Yasujima M, Abe K, Tanno M, Kanazawa M, Yoshida K, Sato M, Takeuchi K, Yoshinaga K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Nephron. 1990;55 Suppl 1:81-4. doi: 10.1159/000186042.
We evaluated the antihypertensive mechanism of enalapril, a long-lasting inhibitor of angiotensin-converting enzyme, in rats made hypertensive by chronic infusion of norepinephrine or vasopressin. The hypertensive effect of norepinephrine (1.8 mg/kg/day intraperitoneal (i.p.] or vasopressin (7.2 U/kg/day i.p.) was completely abolished by simultaneous administration of enalapril (6 mg/kg/day i.p.). The antihypertensive effect of enalapril was not reversed by simultaneous administration of subpressor doses of angiotensin II (36 and 100 micrograms/kg/day i.p.). However, the hypertensive effects of angiotensin II at pressor doses (600 and 900 micrograms/kg/day i.p.) in enalapril-infused rats were not different from those in vehicle-infused rats. These results indicate that the hypotensive effect of enalapril may in part depend on a reduced sensitivity of the vasculature to norepinephrine and vasopressin, independent of inhibition of angiotensin II formation.
我们评估了长效血管紧张素转换酶抑制剂依那普利对通过慢性输注去甲肾上腺素或血管加压素制成高血压的大鼠的降压机制。同时给予依那普利（6毫克/千克/天，腹腔注射）可完全消除去甲肾上腺素（1.8毫克/千克/天，腹腔注射）或血管加压素（7.2单位/千克/天，腹腔注射）的升压作用。同时给予低于升压剂量的血管紧张素II（36和100微克/千克/天，腹腔注射）不会逆转依那普利的降压作用。然而，在输注依那普利的大鼠中，血管紧张素II升压剂量（600和900微克/千克/天，腹腔注射）的升压作用与输注溶媒的大鼠无差异。这些结果表明，依那普利的降压作用可能部分取决于血管系统对去甲肾上腺素和血管加压素的敏感性降低，与抑制血管紧张素II的形成无关。
