Adrenoceptors in SHR: alterations in binding characteristics and intracellular signal transduction pathways.

There is much data on altered adrenoceptor function in the heart, blood vessel and kidney from spontaneously hypertensive rats (SHR). The enhancement of vascular and renal alpha-adrenoceptor function, i.e. vasoconstriction and retention of water and sodium, may contribute to the development and maintenance of the hypertension, whereas cardiac alpha1-adrenoceptor may be of minor physiological significance. Alpha1-adrenoceptor-mediated signal transduction as a whole is increased in SHR vascular tissues, but the intracellular signaling per receptor in the kidney seems to be decreased despite increased alpha1-adrenoceptor density. On the other hand, cardiac and vascular beta-adrenoceptor responsiveness is attenuated in SHR. Reduced vasorelaxation mediated by beta-adrenoceptors may also contribute to high blood pressure. The impaired cardiovascular beta-adrenoceptor function in SHR does not appear to be necessarily explained by alterations observed at receptor levels. Alterations in signal transduction should be also considered. Limited data on renal beta-adrenoceptor density and its signaling suggest decreased or unaltered cyclic AMP formation per receptor in SHR. We will review alterations in both binding characteristics and each component of intracellular signal transduction pathways in cardiovascular and renal adrenoceptors of SHR.