lisinopril and Arteriosclerosis

Acute renal failure is a well recognized complication from the use of angiotensin-converting enzyme inhibitors in patients with severe bilateral renovascular disease. A 54-year-old woman presented with acute pulmonary edema with intractable hypertension and a history of lower limb claudication. The addition of lisinopril to her antihypertensive regimen resulted, within 48 h, in the development of acute renal failure that remitted with cessation of the drug. She was found to have a heavily calcified occlusion of her aortic arch and another occlusion of the aorta below the renal arteries. Angiography and Doppler ultrasonography showed normal renal arteries. This is the first reported case of angiotensin-converting enzyme inhibitor-induced renal failure occurring in a patient with atherosclerotic occlusion of the aorta. The literature on suprarenal aortic occlusion is reviewed to determine the manner of presentation, prevalent risk factors and physical findings that typify this unique clinical entity.

Topics: Acute Kidney Injury; Adult; Aged; Angiography; Angiotensin-Converting Enzyme Inhibitors; Aortic Valve Stenosis; Arteriosclerosis; Female; Humans; Lisinopril; Male; Middle Aged; Renal Artery; Renal Artery Obstruction; Risk Factors; Ultrasonography, Doppler

Long-term treatment with angiotensin-converting enzyme (ACE) inhibitors as well as angiotensin II type 1 (AT(1)) receptor antagonists and statins reduces cardiovascular mortality in patients with coronary artery disease as well as chronic heart failure. Little is known about the acute effects of these compounds on vascular reactivity of coronary resistance vessels. Coronary arterioles were obtained from patients undergoing coronary bypass operation (atherosclerosis group) or valve replacement (control group). Responses to endothelium-dependent agonists (histamine, serotonin, and acetylcholine) as well as to the endothelium-independent agonist sodium nitroprusside (SNP) were investigated under baseline conditions and after incubation (15 min) with lisinopril (ACE inhibitor), candesartan (AT(1) receptor antagonist), or fluvastatin. In atherosclerotic vessels, vasorelaxation was significantly reduced to all endothelium-dependent agonists but not, however, to SNP (77 +/- 8, -24 +/- 16, -46 +/- 24, and 98 +/- 8% relaxation for histamine, serotonin, acetylcholine, and SNP, respectively). Lisinopril and fluvastatin but not candesartan significantly improved the responses to the endothelium-dependent agonists (lisinopril: 94 +/- 4, 17 +/- 22, and -20 +/- 13%; fluvastatin: 96 +/- 8, 23 +/- 21, and -25 +/- 18% relaxation for histamine, serotonin, and acetylcholine, respectively). The effect of lisinopril was prevented by pretreatment with a bradykinin antagonist (HOE-130) and dichloroisocoumarine, an inhibitor of kinine-forming enzymes. Pretreatment with a nitric oxide (NO) synthase inhibitor abolished the improvement of endothelial function by lisinopril and fluvastatin. Vascular reactivity in the control group was not influenced by any of the pharmacological interventions. The data demonstrate that in atherosclerosis, endothelium-dependent relaxation of coronary resistance arteries is severely compromised. The impairment can acutely be reversed by ACE inhibitors and statins via increasing the availability of NO.

Topics: Acetylcholine; Aged; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Arterioles; Arteriosclerosis; Benzimidazoles; Biphenyl Compounds; Coronary Disease; Coronary Vessels; Endothelium, Vascular; Fatty Acids, Monounsaturated; Female; Fluvastatin; Histamine; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; In Vitro Techniques; Indoles; Lisinopril; Male; Middle Aged; Muscle Contraction; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase; Nitric Oxide Synthase Type I; Nitroprusside; Serotonin; Tetrazoles; Vascular Diseases; Vascular Resistance; Vasodilator Agents

Arterial injury by a balloon catheter produces marked smooth muscle cell proliferation and the participation of angiotensin II in this response has been suggested. In this study, we examined the effect of a novel angiotensin II type I receptor antagonist, TCV-116, on neointimal formation after rat carotid artery balloon injury. Oral administration of TCV-116 at doses of 1, 5 or 10 mg/kg/day significantly reduced the cross-sectional intimal area by 30%, 46% and 54%, respectively, and reduced the ratio of the intimal to medial cross-sectional areas by 23%, 41% and 50%. An angiotensin-converting enzyme inhibitor, lisinopril, had an effect similar to that of TCV-116. The effect of both drugs was significantly correlated with the reduction of both blood pressure and cardiac hypertrophy. We conclude that TCV-116 can prevent neointimal formation after balloon injury as well as reducing blood pressure and preventing cardiac hypertrophy.

Topics: Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Arteriosclerosis; Benzimidazoles; Biphenyl Compounds; Blood Pressure; Carotid Artery Diseases; Carotid Artery, Common; Catheterization; Hypertension; Lisinopril; Male; Prodrugs; Rats; Rats, Inbred SHR; Rats, Sprague-Dawley; Tetrazoles; Tunica Intima

Topics: Angioplasty, Balloon; Angiotensin-Converting Enzyme Inhibitors; Arteriosclerosis; Atherectomy; Cell Division; Cells, Cultured; Colchicine; Dipeptides; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Etoposide; Humans; Lisinopril; Muscle, Smooth, Vascular; Prednisolone; Propranolol; Recurrence; Vincristine