Participation of central noradrenergic neurons in experimental hypertension

Abstract

A hyperactivity of both the peripheral sympathetic fibers and the adrenal medulla has been shown to be in part responsible for an elevation of blood pressure in rats made hypertensive with DOCA and sodium. Such a generalized activation suggested that the primary dysfunction responsible for this peripheral sympathetic hyperactivity could be localized at a higher level of the blood pressure regulatory mechanism. The norepinephrine turnover rate was studied after blockade of the biosynthesis with α-methyl-p-tyrosine in various regions of the central nervous system. The norepinephrine turnover was found to be increased in most vascular peripheral organs, whereas it was significantly reduced in the brain stem of hypertensive animals compared with that in normotensive animals. On the other hand, the turnover rate was found normal in the spinal cord and in the telediencephalic portion of the brain. The section of the spinal cord at C6–C7 level resulted in a rapid fall in blood pressure within normotensive levels in hypertensive animals while the norepinephrine turnover was restored to normal in peripheral organs. However, the norepinephrine turnover rate remained markedly reduced in the brain stem of these spinalectomized hypertensive rats despite the lowering in blood pressure, thus indicating that the changes observed in the function of catecholaminergic neurons of the brain stem are not secondary to the elevation of blood pressure but could rather be a determinant factor in the induction of the peripheral sympathetic hyperactivity in this form of experimental hypertension.