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Arzneimittelforschung. 1984;34(9):1035-7.
Effect of nisoldipine on electrophysiological parameters in patients pretreated with beta-blockers.

Klein HH, Schwarck H, Rauschning W, Kreuzer H.

The effect of the new 1,4-dihydropyridine calcium antagonist nisoldipine on electrophysiological parameters was investigated in 10 patients who were pretreated with a beta-blocker. 9 patients received atenolol (75 mg/d) and 1 patient pindolol (15 mg/d) at least for three days prior to the electro-physiological study. Before and after the intravenous injection of nisoldipine (1.5 micrograms/kg body weight) the sinus node function (spontaneous sinus node cycle length, sinus node recovery time, rate corrected sinus node recovery time), the conduction times from the high right atrium to the apex of the right ventricle, and the refractoriness of the different compartments of the heart were assessed. Arterial blood pressure was measured with the cuff method. Nisoldipine induced a slight but significant increase of the heart rate without effecting the blood pressure significantly. All other measured electrophysiological parameters remained unaltered, especially the conduction time of the av node. It is concluded that concerning electrophysiology nisoldipine can safely be combined with beta-blockers because this calcium antagonist does not exert an electrophysiological effect.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6150715&dopt=Abstract




Electrophoresis. 1994 Feb;15(2):240-3.
Capillary zone electrophoresis for the rapid screening of banned drugs in sport.

Gonzalez E, Laserna JJ.

Department of Analytical Chemistry, Faculty of Sciences, University of Malaga, Spain.

Capillary zone electrophoresis was used to analyze some drugs illegally used in sports. The spectroscopic characteristics and electrophoresis migration parameters of diuretics, narcotics-analgesics and beta-blockers were established. Analytical figures of merit including parameters on the precision of migration and limits of detection are discussed. Results for the separation of drugs of different doping families are discussed. An analysis of urine from a patient receiving daily doses of atenolol is presented.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7913016&dopt=Abstract




Arch Int Pharmacodyn Ther. 1987 May;287(1):31-47.
Pharmacological and electrophysiological analysis of the effects of nicotine on cat blood pressure.

Koley J, Saha JK, Koley BN.

Nicotine (20-60 micrograms/kg) produced an initial vasodepressor response followed by a vasopressor response in anaesthetized cats, the mechanism of which was investigated. The vasodepressor response was antagonized by atropine or by vagotomy and was potentiated by physostigmine or neostigmine. Nicotine increased the single unit activity of different peripheral sympathetic nerves and evoked contraction of nictitating membrane and spleen along with vasopressor response. The vasopressor response was antagonized by phentolamine, prazosin, guanethidine, bretylium, 6-OHDA, hemicholinium-3 or hexamethonium. Propranolol or atenolol pretreatment potentiated the vasodepressor response and was antagonized by atropine. Desensitization by salbutamol did not modify the response to nicotine. The biphasic response to nicotine remained unaltered in yohimbine pretreated, in adrenalectomized, and in acute spinal as well as in decapitated animals; intracarotid or intracerebroventricular administration of nicotine did not produce any response. The biphasic response to nicotine does not involve the stimulation of the central vasomotor centre. In conclusion, these results suggest that the vasodepressor response is due to the vagal cholinergic mechanism. The vasopressor response is a consequence of activation of different peripheral adrenergic nerves causing increased release of the adrenergic transmitter at the neuroeffector region and the alpha 1-adrenoceptor mediate vasoconstriction in the systemic vascular bed.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2888442&dopt=Abstract













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