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Catecholamine blockade

Class II catecholamine blockade. Propranolol and other p-adrenoceptor antagonists reduce background sympathetic tone in the heart, reduce automatic discharge (phase 4) and protect against adrenergically stimulated ectopic pacemakers. [Pg.499]

Cocaine and desipramine inhibit the reuptake of monoamine neurotransmitters whereas amphetamine, which is a phenylalkylamine - similar in structure to the catecholamines, see Fig. 4 - competes for uptake and more importantly, evokes efflux of the monoamine neurotransmitters. All of them exert antidepressant effects. Cocaine and amphetamine are addictive whereas tricyclic antidepressants and their modern successors are not. The corollaty of the addictive properties is interference with DAT activity. Blockade of DAT by cocaine or efflux elicited by amphetamine produces a psychostimulant effect despite the different mechanisms even the experienced individual can hardly discern their actions. Because of the risk associated with inhibiting DAT mediated dopamine clearance the antidepressant effects of psychostimulants has not been exploited. [Pg.841]

Other potential adverse effects from P-blockers include fatigue, sleep disturbances, malaise, depression, and sexual dysfunction. Abrupt P-blocker withdrawal may increase the frequency and severity of angina, possibly because of increased receptor sensitivity to catecholamines after longterm P-blockade. If the decision is made to stop P-blocker therapy, the dose should be tapered over several days to weeks to avoid exacerbating angina. [Pg.77]

Drugs used in the treatment of hypertension vary greatly in their mode of interference with sympathetic nerve function. In the case of methyldopa the mechanism is complex and still largely unknown. Others, such as guanoxan, guanochlororbethanidine, involve varying degrees of, for example catecholamine depletion, blockade of subsequent release of noradrenaline and, occasionally, a weak receptor-blockade. Bethanidine is perhaps the best-known of this series and... [Pg.27]

The bicyclic amidoximes (LXIV) and (LXV) cause a reduction in blood pressure in various animal species, but apparently they are not adrenergic neurone blocking agents [270]. The activity of (LXIV)i thought to be mainly due to catecholamine release and subsequent depletion, whilst the action of (LXV) involves blockade at a-receptors [270]. [Pg.167]

Changes in adrenergic function are complex. Inhibition of neuronal catecholamine reuptake gives rise to superimposed indirect sympathomimetic stimulation. Patients are supersensitive to catecholamines (e.g., epinephrine in local anesthetic injections must be avoided). On the other hand, blockade of ai-receptors may lead to orthostatic hypotension. [Pg.232]

Deficiency of adrenal medullary catecholamines appears to give no ill effects, and replacement therapy is therefore not used, but adrenal medullary tumours, phaeochromocytomas, secrete excess catecholamines often causing hypertension with dramatic episodes of headache, palpitations, pallor, sweating and anxiety. This condition is normally treated surgically, but preoperative preparation is mandatory to avoid catastrophic effects of surges of catecholamine release. A combination of alpha- and beta-adrenergic receptor blockade is normally used, with drugs such as phenoxybenzamine or doxazosin as alpha-blockers, and propranolol as a non-selective beta-blocker. [Pg.768]

Isoflurane (Forane) is a structural isomer of enflurane and produces similar pharmacological properties some analgesia, some neuromuscular blockade, and depressed respiration. In contrast, however, isoflurane is considered a particularly safe anesthetic in patients with ischemic heart disease, since cardiac output is maintained, the coronary arteries are dilated, and the myocardium does not appear to be sensitized to the effects of catecholamines. Also, blood pressure falls as a result of vasodilation, which preserves tissue blood flow. Isoflurane causes transient and mUd tachycardia by direct sympathetic stimulation this is particularly important in the management of patients with myocardial ischemia. [Pg.304]

The sympathomimetic drugs are discussed in Chapter 10. In brief, the most commonly abused of these drugs, such as cocaine, work primarily as indirect agonists of the catecholamine neurotransmitter systems via inhibitory actions upon the transmitter reuptake system. Considerable evidence supports a role for dopamine in mediating the rewarding effects of cocaine. There is also evidence that blockade of serotonin uptake may contribute to cocaine s actions. [Pg.411]

Catecholamines also appear to modulate this cortex (reviewed in Coull et ak, 2001). Studies in both monkeys and humans have found that clonidine, but not guanfacine, can impair alerting abilities in the Posner task, likely because of reducing NE release. Dopamine receptor blockade also impairs performance. [Pg.103]

Schmidt. M.E., Matochik, J.A., Goldstein, D.S., et al. Gender differences in brain metabolic and plasma catecholamine responses to alpha2-adrenoceptor blockade. [Pg.363]

Migraine Effective in reducing migraine episodes due to blockade of catecholamine induced vasodilatation in the brain vasculature. Propranolol decreases the incidence and severity of the attack. [Pg.150]

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. [Pg.184]

The pharmacologic actions of phenoxybenzamine are primarily related to antagonism of -receptor-mediated events. The most significant effect is attenuation of catecholamine-induced vasoconstriction. While phenoxybenzamine causes relatively little fall in blood pressure in normal supine individuals, it reduces blood pressure when sympathetic tone is high, eg, as a result of upright posture or because of reduced blood volume. Cardiac output may be increased because of reflex effects and because of some blockade of presynaptic k2 receptors in cardiac sympathetic nerves. [Pg.201]

Release of stored catecholamines from pheochromocytomas may occur in response to physical pressure, chemical stimulation, or spontaneously. When it occurs during operative manipulation of pheochromocytoma, the resulting hypertension may be controlled with cx-receptor blockade or nitroprusside. Nitroprusside is preferred because its effects can be more readily titrated... [Pg.202]


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See also in sourсe #XX -- [ Pg.186 ]




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