Interaction between lifetime captopril treatment and NaCl-sensitive hypertension in spontaneously hypertensive rats and Wistar-Kyoto rats

Design Previous studies that were based on daytime arterial pressure record ings indicate that lifetime treatment with captopril exacerbates the hypert ensive response to a high NaCl diet in spontaneously hypertensive rats (SHR ) but has no such effect in normotensive Wistar-Kyoto (WKY) rats. The prese nt study used 24-h recording methods to examine the hypothesis that during the normal waking hours of rats (night-time) the hypertensive response to a high NaCl diet is exacerbated in SHR and induced in WKY rats treated with lifetime captopril, Methods SHR and WKY rats were (1)untreated, (2), lifetime captopril treated or (3) lifetime captopril treated but removed from the treatment 2 weeks p rior to exposure to a high (8%) NaCl diet. Results Compared to untreated SHR, in SHR that were continuously treated wi th captopril, the high NaCl diet caused a more rapid and greater rise in ar terial pressure. Discontinuation of the captopril treatment did not signifi cantly diminish this NaCl-sensitivity. In untreated WKY rats, the high NaCl diet did not alter mean arterial pressure, but in the lifetime captopril-t reated WKY rats the high NaCl diet induced a rapid rise in arterial pressur e. In WKY rats, discontinuation of the lifetime captopril treatment did not diminish this NaCl-induced rise in arterial pressure, even though baseline mean arterial pressure in this group is similar to that in untreated WKY r ats. Conclusions Lifetime captopril treatment accelerates the hypertensive respo nse to a high NaCl diet in SHR, and it induces a similar response in WKY ra ts, In both strains, the lifetime captopril treatment causes a change in th e response that is not dependent on concurrent administration of the drug. This finding further suggests that lifetime captopril treatment causes a lo ng-term resetting of cardiovascular response mechanisms. J Hypertens 1999, 17:983-991 (C) Lippincott Williams & Wilkins.