Search

Angiotensin-converting enzyme (ACE) is a well-known zinc-metallopeptidase that converts angiotensin I to the potent vasoconstrictor angiotensin II and degrades bradykinin, a powerful vasodilator, both for the regulation of vascular tone and cardiac functions. Other natural substrates of ACE were identified broadening the functions of this enzyme within different physiological contexts such as neuronal metabolism, hematopoiesis, digestion, and reproduction. In this context, ACE has an essential role in diseases, for instance, hypertension, Alzheimer's disease, oxidative stress, sperm maturation and fertility, intraocular pressure, bone metabolism, fibrillary glomerulonephritis, among others. This book describes the role of ACE as a part of the Renin-Angiotensin-System, on different metabolic processes related to some diseases, such as the examples already mentioned. Moreover, ACE is related to adipose tissue. The modulation of ACE can modulate hypertension and diseases related to this enzyme. Captopril is the first successful ACE inhibitor in the treatment of hypertension; however, it has adverse effects such as dry cough, dizziness, lightheadedness or loss of taste and others. The search for alternatives to Captopril has increased research on bioactive peptides. Then, several book chapters describe how ACE can be modulated by bioactive peptides, which are short amino acid sequences previously encrypted in whole proteins and liberated through the digestion process. Animal and vegetal proteins can be used as a source of bioactive peptides. Milk, milk-derived food products and lionfish are examples of animal proteins, while several legumes such as beans and peanuts are vegetable sources of bioactive peptides.

The renin-angiotensin system and the mechanisms regulating this system developed during the adaptive evolution of verte­ brates, along with many other systems involved in the in­ tegrated survival of the organism. Because animal species have evolved from common ancestral populations, a basis for the comparison of body structures and physiological processes ex­ ists among animal groups belonging to different classifications. The comparative approach provides a better understanding of the structure and function of adaptive systems and facilitates the development of general principles governing these systems among animal groups; further, this approach reveals significant characteristics specific to certain animal groups. As the evolu­ tion of adaptation of animals to environmental conditions is explored, directions for future research are suggested. In this book, advances in research on the renin-angiotensin system are described with emphasis on the comparative aspects. However, since studies on the renin-angiotensin system of birds, reptiles, amphibians and fishes are limited compared with those con­ ducted in mammals, in some chapters descriptions are con­ cerned primarily with mammals. It has taken a long time to write this volume, and the topic is a broad one, with new data always emerging; therefore, certain aspects, and sometimes the most recent information, may not be included. Chapters 1-3 and sections 8. 1-8. 4,8. 6, 8. 7 were written by H. K. ; Chapters 4-7 and Section 8. 5 by Y. T. ; Chapter 9 was written by both authors. H. Uemura, M. Nozaki, Y. Okawara, We are indebted to Drs.

The special issue of Molecular and Cellular Biochemistry focuses on `Control of Gene Expression by Catecholamines and the Renin-Angiotensin System'in health and disease. In recent years, great progress has been made in the understanding of catecholamine and angiotensin II modulated gene expression. There is also increasing evidence that catecholamine and angiotensin II induced cellular injury not solely arises from classical pathways but also from a perturbed gene expression. Taking into account that catecholamines and angiotensin II are vital for a balanced gene expression of many cells, the intriguing possibility arises that various disease are initiated or aggravated by such an imbalance. Catecholamine and angiotensin II influences can be in excess arising from, for example, hypercaloric food intake or psychosocial stress. During early progression of heart failure, sympathetic activity and angiotensin II influences also become increased. Due to beta-adrenergic receptor downregulation, depressed catecholamine influences are expected in the final stage of heart failure. An imbalanced influence of catecholamines and angiotensin II on gene expression leads to disordered molecular structures of the cell and an impaired cell function. This focused issue is organized into chapters concentrating on catecholamines, angiotensin II, and the interaction between catecholamines and angiotensin II. Basic biochemical processes are covered in detail and the potential of these pathways for explaining chronic diseases associated with excess catecholamine and angiotensin II influences should become apparent. It is hoped that this focussed issue triggers novel research into the development of drugs that are targeted at diseases characterized by an imbalanced gene expression involving catecholamines and angiotensin II.