Effect of depletion of spinal noradrenaline by 6-hydroxydopamine on the development of renal hypertension in rats.

SUMMARY 1. A single injection in rats of 250 μg of 6-hydroxydopamine HCl (6-OHDA) into the subarachnoidal space of the spinal cord of rats resulted in a lasting, selective depletion of spinal noradrenaline. Dopamine levels in the spinal cord and catecholamine levels in various brain regions were not markedly affected. 2. When ether anaesthesia was used spinal noradrenaline was found to be almost completely depleted by the administration of 6-OHDA. Only partial depletion was achieved when pentobarbitone anaesthesia or neuroleptic analgesia was used. 3. The blood pressure rise caused by electrical stimulation of the posterior hypothalamus was not affected by 6-OHDA treatment 7 days previously. 4. 6-OHDA administration did not influence the development of two-kidney Goldblatt hypertension. When 6-OHDA was administered 7 days before clipping, a slight delay of the development was observed, but this did not occur when 6-OHDA treatment was given 3–4 h before clipping. 5. It is concluded that intact spinal noradrenergic neurotransmission is neither a prerequisite for the development of two-kidney Goldblatt hypertension, nor for the pressor response to hypothalamic stimulation.