Angiotensin Converting Enzyme Inhibitors [1 ed.] 9781607410959, 9781606926192

Citation preview

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

ANGIOTENSIN CONVERTING ENZYME INHIBITORS

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

No part of this digital document may be reproduced, stored in a retrieval system or transmitted in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services.

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

ANGIOTENSIN CONVERTING ENZYME INHIBITORS

ANNE N. DEBRUE

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

EDITOR

Nova Biomedical Books New York

Copyright © 2009 by Nova Science Publishers, Inc.

All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance upon, this material. Any parts of this book based on government reports are so indicated and copyright is claimed for those parts to the extent applicable to compilations of such works. Independent verification should be sought for any data, advice or recommendations contained in this book. In addition, no responsibility is assumed by the publisher for any injury and/or damage to persons or property arising from any methods, products, instructions, ideas or otherwise contained in this publication. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS.

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

Library of Congress Cataloging-in-Publication Data Available upon request. ISBN: 978-1-60741-095-9 (E-Book)

Published by Nova Science Publishers, Inc    New York

Contents Preface Chapter 1

Angiotensin Converting Enzyme Inhibitors Macaulay A. C. Onuigbo and Nnonyelum T. C. Onuigbo

Chapter 2

Adverse Effects of Angiotensin-Converting Enzyme Inhibitor: A Review of the Literature Hiromichi Yoshida, Shigeru Hasegawa, Haruyuki Hayashi and Yasubumi Irie

Chapter 3

Chapter 4

Chapter 5 Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

vii

Chapter 6

Chapter 7

Plant-Derived Substances as ACE Inhibitors – BiosynthesisActivity Relationship of Flavonoids, Terpenes and Sterols on Angiotensin-Converting Enzyme Activity in Human Endothelial Cells Ingrid A-L Persson and Karin Persson The Proper Use of Angiotensin-Converting Enzyme Inhibitors in Patients with Chronic Kidney Disease Hiroshi Nonoguchi, Takeaki Inoue, Yushi Nakayama, Yuichiro Izumi and Takeshi Nakanishi Angiotensin-Converting Enzyme Inhibitors in Coronary Artery Disease and Preserved Left Ventricular Systolic Function Fadi Alqaisi and Mouaz H. Al-Mallah Dual Blockade of the Renin-Angiotensin System: Angiotensin Converting Enzyme Inhibition, Angiotensin Receptor Blockade and Renin Inhibition George S. Stergiou and Efthimia G. Nasothimiou Angiotensin-Converting Enzyme Inhibitors in Patients with Bilateral Atherosclerotic Renal Artery Stenosis Sarabjeet Singh, Bipin Thapa, Roopashree Prabhu, Rohit Arora and Sandeep Khosla

1

43

63

95

113

129

147

vi Chapter 8

Angiotensin Converting Enzyme Inhibitors in Renal Disease Nicolas Roberto Robles

Chapter 9

The Kallikrein- Kinin Pathways in Mediating the Hypotensive Action of Angiotensin Converting Enzyme (ACE) Inhibitors J. N. Sharma

185

Angiotension Converting Enzyme Inhibitors: Improving Utilization and Adherence Micah L. Thorp

199

Chapter 10

Chapter 11 Index

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

Contents

Angiotensin Blockade in Pediatric Chronic Kidney Disease Lavjay Butani

163

211 219

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

Preface Angiotensin II is a very potent chemical that causes the muscles surrounding blood vessels to contract, thereby narrowing the vessels. The narrowing of the vessels increases the pressure within the vessels causing high blood pressure (hypertension). Angiotensin II is formed from angiotensin I in the blood by the enzyme angiotensin converting enzyme (ACE). ACE inhibitors are medications that slow (inhibit) the activity of the enzyme ACE, which decreases the production of angiotensin II. As a result, the blood vessels enlarge or dilate, and blood pressure is reduced. This lower blood pressure makes it easier for the heart to pump blood and can improve the function of a failing heart. In addition, the progression of kidney disease due to high blood pressure or diabetes is slowed. ACE inhibitors are used for controlling blood pressure, treating heart failure, preventing strokes, and preventing kidney damage in people with hypertension or diabetes. They also improve survival after heart attacks. Because they prevent early death resulting from hypertension, heart failure or heart attacks, ACE inhibitors are one of the most important group of drugs. This new book presents important research in this field. Chapter 1 - The angiotensin converting enzyme inhibitors (ACEIs), by inhibiting the angiotensin converting enzyme (ACE), block the generation of the octapeptide, angiotensin II, a potent vasoconstrictor molecule, with effects in cardiovascular homeostasis, renal sodium reabsorption, glomerulo-tubular balance and the stimulation of aldosterone from the adrenal glands. With knowledge of the involvement of the renin angiotensin aldosterone system (RAAS) in the pathophysiology of hypertension, the ACEIs were approved for treatment of hypertension in the 1980’s. In 1998, this author, in an editorial published in the Southern Medical Journal, described the ACEIs as representing a major cornerstone in cardiovascular therapeutics. With accumulated research evidence for a pathogenetic role for angiotensin II in cardiac apoptosis and remodeling post-myocardial infarction, in left ventricular hypertrophy, remodeling and fibrosis, in renal mesangial matrix expansion and renal glomerulosclerosis, the ACEIs now have established roles in the management of hypertension, heart failure with systolic dysfunction, cardio-protection after myocardial infarction, cardio-renal protection in diabetic patients, reno-proetction in both types 1 and 2 diabetic nephropathy, and in non-diabetic nephropathies, and overall reduction in cardiovascular morbidity and mortality. They rank among the most prescribed antihypertensives in the US. Significant adverse effects associated with the ACEIs include cough

