Cellular and Molecular Mechanisms in Hypertension (Advances in Experimental Medicine and Biology, 308)

Hypertension is recognized to be one of the major risk factors for the development of peripheral vascular disease. The last decade has witnessed several major advances in therapy for hypertension, including the development of angiotensin-converting enzyme inhibitors and calcium channel blockers. These compounds have greatly improved the ability to control blood pressure and to reduce the impact of this risk factor on morbidity and mortality. In spite of these advances, cardiovascular disease remains a major health problem in most modern industrialized countries with related deaths exceeding those from all other causes combined. In contrast to these advances in therapy, our understanding of the basic mechanisms responsible for the pathogenesis of hypertension remains incomplete. Recent studies have produced new insights into the nature of the regulation of muscle contraction in both heart and blood vessels as well as the changes in muscle function that occur in hypertension. However, the effects of antihypertensive therapy, both in terms of restoring normal function and in producing reversal of hypertension-associated changes, has not been as thoroughly studied, especially in the vasculature. Studies in the heart suggest that the efficacy of different therapeutic agents in restoring normal function and reversing hypertensive changes vary substantially with the mechanism of action of the therapeutic agent. It has also been recently determined that some therapeutic agents produce adverse effects on plasma lipid profiles, which could lead to the secondary acceleration of the atherosclerotic process, while at the same time normalizing blood pressure. Front Matter....Pages i-ix Ionic Channels of Vascular Smooth Muscle in Hypertension....Pages 1-7 Regulation of the Ca 2+ Sensitivity of Vascular Smooth Muscle Contractile Elements....Pages 9-25 Potassium Channel Activators in Vascular Smooth Muscle....Pages 27-43 Effects of Hypertension on Arterial Gene Expression and Atherosclerosis....Pages 45-53 Altered Phospholipase Activities Related to α 1 -Adrenergic Receptor Supersensitivity of Aortas from Aldosterone-Salt Hypertensive Rats....Pages 55-69 Role of Contractile Agonists in Growth Regulation of Vascular Smooth Muscle Cells....Pages 71-79 Calcium Dependent Regulation of Vascular Smooth Muscle Contraction....Pages 81-94 Calcium-Regulated Protein Kinases Low K m cGMP Phosphodiesterases: Targets for Novel Antihypertensive Therapy....Pages 95-105 Molecular Aspects of Voltage-Dependent Ion Channels....Pages 107-117 Regulation of Ionic Channels by G Proteins....Pages 119-134 Excitation-Contraction Coupling in the Heart....Pages 135-142 Regulation of Human Cardiac Myosin Heavy Chain Gene Expression by Thyroid Hormone....Pages 143-147 Regulation of Cardiac Muscle Function in the Hypertensive Heart....Pages 149-173 Left Ventricular Hypertrophy: Dissociation of Structural and Functional Effects by Therapy....Pages 175-190 Ca/CaM-Stimulated and cGMP-Specific Phosphodiesterases in Vascular and Non-Vascular Tissues....Pages 191-197 Hemodynamic Response of Conscious Rats and Dogs to the Protein Kinase C Inhibitor Staurosporine....Pages 199-204 Effects of Bufalin on Renal Venous Outflow, Urine Flow and Natriuresis in the Anesthetized Dog....Pages 205-210 Role of Phosphatidylinositol Turnover in the Contraction of the Rat Aorta....Pages 211-216 Reduced Aortic and Arteriolar Growth by Captopril in Normotensive and Renal Hypertensive Rats....Pages 217-221 Structure and Function of the Adrenergic Receptor Family....Pages 223-238 Back Matter....Pages 239-247