Β-adrenergic Blocking Drugs Research Articles

Influence of adrenergic blocking drugs on central angiotensin effects.

The central effects of angiotensin in unanes thetized rats were studied before and after administration of adrenergic blocking drugs. Intraventricular injections of prevented angiotensin-induced drinking, sympathetic stimulation, and vasopressin release. Administration Phentolamine of various β-adrenergic blocking drugs, either intraarterially or intraventricularly, did not alter central angiotensin activity in a manner which could be correlated with β-adrenergic blockade. Local anesthetics inhibited central angiotensin pressor and drinking effects. Centrally administered phentolamine or tetracaine appear to be useful tools for further studies of the actions of angiotensin on the central nervous system.

Reduction in the rise of systolic blood pressure during human coitus by the beta-adrenergic blocking agent, propranolol.

Summary. The ingestion of 120 to 160 mg of the β-adrenergic blocking agent, propranolol, caused a significant reduction in the rise of systolic blood pressure which occurs during human coitus. The accompanying tachycardia was also reduced. If used with caution and with careful selection of patients, the β-adrenergic blocking drugs may allow patients with ischaemic heart disease or hypertension a safer and more normal marital life, since the ease of attainment and the intensity of orgasm was not impaired.

Possible dopaminergic pathway from substantia nigra to putamen

Summary Evidence is presented suggesting that dopamine is a synaptic transmitter in the putamen, released from the terminals of axons whose cell bodies lie in the substantia nigra. Electrical stimulation of the substantia nigra (SN) with single rectangular pulses resulted in a negative focal potential being recorded in the putamen. An action potential was often associated with the negative focal potential. The latency of such SN-evoked units varied between 4.5 and 10 msec, indicating that the nigro-putamen fibres conduct impulses quite slowly (0.6–1.4 m/sec) and are of small diameter, probably consisting of C-type fibres. This is in agreement with fluorescent microscopy findings of poorly myelinated dopamine-containing fibres. An increase in the neuronal discharge frequency caused by both iontophoretically applied dopamine and repetitive stimulation of the substantia nigra was observed with 43 neurones (77%). This excitant action was blocked more readily by α-adrenergic antagonists and on a few occasions potentiated by monoamine oxidase inhibitors. On other neurones (37 in number) dopamine caused a depression of neuronal discharge which was antagonized more successfully by β-adrenergic blocking drugs. Several other monoamines were tested on neurones in the putamen including l -noradrenaline, p-tyramine, l -DOPA, homovanillic acid and 5-hydroxytryptamine. The actions of l -DOPA and homovanillic acid, the precursor and breakdown product of dopamine, were weak in comparison to those of dopamine.

The effect of chronic adrenergic blockade on the inhibition by epinephrine of growth hormone and insulin release in sheep.

Infusion of epinephrine inhibited growth hormone (GH) and insulin responses of intact sheep to arginine (0.5 gm/kg). Chronic exposure to the α-adrenergic receptor blocker phentolamine prevented the epinephrine inhibition of insulin release but a similar treatment with propranolol, a β-adrenergic blocking drug was ineffective. Neither phentolamine nor propranolol could counteract the inhibitory effect of epinephrine on GH secretion. It is suggested that the mechanisms mediating the effects of catecholamines on GH release and insulin secretion are different.

Comparative Effects of Propranolol and Chlordiazepoxide in Anxiety States

Propranolol is a β-adrenergic blocking drug and so relieves symptoms due to excessive adrenaline release, and in particular slows the pulse rate, even in normal subjects (Bollinger et al., 1965). Because of this, Granville-Grossman and Turner (1966) undertook a double-blind trial of propranolol against placebo, showing that it was effective in anxiety. The General Practitioner Research Group has used chlordiazepoxide in comparative trials to new drugs in the treatment of anxiety (G.P. Clinical Trials 1968), under grants from the National Institute of Mental Health, U.S. Public Health Service (MY–4135 (CI), MH 0413–05 and PH 43–65–626). It was therefore decided to compare propranolol in like manner to chlordiazepoxide, in cases of anxiety neurosis seen in general practice.

Effects on Myocardial Contractility, Hemodynamics and Cardiac Metabolism of a New Beta-Adrenergic Blocking Drug, Sotalol

Effects of a recently Introduced β-adrenergic blocking drug—sotalol (MJ 1999), on myocardial contractility, hemodynamics and lactate/pyruvate extraction of the heart were examined in closed-chest anesthetized dogs. It was found that the drug resulted in a diminution of myocardial contractile state as indicated by a downward and leftward shift of the force-velocity curve. Decrease in heart rate and rate dependent functions of the heart was pronounced. Thus, significant drop in velocity of shortening, mean systolic ejection rate and the rate of left ventricular pressure rise was noted. On the other hand, due to prolongation of the systolic time, stroke output, stroke work and T.T.I. per beat remained essentially unchanged. Related to the decline in heart rate, however, these parameters, when calculated per minute, fell. LVEDP showed no significant increase. Arteriovenous difference in lactate/pyruvate ratio and lactate extraction ratio of the heart were not altered significantly.

