α-Adrenoreceptors in Hypertension

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Abstract
The most important central autonomic pathways in the control of arterial blood pressure are the baroreceptor reflex pathway and descending pathways from the hypothalamus. Central neurotransmitters in these pathways are L-glutamate, substance P, norepinephrine (NE). γ-aminobutyric acid, epinephrine, neuropeptide Y, and acetylcholine. At peripheral autonomic neurovascular junctions, there are prejunctional α2- and dopamine-2 receptors, which inhibit NE release, and β- and serotonin receptors, which stimulate NE release. Postjunctional α1-receptors open sodium channels, open calcium channels via phosphoinositol release, and release intracytoplasmic calcium. Postjunctional α2-receptors, which are extrasynaptic, inhibit adenylate cyclase and also open calcium channels. In animal models of hypertension, changes in α-receptor density have been reported. In spontaneously hypertensive rats, increased renal β- and α2-receptors, respectively, may enhance renin release and cause sodium and water retention. In experimental (renovascular) hypertension, vascular postsynaptic (vasoconstrictor) α1- and α2-receptors are increased. In both models of hypertension, β-receptors are down-regulated. Selective α1-antagonists, such as indoramin and prazosin, decrease arterial blood pressure by postsynaptic α1-blockade; α2-receptor inhibition of NE release is unaffected so that there is no β-receptor-mediated tachycardia.

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