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In the rat kidney catecholaminergic nerve elements were identified by fluorescence histochemistry in perivascular plexuses around corticula arteries and juxtaglomerular arterioles and in medullary vascular bundles. Fluorescence was abolished in all areas 24 h after treatment with 6-hydroxydopamine (6-OHDA; 150 mg/kg i.v.). Protection of noradrenergic endings from destruction by 6-OHDA was afforded by pretreatment with desipramine (DMI; 25 mg/kg i.p.) which restored fluorescence towards control levels. By semiquantitative analysis fluorescence was identical in juxtaglomerular regions but slightly reduced around larger vessels in (DMI + 6-OHDA)-treated rats when compared to controls. Changes in tissue noradrenaline content, but not dopamine content, paralleled the changes in nerve fluorescence. Noradrenaline content was 4.10 pmol/mg protein (s.e.m. = 0.22, n = 32) in controls and was reduced by 90% to 0.40 pmol/mg (s.e.m. = 0.05, n = 23) in 6-OHDA-treated and by 26% to 3.01 pmol/mg (s.e.m. = 0.21, n = 23) in (DMI + 6-OHDA)-treated rats. Kidney dopamine content was 0.38 pmol/mg protein (s.e.m. = 0.05, n = 32) in controls and was reduced by 55% to 0.18 pmol/mg (s.e.m. = 0.02, n = 17) in 6-OHDA-treated and by 53% to 0.17 pmol/mg (s.e.m. = 0.02, n = 23) in (DMI + 6-OHDA)-treated rats. The renin response to haemorrhage was examined in pentobarbitone sodium-anaesthetized rats as a test of functional integrity of renal nerves in the three groups. Progressive 1 ml haemorrhages (to total blood loss of 4 ml, 1.3% body weight) resulted in similar increases in plasma renin activity in controls and (DMI + 6-OHDA)-treated animals but the response was significantly attenuated in 6-OHDA-treated rats. Renal catecholaminergic nerves appear to be predominantly noradrenergic. It is doubtful if a significant intrarenal dopaminergic system exists in the rat.
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McGrath et al. (1983) studied this question.
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