Surface tension effects of beta-adrenergic blocking drugs.

Journal Article Surface tension effects of β-adrenergic blocking drugs Get access Joseph V Levy Joseph V Levy Research Laboratories, Presbyterian Hospital, Pacific Medical Center, San Francisco, California 94115, U.S.A Search for other works by this author on: Oxford Academic Google Scholar Journal of Pharmacy and Pharmacology, Volume 20, Issue 10, October 1968, Pages 813–815, https://doi.org/10.1111/j.2042-7158.1968.tb09652.x Published: 12 April 2011 Article history Received: 02 July 1968 Published: 12 April 2011

Relation between β-adrenergic blocking potency and cardiotoxicity in a series of β-adrenergic receptor blocking drugs

Relation between β-adrenergic blocking potency and cardiotoxicity in a series of β-adrenergic receptor blocking drugs

Hormonal alteration of the response of the rat uterus to catecholamines

The influence of circulating ovarian hormones on the uterine response to catecholamines in the rat has been studied. Uterine smooth muscles from untreated ovariectomized rats, or from ovariectomized rats under the influence of progesterone, are relaxed by norepinephrine. This response is blocked by β-adrenergic blocking drugs. Samples taken from estrogen-dominated rat uteri, on the other hand, are usually stimulated by norepinephrine, a response which can be prevented by α-adrenergic blocking agents. Thus, the response of the rat uterus to norepinephrine appears to depend on a balance between α and β adrenergic receptors in the myometrium, and this balance is in turn regulated by the ovarian hormones.

Hyperdynamic Beta-Adrenergic Circulatory State

THE DESIGNATION of α- and β-adrenergic receptors in vascular smooth muscle 1 has proved useful in describing adrenergic function. Alpha-receptors, when stimulated, produce peripheral vasoconstriction which can be blocked by such pharmacological agents as phenoxybenzamine or phentolamine. Stimulation of β-receptors produces increased inotropic and chronotropic myocardial activity, as well as peripheral vasodilation; these responses can be blocked by dichloroisoproterenol, pronethalol, or propranolol. Use of β-adrenergic blocking drugs in treatment of hypertension may at first seem paradoxical, since inhibition of a neural mechanism serving vasodilation is contrary to current physiological thinking. However, vascular resistance is not the sole determinant of pressure; blood flow is the other dependent variable. If, therefore, elevated blood pressure could be ascribed to an increase in flow or its determining variables, heart rate and stroke volume, normalization of these factors may provide a specific therapeutic measure in its reduction. Increased β-activity can, therefore, produce hypertension if blood

Hyperdynamic beta-adrenergic circulatory state

THE DESIGNATION of α- and β-adrenergic receptors in vascular smooth muscle¹has proved useful in describing adrenergic function. Alpha-receptors, when stimulated, produce peripheral vasoconstriction which can be blocked by such pharmacological agents as phenoxybenzamine or phentolamine. Stimulation of β-receptors produces increased inotropic and chronotropic myocardial activity, as well as peripheral vasodilation; these responses can be blocked by dichloroisoproterenol, pronethalol, or propranolol. Use of β-adrenergic blocking drugs in treatment of hypertension may at first seem paradoxical, since inhibition of a neural mechanism serving vasodilation is contrary to current physiological thinking. However, vascular resistance is not the sole determinant of pressure; blood flow is the other dependent variable. If, therefore, elevated blood pressure could be ascribed to an increase in flow or its determining variables, heart rate and stroke volume, normalization of these factors may provide a specific therapeutic measure in its reduction. Increased β-activity can, therefore, produce hypertension if blood

Pronethalol-induced reversal of adrenergic vasodepression.

SEVERAL substances have been described as causing reversal of the adrenergic vasodepression observed after blockade of α-receptors, adrenaline reacquiring its usual pressor action. However, when tested in animals treated with long-acting, potent and almost irreversible adrenergic blocking drugs like the β-haloalkylamines dibenamine and phenoxybenzamine, only some pressor agents as, for example, ephedrine, vasopressin, methoxamine, phenylephrine and barium chloride1–3 provoke with regularity negation of adrenergic blockade. In an attempt to investigate the mechanism of this anti-adrenolytic action further, we used the β-adrenergic blocking drug, pronethalol (‘Nethalide’, ‘Alderlin’, ref. 4) and made the unexpected finding that it also causes restoration of the pressor action of adrenaline, when injected after blockade of α-receptors.

The presence of a substance with positive inotropic activity in blood plasma of a variety of animals

1. 1. The possibility that blood plasma of a variety of animals contains a relatively low molecular weight fraction with positive inotropic activity similar to that found in human blood plasma was investigated. 2. 2. Five per cent cross-linked polyacrylamide gel was used to isolate the fraction with a molecular weight in the range 4,000–10,000. 3. 3. When isolated from the plasmas of lampreys, fish, toads, tortoises, lizards, monkeys, rats, rabbits, guinea-pigs, dogs and domestic fowls this fraction was found to possess positive inotropic activity (on the isolated toad ventricles) which was not blocked by the β-adrenergic blocking drug, pronethalol.