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Department of the Regius Professor of Medicine, Radcliffe Infirmary, Oxford, OX2 6HE

1. The effect on renal blood flow regulation of unilateral renal denervation followed by administration of a prostaglandin synthesis inhibitor has been studied in nine conscious rabbits.

2. Renal blood flow distribution was estimated using radioactive microspheres injected via a pre-implanted left ventricular cannula. Cardiac output was estimated by thermodilution. Measurements were made before and after intravenous injection of Meclofenamate, Parke Davis Ltd (4 mg/kg).

3. Renal denervation caused a fall in renal cortical catecholamine concentration of approximately 50% by 48 hr.

4. Resting renal blood flow did not differ significantly between denervated and innervated kidneys.

5. Meclofenamate caused a significant rise in arterial pressure from a mean of 59 to 70 mmHg. In innervated kidneys, Meclofenamate caused a fall in renal blood flow from 8·1 ± 0·6 (mean ± S.E. of mean) to 6·5 ± 0·4 ml./min.g kidney weight while in denervated kidneys it caused a fall from 8·9 ± 0·7 to 6·25 ± 0·3 ml./min.g.

After Meclofenamate flow was redistributed away from the inner cortex in the innervated kidney and paradoxically towards the inner cortex in the denervated one.

6. It was concluded that in conscious animals, resting sympathetic tone has little effect on renal blood flow. The exaggerated reduction in flow in the outer cortex of the denervated kidney following Meclofenamate may indicate denervation hypersensitivity to circulating catecholamines unmasked by reduced synthesis of vasodilator prostaglandins. Alternatively, renal sympathetic nerves may normally prime prostaglandin synthesis in the outer cortex.