Chemical formula: C₈H₁₁NO₂ Molecular mass: 153.178 g/mol PubChem compound: 681
Dopamine exerts positive inotropic and chronotropic effects on the myocardium, acting as an agonist at beta-adrenergic receptors. In addition to its direct action on beta-adrenergic receptors, dopamine acts indirectly by releasing noradrenaline from sympathetic storage sites.
Depending on the vascular bed being studied and the dose administered, dopamine can cause relaxation or contraction of vascular smooth muscle.
Unlike other endogenous catecholamines or sympathomimetic amines, Dopamine caused vasodilation in renal, coronary, mesenteric and intracerebral arterial vascular beds in anaesthetised dogs. This vasodilator effect is not antagonised by beta-adrenergic blockers, atropine or antihistamines. However, butyrophenones, phenothiazines, apomorphine and bulbocapnine selectively attenuate dopamine-induced vasodilatation, thus suggesting the existence of specific dopamine vascular receptors similar to those in the basal ganglia and other areas in the central nervous system.
Dose response studies indicate that with a sufficiently large dose, the vasoconstrictor effect of dopamine predominates over its vasodilator effect. This dopamine-induced vasoconstrictor effect is antagonised by alpha-adrenoreceptor blocking agents such as phentolamine and phenoxybenzamine, indicating that vasoconstriction results from the action of dopamine on alpha-adrenergic receptors.
Intravenous infusions of dopamine (2.6 to 7.1μg/kg/min) to seven normal subjects increased estimated average renal plasma flow from 507 to 798ml/min, inulin clearance from 109 to 136ml/min and average sodium excretion from 171 to 571μEq./min. Although the diuretic and natriuretic effects of dopamine may result from vasodilatation in renal vascular bed (vide supra), disassociation between natriuresis and increments in renal blood flow has been observed, suggesting that other mechanisms such as redistribution of intrarenal blood flow may be involved.
Dopamine is inactive when taken orally and its vasoconstrictor properties preclude its administration by subcutaneous or intramuscular injection. Dopamine hydrochloride is administered by intravenous infusion
Dopamine is a metabolic precursor of noradrenaline and, whereas a proportion is excreted as the metabolic products of noradrenaline.
The plasma half-life of dopamine is approximately two minutes. Dopamine is metabolised in the liver, kidneys, and plasma by monoamine oxidase (MAO) and catechol-0-methyltransferase to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid which are rapidly excreted in the urine. In patients receiving MAO inhibitors, the duration of action of dopamine may be as long as 1 hour. About 25% of a dose of dopamine is metabolised to norepinephrine within the adrenergic nerve terminals.
Dopamine is excreted in urine principally as HVA and its sulfate and glucuronide conjugates and as 3, 4-dihydroxyphenylacetic acid. A very small fraction of a dose is excreted unchanged. Following administration of radio labelled dopamine, approximately 80% of the radioactivity reportedly is excreted in urine within 24 hours.
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