Figure 721

Peripheral (^-adrenergic antagonists. (^-Adrenergic antagonists induce dilation of both resistance (arterial) and capacitance (venous) vessels by selectively inhibiting postjunctional (^-adrenergic receptors [6,9]. The net physiologic effect is a decrease in peripheral resistance; reflex tachycardia and the attendant increase in cardiac output do not predictably occur. This is due to their low affinity for prejunctional ( 2-adrenergic receptors, which modulate the local control of nor-epinephrine release from sympathetic nerve terminals by a negative feedback mechanism (see Fig. 7-22) [11]. NE—norepinephrine.

Adrenergic synapse. Nerve activity releases the endogenous neurotransmitter noradrenaline (NA) and also adrenaline from the varicosities. Noradrenaline and adrenaline reach the postsynaptic a-adrenoceptors (or ^-adrenoceptors) on the cell membrane of the target organ by diffusion. On receptor stimulation, a physiologic or pharmacologic effect is initiated. Presynaptic a2-adrenocep-tors on the membrane (enlarged area), when activated by endogenous noradrenaline as well as by exogenous agonists, inhibit the amount of transmitter noradrenaline released per nerve impulse. Conversely, the stimulation of presynaptic ^-receptors enhances nora-drenaline release from the varicosities. Once noradrenaline has been released, it travels through the synaptic cleft and reaches both a- and ^-adrenoceptors at postsynaptic sites, causing physiologic effects such as vasoconstriction or tachycardia. (Adapted from Van Zwieten [11].)


Generic (trade) name

First dose, mg

Usual daily dose, mg

Maximum daily dose, mg

Duration of action

Prazosin (G) (Minipress) Terazosin (Hytrin) Doxazosin (Cardura)

1 1

2-6 bid/tid 2-5 QD/bid 2-4 QD

0 0

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