Yasujima M, Abe K, Tanno M, Yoshinaga K
Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Adv Exp Med Biol. 1989;247A:35-8. doi: 10.1007/978-1-4615-9543-4_6.
To assess the mechanism by which inhibitors of angiotensin converting enzyme (ACE) lower blood pressure, we evaluated the role of endogenous angiotensin II in the antihypertensive effect of MK 421, a long-lasting ACE inhibitor, in rats made hypertensive by chronic infusion of norepinephrine or vasopressin. The hypertensive effect of norepinephrine (1.8 mg/kg/day, ip) or vasopressin (7.2 U/kg/day, ip) was inhibited by the simultaneous administration of MK 421 (6 mg/kg/day, ip). Additional administration of angiotensin II at a subpressor dose (36 micrograms/kg/day, ip) did not revert the antihypertensive effect of MK 421 in rats made hypertensive by chronic infusion of norepinephrine or vasopressin. The present results suggest that the hypotensive effect of ACE inhibitors may depend on a reduced sensitivity of the vasculature to vasoconstrictor substances. In addition, it is also suggested that the suppressed angiotensin II may not be essential for the antihypertensive effect of ACE inhibitors in rats made hypertensive by chronic infusion of norepinephrine or vasopressin.
为评估血管紧张素转换酶（ACE）抑制剂降低血压的机制，我们在通过慢性输注去甲肾上腺素或加压素诱发高血压的大鼠中，评估了内源性血管紧张素II在长效ACE抑制剂MK 421降压作用中的作用。同时给予MK 421（6毫克/千克/天，腹腔注射）可抑制去甲肾上腺素（1.8毫克/千克/天，腹腔注射）或加压素（7.2单位/千克/天，腹腔注射）的升压作用。以低于升压剂量（36微克/千克/天，腹腔注射）额外给予血管紧张素II并不能逆转MK 421对通过慢性输注去甲肾上腺素或加压素诱发高血压大鼠的降压作用。目前的结果表明，ACE抑制剂的降压作用可能取决于血管系统对血管收缩物质敏感性的降低。此外，还表明，对于通过慢性输注去甲肾上腺素或加压素诱发高血压的大鼠，血管紧张素II的抑制可能并非ACE抑制剂降压作用所必需。
