Abstract: | Norepinephrine (NE) release and pressor response to sympathetic stimulation were studied in dogs under furosemide-induced acute volume depletion. The rise in blood pressure observed following carotid clamping proved similar before and after acute salt and water depletion in the first group of animals and NE rose comparably in these two conditions. Similar results were obtained in a second group of dogs that received an angiotensin II converting enzyme inhibitor (CEI). This study shows that contrary to isotonic saline loading, acute salt and water depletion cause a progressive increase in NE plasma levels. Moreover, these results clearly demonstrate that the decrease in sympatho--adrenergic response and the predominant role played by the renin--aniotensin system during chronic salt depletion are not observed in acute conditions. |