Background: Recent years have witnessed an astonishing proliferation in the number of known adrenoceptor subtypes and related signaling pathways, all of which can potentially be altered in hypertension. Although numerous reports have suggested altered adrenoceptors, guanine nucleotide binding regulatory proteins (G proteins) or effector mechanisms in hypertensive animals or patients, only few clear trends have emerged.

Cardiac and vascular adrenoceptor function: Cardiac ß-adrenoceptor function is desensitized in various forms of hypertension but it is not clear whether alterations in signaling contribute to this desensitization in addition to the well documented decrease in ß-adrenoceptor numbers. Vascular o-and ß-adrenoceptor responsiveness are increased and decreased, respectively, in hypertensive animals and patients but the molecular site underlying these alterations has not unequivocally been established. Renal adrenoceptor function: Renal o-and og-adrenoceptor numbers are frequently increased in genetically hypertensive rats but o-adrenoceptor-stimulated inositol phosphate formation is unchanged or decreased and o-adrenoceptor functions remain unclear. Renal ß-adrenoceptor numbers are elevated in many forms of hypertension but it is not clear whether this is accompanied by alterations in receptor function.