Smoking, diet, stress, coping, and exercise, among other behaviors and psychological states, are now clearly implicated in the development of cardiovascular diseases. Prevention, based largely on altering behaviors that contribute to this chronic disease, is now as important a goal as is treatment of those already afflicted. This volume, based on a recent meeting of the Academy of Behavioral Medicine Research, addresses several important areas of research in the general area of cardiovascular disease. The topics covered reflect on important aspects of this phenomenon, such as the long-term development of coronary artery disease; central nervous system (CNS) regulation of blood pressure, heart rate, and sympathetic tone playing a pivotal role in sympathetic activity and hypertension; learned blood pressure modulation and baroreceptor activation as a means of reducing the aversiveness of stress or noxious stimulation; and the notion that symptoms of heart disease or infarction may occur in the absence of organic heart disease. Having been impressed by the recent advances in the field, the editors of this book capture the wealth of newly acquired knowledge about behavioral factors in cardiovascular disease and how the body's nervous, endocrine, and cardiovascular systems work together.

The presence of monotypism in thick atherosclerotic lesions of black females with G-6-PD mosaicism first reported by the Benditts (1973) has been confirmed in two other laboratories. However, we believe that it is premature to conclude that the finding of monotypism necessarily indicates monoclonal origin of athero sclerotic lesions. We have suggested two alternative explanations for the obser vation of monotypism which we believe must be shown to be invalid before accept ing monoclonal origin as the only plausible way to account for the observed G-6-PD monotypism. One of these two alternatives relates to clonal heterogeneity of cell growth potential, i. e. , during the course of progressive growth of a le sion, progeny of one cell may overgrow all others in a portion of the lesion. The other alternative is that one of the G-6-PD alleles may be linked to genes that afford a preferential survival characteristic in the abnormal environment present in atheroscerotic lesions. Thus, cells with one allele may be able to grow better than cells with the other allele, and this characteristic may be unrelated to "A-ness" or "B-ness". We have studied initiation of lesions in He diet-fed swine and demonstrated that all active lesions that were studied were of multiple cell origin (not monoclo nal). We have studied cell growth patterns in developing atherosclerotic lesions in He diet-fed swine and found evidence consistent with clonal heterogeneity in growth potential of lesion cells.

The relationship between angiotensin II and hypertension was established in 1898 when angiotensin II was shown to modulate systemic blood pressure. Over the intervening decades, a complete characterization of the renin-angiotensin system (RAS) has been achieved, and our understanding of its biochemistry and physiology has led to the directed development of agents such ·as ACE inhibitors and receptor antagonists capable of controlling hypertension. More recently, it was shown that angiotensin II is secreted within certain tissues and that these tissue-specific systems operate independently of the systemic RAS. The novel concept that angiotensin II regulates a number of cardiovascular processes that are unrelated to blood pressure has renewed the interest of both basic and clinical scientists in angiotensin II. The association between angiotensin II and cardiac growth, in particular, has indicated that therapies currently in use for hypertension may have direct application to the treatment of heart failure. The Manitoba Cardiovascular Forum on Angiotensin Receptor Blockade in Winnipeg was convened October 18-20, 1996 to examine the clinical and basic aspects of angiotensin receptor biology as they apply to hypertension and heart failure. In addition, the potential treatment of these conditions using specific angio tensin receptor antagonists was addressed within the context of their immediate therapeutic application and future potential.

The first comprehensive overview of the effects of hypertension on the brain. The book discusses not only the relationship between hypertension and stroke, but also the much less studied relationship between hypertension and cognitive decline and neurodegenerative diseases such as Alzheimer's. It seeks to answer two important questions. First, what are the conditions under which hypertension is associated with stroke, cognitive decline, and neurodegenerative disease? And second, what are the biological mechanisms by which hypertension alters brain homeostasis? By looking at the biological mechanisms of these relationships, this book provides insight to neuroscientists and neurologists regarding why anti-hypertension treatments make a big difference in the case of stroke, but have very little impact on cognitive decline and brain aging.