Upregulation of renal α2-adrenergic receptors is not indicative of salt-related increases in blood pressure in spontaneously hypertensive rats

Abstract

The aim of the present study was to determine if elevations in salt intake were coupled to increases in renal α2-adrenergic receptors in SHR that differ in their blood pressure response to high salt diets. Salt-resistant spontaneously hypertensive rats (SHR-R), which do not increase their blood pressure in response to high salt intake, and salt-sensitive spontaneously hypertensive rats (SHR-S), which do exhibit significant elevations in blood pressure on high salt diets (3.15% NaCl), were used. Radioligand binding studies using [3H]rauwolscine were performed on 6- and 11-week-old SHR-S and Wistar-Kyoto (WKY) rats to determine the effects of age, strain, and salt intake on α2-adrenergic receptor number and affinity. One week of high salt intake significantly increased blood pressure 22% in 6-week-old SHR-S and increased the blood pressure of 11-week-old SHR-S 12% without altering WKY rat controls. This treatment did not significantly increase renal α2-adrenergic receptors in either SHR-S or WKY rats. SHR-S had significantly higher numbers of renal α2-adrenergic receptors than WKY rats on the high salt diets. One week of high (3.15%) or low (0.05%) salt intake did not significantly alter renal α2-adrenergic receptor number in 11-week-old SHR-S or WKY rats; however, blood pressure was significantly elevated in the SHR-S (175.0±3.5 versus 196.0±3.0 mm Hg). Two weeks of high salt intake did produce significant 37-48% increases in renal α2-adrenergic receptor numbers in both SHR-S and SHR-R; however, this treatment increased blood pressure significantly only in the SHR-S. The results of these studies show that salt-induced increases in blood pressure in the SHR-S occur previous to significant increases in renal α2-adrenergic receptors that are seen in both SHR-S and SHR-R after 2 weeks of high salt treatment. These findings suggest that salt-induced increases in blood pressure are independent of the upregulation of renal α2-adrenergic receptors.