Captopril and dihydralazine both prevented genetic hypertension development in spontaneously hypertensive rats, reducing mean blood pressure to 117 mmHg compared to 160 mmHg in controls.
Absolute Event Rate: 117% vs 160%
p-value: p=<0.001
When administered to young spontaneously hypertensive rats (SHRs), dihydralazine (25 mg kg-1, daily) and captopril (100 mg kg-1, daily) prevent with the same efficacy genetic hypertension development (GHD). Dihydralazine treatment increased vascular mesenteric compliance, as shown by a significant decrease in the stiffness of the vessels (-27%), and induced slight reductions in contractility (-12%) and in wall to lumen (W/L) ratio (-15%). After treatment withdrawal, all these parameters returned to control values within 7 weeks, as did blood pressure. Captopril treatment also strongly increased the mesenteric vessels compliance, vessel stiffness being decreased by 16%, and reduced their contractility (-15%) and their W/L ratio (-30%). These effects as well as those exerted on blood pressure persisted up to 7 weeks after treatment ceased although there was a slight trend to a progressive reduction in the intensity of both phenomena. These experiments show that captopril but not dihydralazine has a long-lasting effect in opposing the functional and morphological vascular alterations occurring during GHD in SHRs and this phenomenon probably contributes to a large extent to the sustained preventive effects of the drug against GHD.
Freslon et al. (Tue,) conducted a other in Genetic hypertension development (n=120). Captopril and Dihydralazine vs. Distilled water was evaluated on Mean blood pressure (MBP) at 20 weeks of age (p=<0.001). Captopril and dihydralazine both prevented genetic hypertension development in spontaneously hypertensive rats, reducing mean blood pressure to 117 mmHg compared to 160 mmHg in controls.