CATECHOLAMINE DEPLETORS – INTRODUCTION
Any of a group of sympathomimetic amines (including dopamine, epinephrine, and norepinephrine), the aromatic portion of whose molecule is catechol.
The catecholamines play an important role in the body’s physiological response to stress. Their release at sympathetic nerve endings increases the rate and force of muscular contraction of the heart, thereby increasing cardiac output; constricts peripheral blood vessels, resulting in elevated blood pressure; elevates blood glucose levels by hepatic and skeletal muscle glycogenolysis; and promotes an increase in blood lipids by increasing the catabolism of fats.
CATECHOLAMINE DEPLETORS – INDICATION :
Heart Failure, Advanced age, Systolic Hypertension
CATECHOLAMINE DEPLETORS – INFORMATION :
Most hypotheses of the therapeutic mechanism of action of antidepressant drugs have focused on the role of the monoamines. We examined the effect of catecholamine depletion on antidepressant-induced remission.
The tyrosine hydroxylase inhibitor alpha-methylparatyrosine and the antihistamine diphenhydramine hydrochloride were administered, during separate test sessions, to depressed patients in remission maintained with either norepinephrine reuptake inhibitors (desipramine [n = 7] or mazindol [n = 2]) or serotonin reuptake inhibitors (fluoxetine hydrochloride [n = 9] or sertraline hydrochloride [n = 1]). Because of considerable sedation associated with alpha-methylparatyrosine testing, diphenhydramine was used as an active control rather than an inactive placebo. The effects of alpha-methylparatyrosine and diphenhydramine on depression, anxiety, and plasma catecholamine metabolites were assessed.
Alpha-Methylparatyrosine produced similar significant decreases in plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels in the treatment groups. alpha-Methylparatyrosine produced a robust increase in depressive symptoms on the Hamilton Depression Rating Scale, including depressed mood, decreased concentration, anhedonia, loss of interest, and feelings of worthlessness, helplessness, and hopelessness, in the desipramine-mazindol but not in the fluoxetine-sertraline group. Diphenhydramine had no effects on mood in either treatment group.
The therapeutic effects of norepinephrine reuptake inhibitors, but not serotonin reuptake inhibitors, are reversed by catecholamine depletion. Considered with previous reports that serotonin depletion produces depressive relapses in patients in remission maintained with serotonin reuptake inhibitors, but not norepinephrine reuptake inhibitors, these findings suggest that antidepressants may not work via a single monoamine-related mechanism.
Catecholamine: Pronounced cat·e·chol·amine. An amine derived from the amino acid tyrosine — examples include epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine — that act as hormones or neurotransmitters. There are a number of disorders involving catecholamines, including neuroblastoma, pheochromocytoma, chemodectina, the familial paraganglioma syndrome, dopamine–hydroxalase deficiency, and tetrahydrobiopterin deficiency
A drug may be classified by the chemical type of the active ingredient or by the way it is used to treat a particular condition. Each drug can be classified into one or more drug classes.
Catecholamines include adrenaline, noradrenaline and dopamine. They are physiologically important neurotransmitters, as part of the sympathetic and central nervous systems. Catecholamines act on both the alpha and beta adrenergic receptors. Catecholamines are released in times of stress. They make your heart beat faster with greater force and narrow the blood vessels, causing a rise in blood pressure. The beta1 effects of catecholamine on the heart are due to an increase in intracellular concentration of cyclic-AMP. Cyclic-AMP activates protein kinase A, which phosphorylates sites on calcium channels, including alpha1-subunits. This increases the probability that the channels will open, increasing inward calcium ion current and therefore the force of cardiac contraction. It also increases the calcium ion capture by the sarcoplasmic reticulum, increasing the amount of calcium stored intracellularly available for release by action potential. So the net result of catecholamine action is to elevate and steepen the ventricular function curve. The increase in heart rate results in an increased slope of pacemaker potential owing to a shift in the voltage-dependence of the conductance’s underlying the pacemaker currents so that they are switched on and reach firing threshold, earlier.