publications

A Randomized Controlled Study on the Effects of Bisoprolol and Atenolol on Sympathetic Nervous Activity and Central Aortic Pressure in Patients with Essential Hypertension

A Randomized Controlled Study on the Effects of Bisoprolol and Atenolol on Sympathetic Nervous Activity and Central Aortic Pressure in Patients with Essential Hypertension

Comparison of the effects of nadolol and bisoprolol on the isoprenaline‐evoked dilatation of the dorsal hand vein in man

Comparison of the effects of nadolol and bisoprolol on noradrenaline‐evoked venoconstriction in man in vivo

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