Giudicelli J F, Richer C, Freslon J L, Glasson S, Decourt S
Arch Mal Coeur Vaiss. 1981 Jun;74 Spec No:51-9.
The preventative effects of betablockers and captopril on the development of genetic hypertension in genetically hypertensive rats, were studied after long-term daily dosage by forced feeding, from the 5th to the 20th week of age of the animals. Of the drugs studied, captopril, atenolol and propranolol limited the development significantly, but pindolol only had a modest effect and acebutolol was ineffective. No correlation was found between the degree of prevention of genetic hypertension and the intensity of betablockade. Atenolol and propranolol prevent genetic hypertension by I) reducing cardiac output, a reduction which is not neutralised by the simultaneous change in peripheral resistance, 2) decreasing plasma renin concentrations, and 3) limiting the development of myocardial hypertrophy. Captopril is very effective in preventing the development of genetic hypertension and acts: 1) by causing an early and lasting fall in peripheral resistance related to the suppression of Angiotensin II, and possibly by potentialising the vasodilatation of bradykinins and, 2) by limiting myocardial hypertrophy.
通过从动物5周龄至20周龄长期每日强制灌胃给药，研究了β受体阻滞剂和卡托普利对遗传性高血压大鼠遗传性高血压发展的预防作用。在所研究的药物中，卡托普利、阿替洛尔和普萘洛尔显著限制了高血压的发展，但吲哚洛尔只有适度的效果，醋丁洛尔则无效。遗传性高血压的预防程度与β受体阻滞强度之间未发现相关性。阿替洛尔和普萘洛尔通过以下方式预防遗传性高血压：1）降低心输出量，这种降低不会因外周阻力的同时变化而抵消；2）降低血浆肾素浓度；3）限制心肌肥大的发展。卡托普利在预防遗传性高血压的发展方面非常有效，其作用机制为：1）通过抑制血管紧张素II导致外周阻力早期持续下降，可能还通过增强缓激肽的血管舒张作用；2）限制心肌肥大。
