|| Checking for direct PDF access through Ovid
The effect of haemorrhagic hypotension on plasma catecholamine levels was studied in anesthetized normotensive and DOCA–salt hypertensive rats. The basal levels of plasma norepinephrine (NE) were significantly higher in DOCA–salt hypertensive rats than in normotensive rats. Moreover, the elevations in plasma NE and epinephrine (E) levels induced by haemorrhagic hypotension were found to be markedly potentiated in DOCA–salt hypertensive rats. Pretreatment with the re-uptake blocker (desmethylimipramine) increased both basal and haemorrhage NE levels in DOCA–salt hypertensive as well as in normotensive rats. Consequently, basal and haemorrhage NE plasma levels remained significantly higher in the DOCA–salt hypertensive animals than in the normotensive rats even following neuronal re-uptake blockage. This suggests that the elevated NE concentrations found in the plasma of DOCA–salt hypertensive rats both under basal condition and during haemorrhagic hypotension do not reflect a defective re-uptake. Moreover, in contrast with what is observed in normotensive animals, bilateral adrenalectomy did not induce any increase in basal or haemorrhage NE levels in the DOCA-salt hypertensive rats. This constitutes yet more evidence supporting the existence of an impaired balance of the sympathoadrenal axis in this hypertension model. The present study therefore suggests that the potentiated plasma catecholamine response to haemorrhage in DOCA-salt hypertensive rats is the consequence of an increased sympathoadrenal reactivity and not of an altered neuronal uptake. This hyperreactivity may result from an impaired regulation of the sympatho-adrenal axis in that hypertension model.