How to Induce Arrhythmias with Dopamine

Abstract

Dopamine is one of the most important neurotransmitters in the brain. It is a catecholamine derived from tyrosine and is the precursor of both noradrenaline and adrenaline. Dopamine is a monoamine with positive inotropic activity. It binds to both α-1 and beta-1 adrenergic receptors. It increases the cardiac output by increasing the heart rate and contractility mediated through myocardial β -1 adrenergic receptors. Stimulation of α-1 adrenergic receptors on vascular smooth muscle leads to vasoconstriction and results in increased systemic vascular resistance. Dopaminergic receptors from the renal vasculature are also stimulated by dopamine which leads to dilation of renal blood vessels and increases glomerular filtration rate, renal blood flow, sodium excretion, and urine outputGenerally, dopamine receptors are activated by low doses of dopamine (0.5–2.0 μg/kg/min), which causes a decrease in peripheral vascular resistance and left ventricular afterload. With the increase in dose (2–4 μg/kg/min), there was noted activation of β 1-adrenoceptors which, in turn, leads to increase in the cardiac output. A further increase in the dose (5 μg/kg/min) stimulates α-adrenoceptors resulting in vasoconstriction and amplified peripheral vascular resistance.