Swartz S L
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.
Cardiovasc Drugs Ther. 1987;1(1):39-43. doi: 10.1007/BF02125831.
This review considers the hypothesis that angiotensin converting enzyme (ACE) inhibitors and other antihypertensive drugs may reduce blood pressure by altering the balance of vasoconstrictor and vasodilator hormones. Most cases of essential hypertension are characterized by increased vascular resistance. Since vascular resistance can be viewed as a net balance of offsetting vasoconstrictor and vasodilator neurohumoral forces, and since angiotensin II and norepinephrine can stimulate the synthesis of vasodilator prostaglandins that can in turn counteract peripheral vasoconstriction, we measured changes in vasoconstrictor (angiotensin II) and vasodilator (PGE2) hormones after giving different antihypertensive drugs. We found that the sulfhydryl containing converting enzyme inhibitor captopril increased vasodilator prostaglandin production (PGE2-metabolite) both acutely and chronically. This increase in PGE2-metabolite was not seen with the non-sulfhydryl converting enzyme inhibitor, enalapril.
本综述探讨了一种假说,即血管紧张素转换酶(ACE)抑制剂及其他抗高血压药物可能通过改变血管收缩激素和血管舒张激素的平衡来降低血压。大多数原发性高血压病例的特征是血管阻力增加。由于血管阻力可被视为相互抵消的血管收缩和血管舒张神经体液力量的净平衡,且由于血管紧张素II和去甲肾上腺素可刺激血管舒张前列腺素的合成,而后者又可反过来抵消外周血管收缩,因此我们在给予不同抗高血压药物后测量了血管收缩激素(血管紧张素II)和血管舒张激素(前列腺素E2)的变化。我们发现,含巯基的转换酶抑制剂卡托普利可急性和慢性地增加血管舒张前列腺素的生成(前列腺素E2代谢物)。非巯基转换酶抑制剂依那普利则未出现前列腺素E2代谢物的这种增加。