Catecholamine release in the rat hypothalamic paraventricular nucleus in response to haemorrhage, desipramine and potassium

Abstract

In vivo microdialysis and HPLC were used to measure catecholamine release in the rat hypothalamic paraventricular nucleus (PVN) during haemorrhage. The effects of noradrenaline uptake blockade with 1 μM desipramine (DMI) and a depolarising concentration of potassium (100 mM) through the probe were also examined. Dialysis probes implanted in the PVN of urethane anesthetised rats were perfused with modified Ringer solution at 1.1 μ1/min. Thirty minute collections were analysed for DOPA, noradrenaline, DOPAC, HVA and 5-HIAA. Basal concentrations, in the absence of DMI, were: DOPA 203.6 ± 44.0 pg/ml, noradrenaline 128.0 ± 20.4 pg/ml; DOPAC 5.6 ± 0.7, HVA 5.1 ± 2.2 and 5-HIAA 87.2 ± 17.8 ng/ml. Basal noradrenaline was doubled in the presence of DMI while basal and stimulated DOPA, DOPAC, HVA and 5-HIAA were not affected by DMI. Haemorrhage resulted in a significant noradrenaline release (48% over resting levels) in the presence of DMI (n = 10, P < 0.05); in the absence of DMI, a smaller and non-significant increase (30% over basal levels) was observed. Potassium-induced depolarisation caused a significant two- and four-fold increase in noradrenaline release (P < 0.001), with decreases in the dopamine metabolites DOPAC (31%, 44%) and HVA (35%, 28%), and the serotonin metabolite, 5-HIAA (41%, 33%), in the presence and absence of DMI, respectively. The catecholamine precursor DOPA did not vary throughout either experiment. The results indicate that haemorrhage induces a 48% increase in noradrenaline release in the rat PVN which provides evidence for a role of noradrenergic projections to the PVN in cardiovascular control.