Reduced sympathetic neuronal uptake (uptake1) in a genetic model of desoxycorticosterone-NaCl hypertension.

The effect of desoxycorticosterone (DOC)-NaCl treatment upon sympathetic neuronal uptake of norepinephrine (uptake1) was evaluated in strains of hypertension-resistant (SBN) and -prone (SBH) rats. Uninephrectomized animals were given either a placebo pellet sc and tapwater (untreated) or a 25-mg DOC pellet and 1% NaCl. Four weeks later, tail systolic pressure was significantly higher in DOC-NaCl SBH, 183 +/- 3 mm Hg, than SBN, 141 +/- 2 (P less than 0.01). [3H]Norepinephrine (NE) uptake was determined in heart slices of all four groups by incubation in Krebs buffer at 37 degrees C for 20 min at several concentrations. Preliminary studies confirmed that this is a measure of uptake1. Heart slices of DOC-NaCl-treated SBN and SBH rats had significantly reduced NE uptake at concentrations of 10-80 nM (P less than 0.01); there was no significant difference between SBN and SBH in this regard. Untreated SBH rats have been shown to have a defect in baroreflex regulation when normotensive. The results raise the possibility that the greater increase in arterial pressure caused by DOC-NaCl in SBH compared to SBN may be related to both the inborn difference in reflex function and an acquired reduction in inactivation of norepinephrine by sympathetic neuronal uptake.