ONTOGENY OF SYMPATHETIC RESPONSIVENESS IN SPONTANEOUSLY HYPERTENSIVE RATS .1. RENAL ALPHA-1-ADRENERGIC, ALPHA-2-ADRENERGIC, AND BETA-ADRENERGIC RECEPTORS AND THEIR SIGNALING

We studied the ontogenetic development of renal alpha1-, alpha2-, and beta-adrenergic receptors and their coupling to inositol phosphate and cyclic AMP formation in spontaneously hypertensive and normotensive Wistar-Kyoto rats. Alpha1-, alpha2-, and beta-Adrenergic receptor number was significantly increased in hypertensive compared with normotensive rats, but the increase did not precede blood pressure elevation. Despite increased alpha1-adrenergic receptors, basal and norepinephrine-stimulated inositol phosphate formation remained unchanged in all age groups. Rat kidney contains alpha1A- and alpha1B-adrenergic receptors coupling to inositol phosphate formation by different mechanisms, but the relative contribution of alpha1A- and alpha1B-adrenergic receptors to norepinephrine-stimulated inositol phosphate formation was similar in normotensive and hypertensive rats. Despite increased beta-adrenergic receptors, basal, isoproterenol-, and forskolin-stimulated cyclic AMP accumulation was similar in normotensive and hypertensive rats. We conclude that the number but not the functional responsiveness of renal adrenergic receptors increases in spontaneously hypertensive rats. Thus, the additional receptors are unlikely to contribute to the pathophysiology of elevated blood pressure in this model.