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At least 1,639 records · Page 91Linked to original sources
PubMed1983

Effects of trifluoperazine on beta-adrenergic responses of rat papillary muscle: related to calmodulin?

The beta-adrenergic stimulation of cardiac contraction and relaxation is related to an augmented Ca++ oscillation mediated by cAMP. This Ca++ mobilization may secondarily involve calmodulin in a way modulating the mechanical responses. We tested this possibility by studying interferences of trifluoperazine (which is able to block Ca++-calmodulin) with beta-adrenergic responses in rat heart papillary muscles. Trifluoperazine up to 10(-5) mol/l did not change the basal function. 10(-5) mol/l trifluoperazine augmented the contractile response to isoprenaline above 10(-7) mol/l. The inotropic effects of isoprenaline below 10(-7) mol/l and of the partial beta-agonist prenalterol were not influenced by trifluoperazine. 10(-5) mol/l trifluoperazine attenuated the stimulation of initial relaxation by isoprenaline in the entire concentration range. Thus this beta-adrenergic response was more sensitive to trifluoperazine than the contractile response. But trifluoperazine only slightly and non-significantly attenuated the stimulation of initial relaxation by prenalterol. From experiments on broken cell preparations the present results can be explained in terms of calmodulin blockade and thus inhibition of Ca++ efflux across the sarcolemma and of Ca++ uptake by the sarcoplasmic reticulum. Trifluoperazine effects unrelated to calmodulin can hardly account for the results. Thus a full beta-agonist can apparently mobilize enough Ca++ to activate calmodulin systems important for the final effects on the contraction-relaxation cycle.

Adrenergic beta-Agonists↗
PubMed1984

A method for simultaneous epicardial monophasic action potential recordings from the dog heart in situ.

In order to record epicardial monophasic action potentials (MAP) simultaneously from different regions of intact beating hearts, we developed a tripodal suction electrode device (total weight 1.5 g, distance between the flexible silicone legs 25 mm) which we tested in pentobarbital anaesthetized open chest dogs. The device was easy to apply and gave stable and reproducible recordings. Repolarization times for epicardial left ventricular and endocardial right ventricular MAPs correlated well (r = 0.97, P less than 0.001). There was no correlation between MAP amplitude and repolarization times. The beta 1-adrenergic agonist prenalterol decreased MAP duration, while the new class III antiarrhythmic drug melperone increased MAP duration. Mild ischaemia effected MAP prolongation and severe ischaemia MAP shortening, compared to simultaneous recordings from non-ischaemic ventricular regions. We conclude that the new tripodal suction electrode is a simple device for simultaneous recording of multiple MAPs. The method should be suitable for studies of electrophysiological effects of drugs and other interventions in intact beating hearts.

Action Potentials↗
PubMed1986

The immediate haemodynamic and electrophysiological response to prenalterol during fixed rate pacing in patients with chronic ischaemic heart disease.

The immediate haemodynamic and electrophysiologic effects of intravenous prenalterol 2.5-75 micrograms/kg in patients with coronary heart disease without clinical heart failure were investigated during fixed rate atrial pacing. Right ventricular peak dP/dt increased pronounced and serum concentration dependent after prenalterol concomitant with an increase in stroke volume and a moderate decrease in peripheral vascular resistance. The effects on haemodynamics after prenalterol were thus serum concentration dependent but with marked interindividual variation. AV nodal conduction velocity increased significantly. It is concluded that prenalterol possess pronounced inotropic properties. The haemodynamic response to prenalterol intravenously is to a lesser degree dependent on the chronotropic effects of the drug and it is often unpredictable.

Aged↗
PubMed1976

Beta2-adrenoceptors facilitating noradrenaline secretion from human vasoconstrictor nerves.

Isolated biopsy specimens of human peripheral arteries and veins, preincubated with 3H-(-)- noradrenaline (NA) to label the neural stores of NA, were used to study the Beta-adrenoceptors previously found to increase the secretion of 3H-NA evoked by electrical field stimulation of the adrenergic nerves of this tissue. The increase in nerve stimulation induced secretion of 3H-NA caused by 0.04 muM isoprenaline was prevented by 1 muM propranolol. This beta-blocking drug by itself slightly but significantly depressed the secretion of 3H-NA caused by nerve stimulation in the absence of isoprenaline. While the secretion of 3H-NA was not affected by known beta1-agonists, it was dose-dependently and reversibly increased by two different beta2-agonists. The effect of isoprenaline on 3H-NA secretion was not altered by a selective beta1-antagonist, but strongly reduced or abolished by a beta2-blocking drug. The results indicate that the beta-adrenoceptors involved in the control of NA secretion from the vasoconstrictor nerves of human omental blood vessels are only to a minimal extent stimulated by NA secreted from the nerves, and therefore do probably not mainly serve to mediate local positive feedback control of transmitter secretion; the receptors appear to be beta2 in nature.

