EXPERIMENTAL HYPERTENSION OF THE RAT: RECIPROCAL CHANGES OF NOREPINEPHRINE TURNOVER IN HEART AND BRAIN-STEM

Abstract

In experimental hypertensive rats (DOCA-implantation, 1% saline as drinking-water, encapsulation of the left kidney), the norepinephrine turnover in peripheral sympathetically innervated organs and the central nervous system was determined either by the decay in endogenous norepinephrine after inhibition of tyrosine hydroxylase or by the ecayd in the specific norepinephrine activity after intravenous or intraventricular administration of3H-norepinephrine. In the heart, the norepinephrine turnover was accelerated in proportion to the rise in blood pressure. In hypothalamus and medulla oblongata, the turnover was delayed reciprocally to the acceleration in the heart. No changes were seen in the residual parts of the brain. Administration of chlorisondamine, a quaternary ganglionic blocking agent which does not cross the blood-brain barrier, resulted in a normalization of the increased cardiac norepinephrine turnover, whereas the changes in the brain persisted. Implantation of DOCA alone produced neither a rise in blood pressure nor changes in norepinephrine turnover. The results presented are compatible with the hypothesis that, in this form of experimental hypertension, the delay in norepinephrine turnover in the brain-stem is causally related to the increased activity of the peripheral sympathetic nervous system.