Changes in renal and central noradrenergic activity with potassium in DOCA-salt rats.

We studied the role of the renal and central noradrenergic neurons in the antihypertensive actions of potassium in DOCA-salt hypertensive rats. Supplementation with 0.2% KCl could moderate the development of the DOCA-salt hypertension. The potassium supplement attenuated sodium retention in the DOCA-salt rats, and, thus, sodium "space" at wk 4 was significantly smaller in the KCl-supplemented DOCA-salt rats than in the DOCA-salt rats. Norepinephrine turnover was measured from the rate of decline of tissue norepinephrine concentration after administration of alpha-methyl-p-tyrosine. Renal norepinephrine turnover was markedly accelerated in the DOCA-salt rats compared with the vehicle-treated control rats, but the 0.2% KCl supplements could normalize it. In contrast, turnover time in the hypothalamus and pons medulla was delayed in the DOCA-salt rats compared with the control rats, whereas 0.2% KCl supplements increased the norepinephrine turnover in the brain stem. These results suggest that the potassium-induced hypotensive actions in DOCA-salt rats may be attributed mainly to the augmented urinary sodium excretion. Moreover, it appears that the normalization of the increased renal sympathetic activity, which is intimately related to the central sympathoinhibitory noradrenergic mechanisms, may be involved in the natriuretic and antihypertensive actions of potassium in DOCA-salt hypertensive rats.