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adrenomimetic, is selective for ßr and ß2-adrenocep-tors. Norepinephrine and epinephrine are thus potent vasoconstrictors of vascular beds that contain predominantly a-adrenoceptors, while isoproterenol has little effect in these vessels.

Isoproterenol and epinephrine are potent ß2-adrenoceptor agonists; norepinephrine is a relatively weak ß2-adrenoceptor agonist. Isoproterenol and epinephrine produce vasodilation in skeletal muscle, but norepinephrine does not; rather it produces vasoconstriction through the ^-adrenoceptors. Isoproterenol, epinephrine, and norepinephrine are potent ^-adrenoceptor agonists; thus, all three can stimulate the heart (Table 9.1).

The existence of a ^-adrenoceptor has recently been demonstrated in human adipose tissue along with the ^-adrenoceptor. This observation raises the possibility that eventually therapeutic drugs may selectively alter lipid metabolism and therefore provide therapeutic management of obesity. The (33-receptor and the recently identified subtypes within the a1- and a2-receptor groups (a1A, a1B, etc.) also have not been included in the table, since as yet few therapeutic drugs distinguish among these further subtypes. One exception is tam-sulosin, an antagonist with some selectivity for a1A-receptors in the urinary tract.

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