Decrease in hypothalamic norepinephrine content following renal denervation in the one-kidney, one clip Goldblatt hypertensive rat.
- 1 May 1982
- journal article
- research article
- Published by Wolters Kluwer Health in Hypertension
- Vol. 4 (3) , 369-373
- https://doi.org/10.1161/01.hyp.4.3.369
Abstract
Peripheral and central sympathetic mechanisms contribute to the development and maintenance of increased blood pressure in the 1-kidney model or renal hypertension in the rat. Previous studies demonstrated that the renal sympathetic nerves, in particular, contribute to the maintenance of hypertension in this model, since, renal denervation, performed 2 wk after renal artery clipping, resulted in a significant decrement in blood pressure that was associated with a decrease in peripheral sympathetic activity. To further define the role of the renal nerves in the pathogenesis of hypertension in this model, the systolic blood pressure and norepinephrine and dopamine content of thg hypothalamus, midbrain, pons medulla and spinal cord were determined at 1 wk following renal denervation or sham operation of rats with early established 1-kidney 2 clip hypertension. Age-matched uninephrectomized rats were controls. The blood pressure of denervated animals decreased significantly from 189 .+-. 9.21 to 151 .+-. 6.5 mm Hg (P < 0.001), while that of sham-operated animals did not change. Hypothalamic norepinephrine content of sham-operated animals was significantly greater than that of controls (2.24 .+-. 0.8 .mu.g/g sham vs 1.84 .+-. 0.12 .mu.g/g controls, P < 0.01). Renal denervation resulted in a decrease in hypothalamic norepinephrine content to conrol levels (1.72 .+-. 0.11 .mu.g/g). There was a significant (r = 0.65, P < 0.01) positive correlation between systolic blood pressure and hypothalamic norepinephrine content of renaldenervated and sham-operated animals. The norepinephrine content of other brain regions was not different between groups. Evidently, the renal nerves contribute to the maintenance of hypertension in the 1-kidney 1 clip rat by modulating central sympathetic nervous system activity.This publication has 22 references indexed in Scilit:
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