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

viii

Anne N. DeBrue

and angioedema, more so in the African American, potentially life-threatening hyperkalemia, hypotension, hepatotoxicity, fetal toxicity and death and therefore contra-indicated in pregnancy, neutropenia, anemia, rash and renal failure. The phenomenon of renal failure associated with RAAS blockade in general had mostly been published in the past as retrospective reports and case series as well as individual case reports. These reports of renal failure associated with ACE inhibition had mostly implied a need for the presence of traditionally acknowledged precipitating risk factors. Also, these previous reports had nearly always implied recovery of renal function once the offending ACEI was discontinued. More recently, however, as a result of an ever-increasing CKD/ESRD epidemic in the US, occurring simultaneously with the expanded use of these supposedly reno-protective agents, some concerns had been expressed by some authors regarding possible iatrogenic renal failure with concurrent RAAS blockade. The authors have recently published several reports of this association from the results of our prospective studies including the previously unreported syndrome of late-onset renal failure from angiotensin blockade (LORFFAB) in older CKD patients with normal renal arteries by MRA without precipitating risk factors. In addition, our reports have highlighted a previously under-recognized risk of irreversible ESRD in some patients, the exacerbation of contrast induced nephropathy by concurrent RAAS blockade in elderly CKD patients, and the occurrence of worsening renal failure in CKD patients with unilateral RAS lesions in CKD patients with dual functioning kidneys. The authors submit that a more prudent utilization of RAAS blockade in general, and ACEIs in particular, with close attention to monitoring of kidney function indefinitely, the temporary withholding of the RAAS blocking agents under certain clinical scenarios including before contrast administration and peri-operatively, as well as a willingness to discontinue RAAS blockade when indicated for aggravating renal failure, will only improve patient and renal outcomes, thus furthering the hope of cardio-renoprotection with these agents. Chapter 2 - In contrast to the excellent effectiveness of angiotensin-converting enzyme inhibitor (ACEI) in the treatment of hypertension, cardiac and kidney disease, the uncomfortable adverse effects often lead to discontinuation of the drug. Dry cough is a unique well-known side effect of ACEIs, with a frequency of 1 to 39%, and some of its mechanisms are thought to be associated with a disorder of the kinin metabolism involving bradykinin, substance P, and prostaglandin. Potential life-threatening ACEI-provoked angioedema, for which activation of the kallikrein-kinin system is also reported to be causative, has an incidence of 0.1 to 0.7% among white patients, and airway intervention can be applicable to such angioedema. Hypersensitivity to ACEIs is noted as anaphylactoid reaction that occurs during hemodialysis, and is supposed to be generated by a combination use of polyacrilonitrile dialyser and ACEIs. In contrast, ACEI-induced anemia is thought to be useful for treating erythrocytosis after renal allograft transplantation. In the latter part of this chapter the authors present a rare case, which the authors recently encountered, with allergic pleuritis in eosinophilic infiltrates associated with an ACEI, and review ACEIinduced lung involvement. In conclusion, the authors recommend that all medical participants keep in mind of various potent adverse effects during medication with ACEIs. Chapter 3 - Flavonoids, carotenoids and tocopherols are antioxidants with alleged positive effect on the cardiovascular system. To investigate other possible pharmacological mechanisms, the authors examined common substances from these groups and others derived

Copyright © 2009. Nova Science Publishers, Incorporated. All rights reserved.

Preface

ix

from the same biosynthesis pathway concerning their effect on angiotensin-converting enzyme (ACE) activity in human endothelial cells. Cultured human endothelial cells from umbilical veins (HUVEC) were used and incubated for 10 minutes with flavonoids, terpenes, sterols and precursor molecules. The flavonoids tested were the isoflavone genistein, the flavonol quercetin, the epi-flavan-3-ols epicatechin, epicatechingallate, epigallocatechin, epigallocatechingallate, procyanidin and the biflavan sciadopitysin. The terpenoids tested were the diterpenes α-tocopherol and ginkgolides A, B, C, the sesquiterpene bilobalide, the triterpenes ginsenoside Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and the tetraterpene β-carotene. The sterols tested were stigmasterol, lanosterol and cholesterol. The biosynthesis precursor molecules tested were mevalonic acid, malonic acid, shikimic acid, chorismic acid and the progenitor squalene. The phenol salicin, bilberry extract 25E containing 25% anthocyanidins, cacao extract containing procyanidin oligomers derived from epicatechin, extract of green tea, black tea, Rooibos tea, coffee, the purines caffeine, theobromine and theophylline, Ginkgo biloba, Panax ginseng and liquorice. The human-derived steroids aldosterone, estradiol and testosterone were also tested. Also, the blood lipid-lowering drugs simvastatin and pravastatin were tested. After incubation with the respective substance, ACE activity was analysed with a commercial kit. A significant and dose-dependent inhibition was seen with the flavonoids; genistein 0.5mg/ml ***p