Changes in renal vascular sensitivity and arterial pressure associated with sodium intake during long-term intrarenal norepinephrine infusion in dogs.

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Abstract
Experiments were performed on conscious uninephrectomized dogs to determine the comparative effects of chronic intrarenal and intravenous norephrine (NE) infusion (0.27 microgram/kg/min) on the steady-state values for arterial pressure, plasma renin activity (PRA), and renal function at four levels of sodium intake (5, 40, 120 and 240 mEq/day). Arterial pressure was monitored continuously 24 hr/day with on-line computer techniques. Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and plasma renin activity (PRA) were determined after sodium and water balance was achieved. During intrarenal NE infusion, ERPF and GFR decreased progressively from 15% to 30% and from 24% to 46% respectively, while renal vascular resistance increased progressively from 40% to 140% as sodium intake was increased from 10 to 240 mEq/day. Both ERPF and renal resistance, but not GFR, returned to control levels during intravenous NE infusion at each level of sodium intake and after terminating NE infusion. During intrarenal NE infusion the steady-state value for mean arterial pressure increased from a control of 105 to 118 mm Hg when the sodium intake was 10 mEq/day. Pressure then increased progressively from 118 to 135 mm Hg as the sodium intake was elevated from 10 to 240 mEq/day. Increases in arterial pressure associated with intravenous NE infusion were significantly smaller at each sodium level than those achieved with intrarenal NE infusion. At each level of sodium intake, PRA was elevated during intrarenal NE infusion and returned to control after NE infusion. Intravenous NE infusion did not increase PRA above control levels. The data are compatible with the concept that enhanced renal adrenergic activity could initiate and sustain hypertension chronically by basic alterations in renal function.