Vascular effects of dihydralazine during prevention of genetic hypertension development in SHR rats

Dihydralazine (25 mg/kg, q.d., orally, from the 6th to the 20th week of age) strongly inhibits genetic hypertension development (GHD) without limiting myocardial hypertrophy. However, after treatment withdrawal, the drug no longer opposes GHD. Therefore we have investigated whether dihydralazine-induced transient morphological and functional vascular alterations could explain the drug's biphasic effects against GHD during and after treatment. Dihydralazine increased vascular mesenteric compliance, reduced aortic wall weight and induced slight but not significant reductions in contractile ability and wall to lumen ratio of mesenteric arteries during treatment. When the latter was discontinued, all these parameters again reached the control values within 7 weeks, as was also the case for blood pressure. These experiments show that when the vascular effects of dihydralazine disappear, its preventive effect against GHD also subsides, thus pointing out the major role played by vascular morphological and functional changes in GHD.