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The elusive alpha(1D)-adrenoceptor: molecular and cellular characteristics and integrative roles.

alpha(1)-Adrenoceptors seem to play key roles in cardiovascular, genitourinary, and central nervous system functions. This review will be focused on alpha(1D)-adrenoceptors. These receptors have intrinsic activity, and many of the more commonly used antagonists are in reality inverse agonists. alpha(1D)-Adrenoceptors are phosphorylated in the basal state, and the natural agonists, adrenaline and noradrenaline, increase their phosphorylation; similar effects are induced by direct activation of protein kinase C and through activation of nonadrenergic receptors. Interestingly, a large proportion of alpha(1D)-adrenoceptors are located in intracellular vesicles. Such intracellular location can be changed to surface expression through the use of inverse agonists and coexpression of alpha(1B)-adrenoceptors, which seem to act as pharmacological chaperons for proper plasma membrane insertion. The alpha(1D)-adrenoceptor amino terminus seems to contain a signal that keeps the receptor intracellularly, but interaction with other proteins may also contribute. The precise relationship between the intrinsic activity, phosphorylation, and intracellular location is currently unknown. alpha(1D)-Adrenoceptor activation induces contraction in a variety of vessels, and a role in the control of blood pressure has been suggested. Studies using young prehypertensive and adult spontaneously hypertensive rats as well as knockout mice suggest that vascular alpha(1D)-adrenoceptors are involved in the genesis/maintenance of hypertension.