Dopamine is a naturally occurring catecholamine; it is the immediate biochemical precursor of the norepi-nephrine found in adrenergic neurons and the adrenal medulla. It is also a neurotransmitter in the CNS, where it is released from dopaminergic neurons to act on specific dopamine receptors (see Chapter 31).
Dopamine is a unique adrenomimetic drug in that it exerts its cardiovascular actions by (1) releasing norepi-nephrine from adrenergic neurons, (2) interacting with a-and ( 1-adrenoceptors, and (3) interacting with specific dopamine receptors.
The cardiovascular response to dopamine in humans depends on the concentration infused. Low rates of dopamine infusion can produce vasodilation in the renal, mesenteric, coronary, and intercerebral vascular beds with little effect on other blood vessels or on the heart. The vasodilation produced by dopamine is not antagonized by the (3-adrenoceptor blocking agent propranolol but is antagonized by haloperidol and other dopamine receptor-blocking agents.
Dopamine can exert pronounced cardiovascular and renal effects through the activation of both Dr and D2-receptor subtypes. Stimulation of the Drreceptor, which is present on blood vessels and certain other peripheral sites, will result in vasodilation, natriuresis, and diuresis. D2-receptors are found on ganglia, on sympathetic nerve terminals, on the adrenal cortex, and within the cardiovascular centers of the CNS; their activation produces hypotension, bradycardia, and regional va-sodilation (e.g., renal vasodilation). The kidney appears to be a particularly rich source for endogenous dopamine in the periphery.
The infusion of moderately higher concentrations of dopamine increases the rate and contractile force of the heart and augments the cardiac output. This action is mediated by ^-adrenoceptors and norepinephrine release and is antagonized by propranolol. In contrast to isoproterenol, which has a marked effect on both the rate and the contractile force of the heart, dopamine has a greater effect on the force than on cardiac rate. The advantage of this greater inotropic than chronotropic effect of dopamine is that it produces a smaller increase in oxygen demand by the heart than does isoproterenol. Systolic blood pressure is increased by dopamine, whereas diastolic pressure is usually not changed significantly. Total peripheral resistance is decreased because of the vasodilator effect of dopamine (Fig. 10.4).
At still higher concentrations, dopamine causes a-adrenoceptor-mediated vasoconstriction in most vascular beds and stimulates the heart. Total peripheral resistance may be increased. If the concentration of dopamine reaching the tissue is high enough, vasoconstriction of the renal and mesenteric beds also occurs. The vasoconstrictive action of dopamine is antagonized by a-adrenoceptor blocking agents such as phentol-amine.
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