The Renin-Angiotensin System in Hypertension and Congestive Heart Failure [antikvár]

How to Use The goal of this book is to provide an in-depth introduction This Book to a new form of treatment for hypertension and congestive heart failure. The format and organization of the book facilitate rapid, selective reading. The book is divided into four parts: Part I is an examination of basic pathophysiologic mechanisms, principles of treatment, and the characteristics of ACE inhibition. Part II provides more details of ACE inhibition, which may not be needed immediately but which may provide important reference material at a later time. Part III contains illustrative case histories for diagnostic and therapeutic considerations. Part IV provides a translation of the principles developed in preceding parts into some practical guidelines for therapeutic decision making. © Physiology of the Cardiovascular System Arterial blood pressure is determined by blood volume, cardiac performance, and peripheral vascular resistance: Cardiac Output Cardiac output is the product of stroke volume and heart rate. Stroke Volume In addition to sympathetic nervous system activity to the heart, intrinsic myocardial contractility, and aortic pressure, stroke volume depends on diastolic fiber length, which determines the degree of stretching (preload). In that way, cardiac function is influenced by the available blood volume. Blood volume, in turn, is controlled by a series of regulatory mechanisms, in part involving sodium homeostasis. Heart Rate The baroreceptor reflex is a major determinant of heart rate, acting through the sympathetic and parasympathetic nervous systems. Baroreceptor Function Baroreceptors in the aortic arch respond to intravascular pressure and communicate with the central nervous system via afferent fibers of the vagus nerve. Baroreceptors also act on circulation centers in the brainstem through the carotid sinus nerves and the glossopharyngeal nerve. In turn, these central nervous system centers determine vascular tone and cardiac output via efferent adrenergic nerve fibers. Peripheral Vascular Resistance and the Sympathetic Nervous System Peripheral vascular resistance increases in response to vasoconstriction when a-recep-tors of the vascular smooth muscle cells are activated. The specific neurohumoral transmitter involved is norepinephrine. Epinephrine stimulates both the a- and |3-adrenergic receptors. Because the latter are more sensitive at lower concentrations, epinephrine acts primarily as a vasodilator on the coronary and skeletal vessels by activating 3-receptors. At higher concentrations its vasoconstrictor action dominates by activating the more numerous a-receptors. Thus, at lower concentrations, epinephrine reduces peripheral vascular resistance and diastolic blood pressure, while concurrently increasing heart rate by means of the baroreceptor reflex. In contrast, norepinephrine always induces an increase in peripheral vascular resistance and diastolic pressure, with decreases in heart rate and stroke volume.