Abstract
Renal alpha 1 and alpha 2-adrenergic receptors were quantified in Dahl salt-sensitive and salt-resistant rats, in Okamoto-Aoki spontaneously hypertensive rats (SHR), in Wistar Kyoto "normotensive" (WKY), and in Charles River rats made hypertensive by the Grollman ligature technique and by DOC-NaCl administration after unilateral nephrectomy. The effect of high dietary NaCl on renal alpha receptors was studied in Dahl, SHR, and WKY rats. Renal alpha 1 and alpha 2 receptor densities were higher (p less than 0.05) in SHR and in Dahl salt-sensitive rats than in their normotensive controls. High dietary sodium increased renal alpha 2 receptors and blood pressure in SHR, WKY and Dahl salt-sensitive, but not in resistant Dahl rats. A study of time relationships revealed that the increase in renal alpha 2 receptors preceded most of the blood pressure elevation due to high dietary sodium. Renal alpha-adrenergic receptor densities of surgical (Grollman) and endocrine (DOC-NaCl) forms of rat hypertension were not different from normotensive controls. Thus, renal alpha 2 receptor density and increase thereof by dietary sodium may be: 1) a biochemical marker for genetic forms of hypertension in the rat, and 2) closely linked to the basic mechanism of high blood pressure.
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