The aim of the present study was to determine if elevations in salt intake were coupled to increases in renal a^-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 [3 H]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 o^-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 a^-adrenergjc receptors in either SHR-S or WKY rats. SHR-S had significantly higher numbers of renal o^-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 oj-adrenergic receptor number in 11-week-old SHR-S or WKY rats; however, blood pressure was significantly elevated in the SHR-S (175.0±3S versus 196.0±3.0 mm Hg). Two weeks of high salt intake did produce significant 37-48% increases in renal o^-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 «j-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 o^-adrenergic receptors. (Hypertension 1990;16:49-54)
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