1. Previous studies have indicated that increases in dietary K+ promote diuresis and retard stroke development in stroke-prone spontaneously hypertensive rats (spSHR) fed a Japanese-style diet containing 4% NaCl.

2. It is possible that elevations in dietary K+ retard stroke development by inducing natriuresis and facilitating the clearance of Na+, and that diuretics associated with natriuresis might also be capable of retarding stroke development in spSHR. To test if this was the case, the onset of stroke development in spSHR fed a low (0.75%) K+ diet containing 4% NaCl (controls) was monitored and compared with that in spSHR treated with (a) frusemide, (b) chlorothiazide, (c) amiloride or (d) acetazolamide, and with (e) untreated spSHR fed a high (2.11%) K+ diet.

3. The onset of stroke, as well as death resulting from stroke, occurred at a significantly later age in spSHR fed a high K+ diet than in spSHR fed a low-K+ diet, despite the fact that both groups of spSHR rats had comparable blood pressures.

4. Treatment of spSHR with the above-named diuretics before stroke development did not alter the blood pressure of the rats. The onset of stroke development and death in spSHR treated with chlorothiazide, amiloride or acetazolamide was comparable with that observed in untreated control spSHR. In spSHR treated with frusemide, the onset of stroke was comparable with that of untreated control spSHR, whereas the onset of death after stroke development was accelerated.

5. Post mortems performed on spSHR that developed stroke indicated the presence of haemorrhagic stroke of comparable severity in the six groups of spSHR studied.

6. The results indicate that treatment of spSHR with diuretics at levels which do not alter the animals’ blood pressure does not alter the timing or incidence of stroke development, and does not prolong the lifespan of the animals after stroke has developed.

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