ACE inhibitor

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Related to ACE inhibitors: Beta blockers, Diuretics, Calcium channel blockers, ARBS

ACE inhibitor

A class of drugs (angiotensin-converting enzyme inhibitors) that block the conversion of angiotensin I to angiotensin II, used in the treatment of hypertension and congestive heart failure and in the prevention of microvascular complications of diabetes mellitus (DM).

The renin-angiotensin system is involved in the regulation of blood pressure and electrolyte balance. Angiotensinogen, a globulin formed in the liver, is converted to angiotensin I by renin, an enzyme produced by the juxtaglomerular cells of renal afferent arterioles. Renin release can be triggered by a drop in systemic blood pressure (either directly through baroreceptors or indirectly through reduction in renal tubular fluid, as in hypotension or dehydration) or in serum sodium chloride concentration. Angiotensin I is converted by the ACE, a glycoprotein produced chiefly in the lung, to angiotensin II. (ACE also degrades bradykinin, a vasodilator.) Angiotensin II is a potent vasoconstrictor and neurotransmitter, which raises peripheral vascular resistance and induces sodium retention by stimulating the adrenal cortex to secrete aldosterone. In addition, angiotensin II stimulates cell migration and the growth and proliferation of vascular smooth muscle. Because it plays a pivotal role in the pathogenesis of essential hypertension, congestive heart failure, and diabetic nephropathy, drugs that block production of angiotensin II are useful in those disorders. ACE inhibitors have an established place in the treatment of essential hypertension, congestive heart failure, and left ventricular dysfunction after myocardial infarction. Their effectiveness in hypertension is less marked in black patients than in nonblacks. ACE inhibitors may lessen cardiovascular risk by improving endothelial dysfunction, reducing inflammation, and promoting fibrinolysis by inhibiting plasminogen activator inhibitor-1. The protection afforded by these agents against vascular complications of DM is independent of their effect on blood pressure. They can slow the progression of diabetic nephropathy in patients with Type 1 DM, and of microalbuminuria in those with Type 2 DM, even in the absence of hypertension. Studies have shown a 50% reduction in the risk of the combined end-points of death, dialysis, and renal transplantation in patients with Type 1 DM who were treated with the ACE inhibitor captopril. In addition, ACE inhibitors may prevent development of DM in nondiabetic hypertensive patients. Their potentiation of the effects of bradykinin may account for their ability to enhance insulin sensitivity and may explain their apparent benefit in preventing new-onset Type 2 DM. The usefulness of these agents is limited by their tendency to elevate levels of blood urea nitrogen and creatinine, particularly in conjunction with diuretic therapy and in patients with renal disease or congestive heart failure, and to cause nonproductive cough.

ACE inhibitor

(ās)
n.
Any of a class of drugs that cause vasodilation and are used to treat hypertension and heart failure.

ACE inhibitor

Angiotensin-converting enzyme inhibitor. Any of a family of drugs used to manage hypertension and reduce congestive heart failure (CHF)-related mortality and morbidity.

Examples
Bepridil, captopril, enalapril, lisionopril, losartan, quinapril, ramipril.

ACE inhibitor Effects in Heart Disease
Cardioprotective effects
• Restores balance between myocardial O2 supply and demand;
• Reduces left ventricular preload and afterload;
• Reduces left ventricular mass;
• Reduces sympathetic stimulation.
Vasculoprotective effects
• Antiproliferative and antimigratory effects on smooth muscle and inflammatory cells;
• Antiplatelet effects;
• Improved arterial compliance and tone;
• Improved and/or restored endothelial function;
• Antihypertensive;
• Possible antiatherosclerotic effect. 

Pros
ACEIs are cardioprotective and vasculoprotective; cardioprotective effects include improved haemodynamics and electric stability, reduce sympathetic nervous system (SNS) activity and reduce left ventricular mass; vasculoprotective benefits include improved endothelial function, vascular compliance and tone, and direct antiproliferative and antiplatelet effects. ACEIs also stimulate prostaglandin (PG) synthesis, reduce the size of MIs, and reduce reperfusion injury and complex ventricular arrhythmias.

ACEIs are the treatment of choice in CHF with systolic dysfunction; they are vasodilators which decrease preload and afterload. ACEI-induced reduction in angiotensin II inhibits the release of aldosterone, which in turn reduces sodium and water retention which, by extension, reduce preload; ACEIs improve haemodynamics of CHF by reducing right atrial pressure, pulmonary capillary wedge pressure, arterial BP, as well as pulmonary and systemic vascular resistance; ACEIs increase cardiac and stroke indices by the left ventricle and reduce the right ventricular end-diastolic volumes, thereby increasing cardiac output, while simultaneously reducing cardiac load and myocardial O2 consumption.
 
Adverse effects
• Idiopathic—e.g., rashes, dysgeusia, BMsuppression.
• Class-specific—e.g., hypotension, renal impairment, hyperkaleamia, cough, angioneurotic oedema (the latter 2 of which are mediated by small vasoactive substances—e.g., bradykinin, substance P, and PG-related factors).

