Renal and cardiovascular effects of renal medullary damage with bromoethylamine in dogs.

Bromoethylamine (BEA, 30-40 mg/kg) was administered to dogs to determine whether damage to the inner medulla of the kidney, the putative source of a depressor hormone, causes hypertension in this species. Bromoethylamine produces hypertension in rats but this has not been confirmed in other species, although we have shown that this dose of BEA in dogs abolishes the release of a reno-medullary vasodepressor hormone in response to marked increases in renal perfusion pressure. During acute BEA administration over 1 h to conscious dogs, there were no significant effects on renal blood flow, arterial pressure or total peripheral resistance, but there was a significantly greater diuresis compared to vehicle administration. Over the first 10-14 days after BEA, daily urine output rose 5-10 fold initially and plasma creatinine concentration rose markedly. There was no significant effect on arterial pressure, cardiac output, total peripheral resistance, or renal blood flow over this period. BEA administration caused extensive damage to the thin limbs of the loops of Henle, widespread thrombosis of blood vessels and haemorrhage into the interstitium of the dog renal medulla. Reno-medullary interstitial cells were devoid of lipid droplets, were synthetic, and were associated with increased amounts of extracellular matrix. Thus extensive renal medullary damage by BEA administration to conscious dogs did not alter resting systemic haemodynamics, and these results therefore provide no evidence for a role for the medulla in the maintenance of resting arterial pressure in the dog.