An antihypertensive function in systemic blood pressure control has been attributed to the renal medulla. In order to examine this hypothesis normotensive and spontaneously hypertensive rats of the Muuml;nster strain (SHR) were chemically renomedullectomized by 2-bromoethylamine hydrobromide (BEA), injected intraperitoneally in a single dose of 200 mg/kg body weight. Within 5 weeks blood pressure of the BEA-treated normotensive rats and SHR rose by 17.2 plusmn; 15.2 and 27.7 plusmn; 21.0 mmHg (mean values plusmn; s.d;P 0.01), respectively, returning to baseline after 2 further weeks. Blood pressure was unchanged in the normotensive rats and SHR controls that were given isotonic saline instead of BEA solution. During maximum blood pressure in BEA-treated animals histological signs of severe renomedullary inflammation with papillary necrosis were demonstrable, while urine flow rates were elevated. Despite these disturbances renal function remained normal. These similar responses make it unlikely that a lack of a renomedullary vasodilator plays a major role in the pathogenesis of spontaneous hypertension in the Muuml;nster strain.
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