ACE inhibitor

Angiotensin-converting enzyme inhibitor Pharmacology Any of a family of drugs that are used to manage essential HTN, ↓ CHF-related M&M  Pros ACEIs are cardioprotective and vasculoprotective; cardioprotective effects include improved hemodynamics and electric stability, ↓ SNS activity and ↓ left ventricular mass; vasculoprotective benefits include improved endothelial function, vascular compliance and tone, and direct antiproliferative and antiplatelet effects; ACEIs also stimulate PG synthesis, ↓ the size of MIs, ↓ reperfusion injury and complex ventricular arrhythmias; ACEIs are the treatment of choice in CHF with systolic dysfunction; they are vasodilators which ↓ preload and afterload; ACEI-induced ↓ in angiotensin II inhibits the release of aldosterone, which in turn ↓ sodium and water retention which, by extension, ↓ preload; ACEIs improve hemodynamics of CHF by ↓ right atrial pressure, pulmonary capillary wedge pressure, arterial BP, as well as pulmonary and systemic vascular resistances; ACEIs ↑ cardiac and stroke indices by the left ventricle and ↓ the right ventricular end-diastolic volumes, thereby resulting in ↑ cardiac output, while simultaneously ↓ cardiac load and myocardial O2 consumption; ACEIs also downregulate the SNS, which is linked to the pathogenesis of CHF Adverse effects Idiopathic–eg, rashes, dysgeusia, BM suppression; class-specific–eg, hypotension, renal impairment, hyperkalemia, cough, angioneurotic edema, the latter 2 of which are mediated by small vasoactive substances, eg, bradykinin, substance P, and PG-related factors

ACE inhibitor Effects in Heart Disease

Cardioprotective effects
  • Restores balance between myocardial O2 supply & demand
  • Reduces left ventricular preload and afterload
  • Reduces left ventricular mass
  • Reduces sympathetic stimulation
Vasculoprotective effects
  • Antiproliferative & antimigratory effects on smooth muscle & inflammatory cells
  • Antiplatelet effects
  • Improved arterial compliance and tone
  • Improved and or restored endothelial function
  • Antihypertensive
  • Possibly, antiatherosclerotic effect
After Lonn et al, 1994

Angiotensin-converting enzyme (ACE) inhibitor

A drug that relaxes blood vessel walls and lowers blood pressure.

angiotensin-converting enzyme inhibitor

; ACE inhibitor pharmacological agent preventing conversion of angiotensin I to angiotensin II (thereby controlling vasoconstriction and reducing blood pressure), used in the treatment of heart failure, hypertension (especially diabetic patients with associated nephropathy) and in the long-term management of patients with myocardial infarction; used with care in patients on diuretics and those with renal dysfunction

ACE in·hi·bi·tor

(ās in-hibi-tŏr)
Class of drugs (angiotensin-converting enzyme inhibitors) that blocks conversion of angiotensin I to angiotensin II; used to treat hypertension and other disorders.
References in periodicals archive ?
13) The ACE inhibitor should be discontinued, and the patient should be started on a different class of antihypertensive medication.
And the brain power of those patients newly prescribed ACE inhibitors actually improved over the six month period, compared with those already taking them, and those not taking them at all.
Of note, the same magnitude of improvement in femoral neck bone mineral density was seen after just 5 years of ACE inhibitor therapy In other words, no further divergence in bone mineral density occurred during years 5-10.
sought to determine the risks versus benefits of using ACE inhibitors in patients with severe CKD.
But the only effect by type of antihypertensive the patient was exposed to was a slightly higher risk in those who took an ACE inhibitor that did not cross the blood-brain barrier, with about an 18% higher risk than that seen in the subjects on other antihypertensives.
Clinically, the temporal relationship between the drug and the occurrence of pancreatitis, as well as the evidence of recurrence on re-challenge (8,16-17,19) in several case reports, supports the association between ACE inhibitors and pancreatitis.
1 percent of the children exposed to ACE inhibitors had congenital defects--mainly of the heart and central nervous system--compared with only 1.
ACE inhibitors have been contraindicated in the second and third trimesters for at least a decade because they were known to be associated with conditions including oligohydramnios, intrauterine growth retardation, hypocalvaria, renal dysplasia, anuria, renal failure, and fetal death.
noted that using ACE inhibitors to treat heart failure has reached a plateau in recent years, leaving a substantial gap between current medical practices and optimal care.
The landmark Valiant clinical trial into the drug, also known as valsartan, involving 14,703 patients worldwide found that is as effective at improving survival after a heart attack as the conventional Ace inhibitor treatments for those patients also taking other 'background' treatments such as aspirin, beta-blockers and statins.
The cardiovascular drugs that have the most favorable profile would be the class of alpha-blockers, ACE inhibitors and ARBs--venodilators, nitrates and slow calcium channel blockers (with the exception of verapamil, which may cause a significant decrease in heart rate response at peak exercise.
Evidence has shown that the heart drugs called ACE inhibitors and angiotensin receptor blockers (ARBs) spare insulin and preserve heart and kidney function.