Salt enhances responsiveness of terminal aortic vascular bed to sympathetic activity

Haemodynamic and laboratory examinations were performed in 27 essential hypertensives. The participation of the sympathetic system was estimated from the percentage decrease in regional vascular resistance caused by 1 mg prazosin, during varied salt intake (50-80 mEq sodium per day for 9 weeks, followed by 220-250 mEq sodium per day for 10 days), with or without benidipine.

During low salt intake, terminal aortic and renal resistances were decreased by prazosin, but superior mesenteric resistance remained unchanged. In the saltsensitive patients, whose mean arterial pressure increased more than 5 mmHg with salt repletion, salt loading increased superior mesenteric and renal resistances but did not change terminal aortic resistance. This salt-induced vasoconstriction of renal and superior mesenteric arteries is not related to an increase in sympathetic activity, because both plasma noradrenaline concentrations and the percentage decrease in these regional vascular resistances by prazosin remained unchanged after salt loading. On the other hand, terminal aortic area demonstrated an increase in responsiveness to noradrenaline (increased response to prazosin) with salt loading in spite of unchanged terminal aortic resistance. This salt-induced increase in sympathetic responsiveness in the terminal aortic area was inhibited with the addition of benidipine, which abolished development of salt-induced hypertension and its accompanying haemodynamic responses.