ACE inhibitors used in D.M because:1.not affect on blood glucose level
:Reduce progression to severe chronic kidney disaease and failure in patient with type II D.M and protien urea and reduce worsening of protien urea in type II D.M
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.
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.
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