['Previous studies have shown that a fully functional alpha(2B)-adrenergic receptor (AR) is necessary for the development of salt-induced hypertension. The current studies were designed to explore the effect of prolonged inhibition of central alpha(2B)-AR gene expression by antisense (AS) DNA on this hypertension.', 'We developed a plasmid vector driven by a cytomegalovirus promoter, containing a green fluorescent protein reporter gene and AS for rat alpha(2B)-AR protein. Subtotally nephrectomized, salt-loaded hypertensive rats received intracerebroventricular injection of 500 microg of either the AS plasmid (n = 9) or sense plasmid (containing cDNA for alpha(2B)-AR), as control (n = 7).', 'The AS injection produced a fall in SBP from 201 +/- 4 to 171 +/- 5 mmHg within 12 h. The level of BP in the 3 days post-injection was 174 +/- 6, 181 +/- 4 and 184 +/- 6 mmHg on day 1, day 2 and day 3, respectively (P < 0.05), and returned gradually towards baseline in subsequent days, although it remained significantly lower for the 8 days of observation. The control sense plasmid injections produced no significant changes in blood pressure (BP). Neither group had histological evidence of neural tissue disruption.'] Does central alpha2B-adrenergic receptor antisense in plasmid vector prolong reversal of salt-dependent hypertension?