Adrenergic mechanisms do not contribute to salt-induced vasoconstriction in stroke-prone spontaneously hypertensive rat.

The study was done to determine if neurogenic mechanisms participate in salf-induced vasoconstriction in stroke-prone spontaneously hypertensive rats (SHR-SP) in the established stage of hypertension. Either high (8% NaCl) or normal (0.3% NaCI) salt diet was given for 5 weeks to 8-week-old SHR-SP. High salt intake increased mean arterial pressure (MAP) and hindquarter vascular resistance (VR) in SHRSP in the established stage of hypertension (p < 0.01). However, hindquarter sympathetic vascular tone assessed by the difference in hindquarter VR before and after sympathetic denenation was not increased in SHR-SP on high salt diet more than that in rats on normal salt diet. The reduction of MAP by alphaadrenergic blockade produced by a supramaximal dose of intravenous phentolamine in conscious rats was not greater in rats on high salt diet than that in rats on normal salt diet. These results suggest that adrenergic tone was not increased in rats on high salt diet. In addition, the increase in arterial pressure during high salt diet was not altered by destroying noradrenergic neurons by chronic treatment with 6-OHDA, 75 to 100 mg/kg intraperitoneally given every week. Hindquarter vascular responses to direct sympathetic nerve stimulation and tyramine were markedly reduced, and responses to norepinephrine were augmented in rats treated with 6- OHDA, which suggested that sympathetic denenation of the blood vessels had been achieved. These results suggest that high salt diet produces vasoconstriction in SHR-SP in the established stage of hypertension but adrenergic mechanisms do not contribute importantly to salt-Induced vasoconstriction. (Hypertension 4: 288–293, 1982)