Comparison of cilazapril and nifedipine retard on ambulatory blood pressure, metabolic, rheological and platelet function in hypertensive patients.

In a 12 week randomised, double-blind study, a total of 31 patients with a sitting DBP of between 95 and 115 mmHg were enrolled for comparison of the antihypertensive, metabolic and antiplatelet effects of the drugs cilazapril and nifedipine retard. A two week placebo treatment was given before either cilazapril (2.5 mg daily) or nifedipine retard (20 mg twice daily) was administered. After four weeks treatment, those patients with a sitting DBP > 90 mmHg were given a doubling of their initial doses for the next six weeks; the others were maintained at their initial doses. All patients received their drugs and reported any adverse effects every other week. Blood was taken for metabolic, rheological and platelet function tests. Ambulatory BP and heart rate were recorded at the start, fourth and tenth weeks of study. At the end of this trial, there was a significant decrease in both SBP and DBP in the cilazapril group (155 +/- 14 to 142 +/- 12 mmHg systolic, P < 0.01; 106 +/- 6 to 95 +/- 5 mmHg diastolic, P < 0.01). In the nifedipine group, there was also a significant decrease in SBP and DBP (161 +/- 18 to 139 +/- 5 mmHg, systolic, P < 0.01; 101 +/- 6 to 88 +/- 9 mmHg diastolic, P < 0.05) but with a significant increase in heart rate (79 +/- 14 to 91 +/- 10 beats/minute, P < 0.05). There were no significant changes in the biochemical or metabolic parameters in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of endothelium in vascular response of diabetic rats.

The responses of aortas to various vasoactive agents were compared in streptozotocin-induced diabetic male rats and age-matched normal controls. There was a shift of the dose-response curve of norepinephrine (NE) to the right from streptozotocin-induced diabetic rats of 8 weeks duration as compared that of to normal rats. The median effective concentration (EC50) of NE in diabetic aortas to NE was significantly increased from 10(-7.5) M to 10(-7.2) M, while the maximum response of diabetic aortas to NE was not different from that of normal controls. In addition, the EC50 and maximum contractile response to KCl were also not different between the two groups. Meanwhile, the contractions induced by angiotensins I and II, were also significantly attenuated in diabetic aortas. The endothelium-dependent relaxation produced by carbachol in aortic rings which is precontracted with NE was significantly lower in diabetic preparations than that in age-matched control animals. The EC50 of carbachol in diabetic and normal aortas to carbachol were 2.8 x 10(-6) M vs 1.2 x 10(-6) M respectively. These results suggest that deterioration of endothelium might exist in diabetic rats.