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Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a class of medication used primarily for the treatment of high blood pressure and heart failure. [1] [2] This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.
Reflecting the critical role of zinc, ACE can be inhibited by metal-chelating agents. [14] ACE in complex with inhibitor lisinopril, zinc cation shown in grey, chloride anions in yellow. Based on PyMOL rendering of PDB 1o86. The picture shows that lisinopril is a competitive inhibitor, since it and angiotensin I are similar structurally.
There are many classes of antihypertensives, which lower blood pressure by different means. Among the most important and most widely used medications are thiazide diuretics, calcium channel blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin II receptor blockers or antagonists (ARBs), and beta blockers.
Angiotensin-converting enzyme (ACE) inhibitors. ACE inhibitors are drugs that can relax and open up your blood vessels. Angiotensin-2 receptor blockers (ARBs). ... Vasodilators. These help to open ...
Medications used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g., spironolactone). Some medications which increase heart function, such as the positive inotrope milrinone, lead to increased death, and are contraindicated. [9] [10]
Inhibition of ACE with ACE inhibitors leads to decreased conversion of angiotensin I to angiotensin II (a vasoconstrictor) but also to an increase in bradykinin due to decreased degradation. This explains why some patients taking ACE inhibitors develop a dry cough, and some react with angioedema, a dangerous swelling of the head and neck region.
Hydralazine is a direct-acting smooth muscle relaxant and acts as a vasodilator primarily in resistance arterioles, also known as the smooth muscle of the arterial bed. The molecular mechanism involves inhibition of inositol trisphosphate-induced Ca 2+ release from the sarcoplasmic reticulum in arterial smooth muscle cells.
In some cases, your physician may prescribe certain medications, including calcium channel blockers like nifedipine, a vasodilator like sildenafil and ACE inhibitors or angiotensin II blockers ...