The contribution of the sympathetic nervous system and vasopressin to the maintenance of arterial pressure was investigated in high sodium-fed rats 4 weeks after the induction of one-kidney, figure-8 renal wrap hypertension. Arterial pressure was significantly greater In renal-wrapped rats than in shamoperated animals. The contribution of the sympathetic nervous system was assessed functionally by measuring the arterial pressure response to ganglionic blockade and estimating the apparent rate of release of norepinephrine. The contribution of vasopressin was assessed by administration of the vascular antagonist (CH 2 ) 5 Tyr(Me)-AVP. Whole-animal vascular responsiveness and cardiac baroreceptor reflex sensitivity were determined by graded intravenous bolus injections of angiotensin II, vasopressin, and phenylephrine. Hypertensive rats demonstrated an exaggerated reduction in arterial pressure to autonomic blockade before and after blockade of vascular vasopressin receptors. There was a significant 27% increase in the apparent rate of release of norepinephrine into the plasma. Administration of (CH2)jTyr(Me)-AVP did not affect arterial pressure when given alone. However, after ganglionic blockade, inhibition of the vasopressin system elicited similar falls in blood pressure in both normotensive and hypertensive rats. Arterial pressure dose-response effects of phenylephrine, angiotensin II, and vasopressin were similar between renal-wrapped and sham-operated animals; however, cardiac baroreceptur reflex sensitivity was suppressed in the hypertensive rats. These studies indicate that the maintenance of arterial pressure in chronic, high sodium renal-wrap hypertension is associated with an augmented sympathetic nervous system function. hypertension have been used to investigate the relation between sodium and elevated arterial pressure. The work has revealed significant contributions of the sympathetic nervous system and vasopressin to the maintenance of chronic hypertension. Several indexes of augmented sympathetic nervous system function have been documented in sodium-dependent hypertension. In deoxycorticosterone (DOC)-saline hypertension in rats, an exaggerated depressor response to ganglionic blockade, 1 elevations in plasma catecholamines, 2 increases in norepinephrine turnover, 34 and an augmented apparent rate of release of norepinephrine 5 have been observed. In addition, peripheral chemical sympathectomy with 6-hydroxydopamine 6 is effective in preventing this model of hypertension. In Dahl saltsensitive rats, an augmented ganglionic blockade response, 7 an elevation in splanchnic nerve activity,