The effects of time and dose on the relative beta 1‐ and beta 2‐ adrenoceptor antagonism of betaxolol and atenolol.

Lipworth, BJ; Irvine, Nicola; McDevitt, DG

doi:10.1111/j.1365-2125.1991.tb05504.x

Cited by 12 publications

(5 citation statements)

References 30 publications

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“…Medication was administered between 22:15 and 22:45h. The dose of atenolol was chosen based on evidence that the 50 mg dose is highly selective for the /31- [19] with negligible antagonism at the /32" adrenoceptor [20]. The HRV parameters were compared between the two doses of celiprolol alone, and when celiprolol was co-administered with propranolol 160 mg or atenolol 50 rag.…”

Section: Methodsmentioning

confidence: 99%

Heart rate variability effects of an agonist or antagonists of the β-adrenoceptor assessed with scatterplot and sequence analysis

Silke

Riddell

1998

Clinical Autonomic Research

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There is evidence that the processes regulating heart rate variations reflect non-linear complexity and show 'chaotic' determinism. Data analyses using non-linear methods may therefore reveal patterns not apparent with conventional statistical approaches. We have consequently investigated two non-linear methods, the Poincaré plot (scatterplot) and cardiac sequence (quadrant) analysis, and compared these with standard time-domain summary statistics, during a normal volunteer investigation of an agonist and antagonists of the cardiac beta-adrenoceptor. Under double-blind and randomized conditions (Latin square design), 12 normal volunteers received placebo, celiprolol (beta 1- and beta 2-adrenoceptor partial agonist), propranolol (beta 1- and beta 2-adrenoceptor antagonist), atenolol (beta 1-adrenoceptor antagonist) and combinations of these agents. Single oral doses of medication (at weekly intervals) were administered at 22:30 hours with sleeping heart rates recorded overnight. The long (SDNN, SDANN) and short-term (rmsSD) time-domain summary statistics were reduced by celiprolol--effects different from the unchanged or small increases after atenolol and propranolol alone. The Poincaré plot was constructed by plotting each RR interval against the preceding RR interval, but unlike previous descriptions of the method, an automated computer method, with a high level of reproducibility, was employed. Scatterplot length and area were reduced following celiprolol and different from the small increases after propranolol and atenolol. The geometric analysis of the scatterplots allowed width assessment (i.e. dispersion) at fixed RR intervals. Differences between the drugs were confined to the higher percentiles (i.e. 75% and 90% of scatterplot length: low heart rate). The long-term time-domain statistics (SDNN, SDANN) correlated best with scatterplot length and area whereas the short-term heart rate variability (HRV) indices (rmsSD), pNN50) correlated strongly with scatterplot width. Cardiac sequence analysis (differences between three adjacent beats; delta RR vs delta RRn+1) assessed the short-term patterns of cardiac acceleration and deceleration, four patterns are identified: +/+ (a lengthening sequencing), +/- or -/+ (balanced sequences), and finally -/- (a shortening sequence). A running count of events by quadrant, together with the average magnitude of the differences was computed. The beta-adrenoceptor partial agonist celiprolol increased acceleration sequences. The duration of beat-to-beat difference shortened after celiprolol; this contrasted with increased duration of beat-to-beat difference after propranolol and atenolol. These results demonstrated a shift towards sympathetic dominance after the beta-adrenoceptor partial agonist celiprolol contrasting in parasympathetic dominance after the beta-adrenoceptor antagonists propranolol and atenolol. These non-linear methods appear to be valuable tools to investigate HRV in health and in cardiovascular disease and to study the implications of alterations in autonomi...

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Section: Methodsmentioning

confidence: 99%

Heart rate variability effects of an agonist or antagonists of the β-adrenoceptor assessed with scatterplot and sequence analysis

Silke

Riddell

1998

Clinical Autonomic Research

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“…The response to NA was then elicited in the presence on 10 pM atenolol. 13,-Adrenoceptor selectivity of atenolol is a concentration-related phenomenon and the concentration used in the present study significantly blocks D2-adrenoceptors (Lipworth et al 1991). A 30 min.…”

Section: Arterial Relaxation To Endothelium-dependent Agents After Kcimentioning

confidence: 62%

Variations of Arterial Responses in vitro in Different Sections of Rat Main Superior Mesenteric Artery