Adrenergic beta-Antagonists↗
PubMed1984

Beta 1- and beta 2-adrenoceptor-mediated secretion of amylase from incubated rat parotid gland.

The present in vitro investigation was undertaken in an attempt to obtain further information on beta-adrenoceptor specificity and action in the rat parotid gland, with regard to amylase secretion. The beta 1-selective agonist prenalterol was roughly 800 times more potent than the beta 2-agonist terbutaline, and about 5 times more effective than noradrenaline in evoking amylase release . Propranolol was the most effective inhibitor of amylase release in all experiments. The beta 1-selective antagonist metoprolol and H104 /08 were also effective blockers of maximal noradrenaline- and prenalterol-induced release. The inhibition curves displayed biphasic shapes when amylase secretion was induced by noradrenaline, but not when prenalterol was the secretagogue. The beta 2-antagonist H35 /25 was without effect on maximal noradrenaline- and prenalterol-stimulated secretion. The amylase release evoked by submaximal concentration of terbutaline was inhibited by the two antagonists H35/25 and IPS 339. In another series of experiments propranolol and metoprolol clearly shifted the noradrenaline concentration-response curve to the right, whereas H35/25 was without effect. The results further demonstrate the major importance of the beta 1-adrenoceptor (noradrenaline-activated) in eliciting amylase release from the rat parotid gland. However, it is also suggested that the beta 2-adrenoceptors (terbutaline-activated) may to some extent serve the same function.

Adrenergic beta-Agonists↗
PubMed1984

Clinical consequences of the lipophilicity and plasma protein binding of antiarrhythmic drugs and active metabolites in man.

In two series of antiarrhythmic drugs tested, as the octanol/water partition coefficient increases so do the following: elimination from the body by biotransformation, first-pass biotransformation in the liver and gastrointestinal tract after oral administration, protein binding to some extent, and penetration into brain tissue. Patients receiving lipophilic beta-adrenoreceptor blocking drugs may experience more central nervous system side effects than those receiving hydrophilic beta blockers. Structural modification of a drug, guided by the concept of bioisosterism, may allow the disassociation of therapeutic from toxic activities. Alpha-1 acid glycoprotein is the major plasma protein that binds the basic antiarrhythmic drugs. Antiarrhythmic drug metabolites are generally more polar (less lipophilic) and less plasma protein-bound than the parent drugs.

Adrenergic beta-Antagonists↗
PubMed1979

Amylase secretion in the rabbit parotid gland when stimulating the sympathetic nerves during parasympathetic activity.

1. In anaesthetized rabbits amylase secretion from the parotid gland was investigated. Secretion was evoked by sympathetic nerve stimulation, either alone or superimposed on a parasympathetic background secretion, imitating the resting secretion present in the waking animal.2. Sympathetic nerve stimulation at frequencies below 1 Hz was alone subthreshold for fluid secretion, but could greatly increase the amounts of amylase present in fluid secretion produced by parasympathetic nerve stimulation. The amylase output due to sympathetic nerve stimulation alone at 10 Hz did not exceed that seen in response to a stimulation at 1 Hz superimposed on parasympathetic activity.3. The amylase output in response to superimposed sympathetic stimulation was not influenced by the rate of fluid secretion, which was altered by stimulating the parasympathetic nerves at different frequencies.4. Sympathetically-evoked amylase secretion was abolished after beta(1)-block. The amylase secretion remaining on parasympathetic activation was sparse.5. It is concluded that secretion of amylase in response to sympathetic nerve stimulation requires the presence of a parasympathetic fluid secretion to be washed along the glandular ducts. Parasympathetic activity may also augment the sympathetic effect on amylase secretion.

Amylases↗
PubMed1975

Long-term beta blockade: possible protection from myocardial infarction.

The clinical behaviour of 90 patients on beta-blocking drugs for established coronary heart disease who were admitted to a coronary care unit with prolonged ischaemic myocardial pain was compared with that of 90 similar patients not on this therapy. Transmural myocardial infarction was confirmed in 30 of the patients on beta-blockers and in 62 controls. A diagnosis of myocardial necrosis without infarction was made in 20 patients on beta-blockers and in 14 controls. Coronary insufficiency was diagnosed in 40 patients on beta-blockers and in 14 controls. The incidence of simus bradycardia, hypotension, syncope, and radiological pulmonary oedema was similar in the two groups. Established beta-blockade, therefore, has not been shown to prejudice the outcome of patients with coronary heart disease admitted to hospital with prolonged ischaemic myocardial pain. On the contrary, it may protect some patients from the development of a myocardial infarction.

Adrenergic beta-Antagonists↗