Dopamine is important mainly as a neurotransmitter and as a precursor to norepinephrine. Circulating dopamine is not normally a significant catecholamine; the presence of dopamine in the urine is largely attributable to high renal concentrations of dopa decarboxylase. At significant circulating levels, dopamine stimulates vascular Di receptors, causing vasodilatation and, particularly, increasing renal blood flow. Very high serum levels of dopamine are required to activate vascular alpha receptors sufficiently to cause vasoconstriction.
Norepinephrine is found in the adrenal medulla and the paraganglia, where it is stored in granulated vesicles. Norepinephrine is also found in brain and spinal cord nerve cells. However, most norepineph-rine is found in the synaptic vesicles of postgan-glionic autonomic nerves in organs that have rich sympathetic innervation: the salivary glands, heart, vascular smooth muscle, liver, spleen, kidneys, and muscles. A sympathetic nerve may have up to 25,000 bulges along the length of its fibers; each synthesizes norepinephrine and stores it in adrenergic storage vesicles, adjacent to target cells.1
Norepinephrine's stimulation of ai-adrenergic receptors increases the flux of calcium into the target cell. Alphai-adrenergic receptors are found in the vascular smooth muscle, heart, and pupillary dilator muscles; activation results in hypertension, some increased force of cardiac contraction, and pupillary dilation. It also stimulates sweating from nonther-moregulatory apocrine "stress" sweat glands (located variably on the palms, axillae, and forehead). Norepinephrine's activation of P-adrenergic receptors causes an increased flux of calcium into the target cell. Norepinephrine has great affinity for Pi-adrenergic receptors (increases cardiac contraction and rate); stimulation of heart rate is counteracted by simultaneous vagal stimulation. Norepi-nephrine has less affinity for P2-adrenergic receptors (vasodilation, hepatic glycogenolysis). With higher norepinephrine levels, hypermetabolism and hyper-glycemia are noted. Norepinephrine also activates
P3-adrenergic receptors (fat cells), causing lipolysis and increased serum levels of free fatty acids.
Epinephrine also stimulates ai-adrenergic receptors, causing "stress" sweating, pupil dilatation, some increased force of cardiac contraction, and vasoconstriction in skin and kidneys. Epinephrine also activates Pi-receptors, increasing cardiac rate and force of contraction. However, simultaneous activation of P2-receptors causes vasodilation in skeletal muscles. Thus, epinephrine has a variable effect on blood pressure, ranging from hypertension to hypotension (rare). Increased hepatic glycogeno-lysis causes hyperglycemia, which is usually mild. Lipolysis results in increased serum levels of free fatty acids. It also increases the basal metabolic rate. Epinephrine crosses the blood-brain barrier poorly, but hypothalamic stimulation occurs with high serum levels.5 This causes unpleasant sensations, ranging from nervousness to an overwhelming feeling of impending doom. These manifestations are distinct from those of noncatecholamine amphetamines, which enter the central nervous system more readily and have other effects.6
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