Tolvanen

Sallinen

et al. 1998

Pharmacology & Toxicology

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Abstract;We examined the control of vascular tone in rat main superior mesenteric artery. Three standard rings (3 mm in length) of the mesenteric artery were cut, beginning 5 mm, 13 mm and 21 mm distally from the mesenteric arteryaorta junction. In noradrenaline-precontracted rings, relaxations to acetylcholine in the absence and presence of the cyclooxygenase inhibitor diclofenac, did not differ in the studied sections. However, the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, attenuated the diclofenac-resistant responses to acetylcholine more effectively in the proximal than the distal section. Glibenclamide, an inhibitor of ATP-sensitive K + channels, diminished relaxations evoked by acetylcholine only in the distal section, whereas the inhibitor of Ca2+ activated K+ channels, apamin, attenuated the responses in all sections. Furthermore, relaxation sensitivity to nitroprusside and isoprenaline was lower in the proximal than distal section. Arterial contractile sensitivity to noradrenaline and potassium chloride was higher, while the maximal contractile force generation was lower in the proximal than the distal part. In conclusion, in different sections of rat main superior mesenteric artery considerable variability was observed in vasoconstrictor and vasodilator responses, as well as in the contribution of endothelial nitric oxide and endothelium-mediated hyperpolarization to vasodilation. Therefore, the present results emphasize the fact that only corresponding vessel segments should be used when investigating the control of arterial tone.Numerous findings concerning arterial physiology and pathophysiology originate from studies performed on the superior mesenteric artery of the rat (Foster et al. 1992;Asano et al. 1993;Parsons et al. 1994). Previous investigations have revealed variations in arterial responses between the superior mesenteric arteries of different species, these arteries and other arteries of the same species, and between the conduit and the resistance part of the same superior mesenteric arteries (Nagao et al. 1992;Hwa et al. 1994;Kong et al. 1994;Roberts-Thomson et al. 1994). However, little is known about the homo-or heterogeneity of vascular tone in the conduit part of the superior mesenteric arteries. Therefore, the present experiments were designed to elucidate possible functional differences within the conduit part of this artery by examining vascular responses to contractile agents and to endothelium-independent anddependent vasodilators in different sections of the main superior mesenteric arteries of Wistar rats. Materials and MethodsAnimals and experimental design. Forty male Wistar rats were obtained from the experimental animal laboratory of University of Tampere. The animals were housed four to a cage in a standard experimental animal laboratory (illuminated 6 a.m.-6 pm., temperature 22'3, and had free access to drinking fluid (tap water) and Author for correspondence: Jari-Petteri Tolvanen, Department of Pharmacological Sciences, University of Tampere, P...

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“…With low plasma concentrations of β 1 -blockers, the selectivity for β 1 -ARs was maintained, but as concentrations increased, selectivity was lost. 8,10 Reduced selectivity of β 1 -blockers is associated with a decrease in pulmonary function. Ellis et al 15 reported that 40 mg propranolol and 100 and 200 mg atenolol decreased the forced expiratory volume in 1 s (FEV 1 ), but 50 mg atenolol did not reduce the FEV 1 .…”

Section: Discussionmentioning

confidence: 99%

The Haemodynamic Effects of Propranolol and Atenolol Medication on Dobutamine Infusion in Patients with Coronary Artery Obstructive Disease

Lee

Kim

et al. 2005

J Int Med Res

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We compared the haemodynamic effects of beta-blockers on dobutamine infusion in 60 patients undergoing coronary artery bypass graft surgery. All patients had been taking propranolol (n = 30) or atenolol (n = 30) pre-operatively for at least 1 month. After sternotomy, dobutamine was infused at 2 microg/kg per min, and the dose increased to 4 microg/kg per min and then 8 microg/kg per min, at 15-min intervals. In both groups, dobutamine infusion did not increase the cardiac index or the heart rate, but was associated with an increase in mean arterial pressure, systemic vascular resistance index and mean pulmonary arterial pressure in a dose-dependent manner. The haemodynamic responses to dobutamine infusion were similar in the two groups. We conclude that pre-operative medication with beta-blockers reduced the inotropic and chronotropic effects of dobutamine infusion. There was no difference between the modification produced by propranolol, a non-selective beta-blocker, and that produced by atenolol, a selective beta1-blocker, however.

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The effects of time and dose on the relative beta 1‐ and beta 2‐ adrenoceptor antagonism of betaxolol and atenolol.

Cited by 12 publications

References 30 publications

Heart rate variability effects of an agonist or antagonists of the β-adrenoceptor assessed with scatterplot and sequence analysis

Heart rate variability effects of an agonist or antagonists of the β-adrenoceptor assessed with scatterplot and sequence analysis

Variations of Arterial Responses in vitro in Different Sections of Rat Main Superior Mesenteric Artery

The Haemodynamic Effects of Propranolol and Atenolol Medication on Dobutamine Infusion in Patients with Coronary Artery Obstructive Disease

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