Effects of renal papillary-medullary lesion on the antihypertensive effect of furosemide and development of salt-sensitive hypertension in Dahl-S rats. 
To test the hypothesis that the long-term antihypertensive action of furosemide is mediated by a renomedullary vasodepressor substance, we measured mean arterial pressure (MAP) by radiotelemetry in Dahl-S rats with either intact or bromoethylamine-induced (BEA, 100 mg/kg i.p.)  lesion of the renal papilla and medulla.  Seven days of recovery after BEA administration, the rats diet was changed from 1 to 4% NaCl, and during days 8 to 31, rats were randomized to daily treatment with placebo or furosemide (50 mg/kg p.o.).  Then furosemide treatment was stopped and the rat food was changed to 1% NaCl diet.  After a 10-day wash-out period, renal function was measured.  BEA produced a rapid (within min) and sustained increase in MAP which was accelerated during 4% NaCl diet.  Furosemide prevented 4% NaCl-induced hypertension in both rats with intact kidneys and in rats with BEA-induced renal papillary-medullary lesion.  A significant decrease in renal plasma flow (-34%) and glomerular filtration rate (-40%) was observed in all BEA-treated rats independent of previous furosemide treatment.  In response to an i.v.  load of isotonic saline (10% body weight), rats with renal papillary-medullary lesion had an impaired ability to excrete sodium.  Histological examination showed that BEA-treated rats had severe lesions of the renal papilla and medulla, with light-to-moderate changes in the renal cortex.  It is concluded that the antihypertensive effect of furosemide is not mediated by a renomedullary vasodepressor substance.  The accelerated NaCI-sensitive hypertension in rats with BEA-induced renal papillary-medullary lesion is related to an impaired ability to excrete excess NaCl.