Oshima T, Matsushita Y, Miyamoto M, Koike H
Eur J Pharmacol. 1983 Jul 22;91(2-3):283-6. doi: 10.1016/0014-2999(83)90479-x.
In order to determine if long-term treatment with captopril affects vascular collagen biosynthesis we administered the agent at a dose of 30 or 100 mg/kg/day p.o. for 6 weeks to spontaneously hypertensive rats. At the 6th week of captopril treatment the aorta was excised and the activity of prolyl hydroxylase, the rate-limiting enzyme of collagen biosynthesis, was measured. Vascular enzyme activity was decreased by 7.0% and 34.6% in the low- and high-dose groups, respectively. A single oral administration of captopril, on the other hand, did not decrease the enzyme activity in the aorta. Furthermore, captopril had no direct inhibitory effect on the enzyme activity in vitro. These findings suggest that the decrease in vascular prolyl hydroxylase activity resulted from a sustained decrease in blood pressure.
为了确定卡托普利长期治疗是否会影响血管胶原生物合成,我们以30或100mg/kg/天的口服剂量给自发性高血压大鼠给药6周。在卡托普利治疗的第6周,切除主动脉并测量胶原生物合成的限速酶脯氨酰羟化酶的活性。低剂量组和高剂量组的血管酶活性分别降低了7.0%和34.6%。另一方面,单次口服卡托普利并未降低主动脉中的酶活性。此外,卡托普利在体外对酶活性没有直接抑制作用。这些发现表明,血管脯氨酰羟化酶活性的降低是由于血压持续下降所致。