McGrath B P, Lim A E, Bode K, Willis G L, Smith G C
Clin Exp Pharmacol Physiol. 1983 Sep-Oct;10(5):543-53. doi: 10.1111/j.1440-1681.1983.tb00223.x.
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.
在大鼠肾脏中,通过荧光组织化学法在皮质动脉和近球小动脉周围的血管周围丛以及髓质血管束中鉴定出了儿茶酚胺能神经成分。在用6-羟基多巴胺(6-OHDA;150mg/kg静脉注射)处理24小时后,所有区域的荧光均消失。用去甲丙咪嗪(DMI;25mg/kg腹腔注射)预处理可保护去甲肾上腺素能神经末梢免受6-OHDA的破坏,使荧光恢复到对照水平。通过半定量分析,近球区域的荧光与对照相同,但在(DMI + 6-OHDA)处理的大鼠中,较大血管周围的荧光与对照相比略有降低。组织去甲肾上腺素含量的变化与神经荧光的变化平行,但多巴胺含量没有变化。对照组中去甲肾上腺素含量为4.10pmol/mg蛋白质(标准误=0.22,n = 32),在6-OHDA处理组中降低了90%至0.40pmol/mg(标准误=0.05,n = 23),在(DMI + 6-OHDA)处理组中降低了26%至3.01pmol/mg(标准误=0.21,n = 23)。对照组中肾脏多巴胺含量为0.38pmol/mg蛋白质(标准误=0.05,n = 32),在6-OHDA处理组中降低了55%至0.18pmol/mg(标准误=0.02,n = 17),在(DMI + 6-OHDA)处理组中降低了53%至0.17pmol/mg(标准误=0.02,n = 23)。在戊巴比妥钠麻醉的大鼠中检查了三组对出血的肾素反应,以此作为肾神经功能完整性的测试。逐渐进行1ml出血(至总失血量4ml,占体重的1.3%)导致对照组和(DMI + 6-OHDA)处理组动物的血浆肾素活性有相似的增加,但6-OHDA处理组的反应明显减弱。肾儿茶酚胺能神经似乎主要是去甲肾上腺素能的。大鼠肾脏中是否存在显著的肾内多巴胺能系统尚不确定。