On the Role of Renal ar-Adrenergic Receptors in Spontaneously Hypertensive Rats

We tested the hypothesis that a genetically determined increase in renal or-adrenergic receptor density might be a pathophysiologically important factor in the spontaneously hypertensive rat model of genetic hypertension. In a first study, we compared renal a,and <*t-adrenergic receptor density with systolic blood pressure in 45 rats of an F2 generation of Wistar-Kyotox spontaneously hypertensive rat hybrids but were unable to detect significant cosegregation between either receptor density or blood pressure. In a second study, we determined renal a,and «j-adrenergic receptor density in Wistar-Kyoto and spontaneously hypertensive rat kidneys that were transplanted into an F, generation of WistarKyoto x spontaneously hypertensive rat hybrids. Although Wistar-Kyoto kidneys lowered blood pressure in these animals and spontaneously hypertensive rat kidneys increased blood pressure, renal a-adrenergic receptor densities were similar in membranes from both types of kidneys. Since rat kidney coexpresses OIAand «,B-adrenergic receptors, we also investigated whether differential regulation of these two subtypes might conceal ongoing alterations. The a^/ttm-adrenergic receptor ratio, however, was similar in Wistar-Kyoto rats, spontaneously hypertensive rats, and F, rats transplanted with a kidney from either strain. Taken together these data do not support the hypothesis that genetically determined alterations of renal o-adrenergic receptor numbers play an important role in the development of elevated blood pressure in the spontaneously hypertensive rat (Hypertension 1992;19-J65-370)