Cellular and Molecular Mechanisms in Hypertension

1. Front Matter

   Pages i-ix

   PDF

2. Vascular Smooth Muscle

   1. Membrane Mechanisms

      1. Ionic Channels of Vascular Smooth Muscle in Hypertension

         • Nancy J. Rusch, William J. Stekiel

         Pages 1-7

      2. Regulation of the Ca2+ Sensitivity of Vascular Smooth Muscle Contractile Elements

         • Junji Nishimura, Cornelis van Breemen

         Pages 9-25

      3. Potassium Channel Activators in Vascular Smooth Muscle

         • Robert H. Cox

         Pages 27-43

   2. Intracellular Mechanisms

      1. Effects of Hypertension on Arterial Gene Expression and Atherosclerosis

         • Aram V. Chobanian

         Pages 45-53

      2. Altered Phospholipase Activities Related to α1-Adrenergic Receptor Supersensitivity of Aortas from Aldosterone-Salt Hypertensive Rats

         • Allan W. Jones, Shivendra D. Shukla, Brinda B. Geisbuhler, Susan B. Jones, Jacquelyn M. Smith

         Pages 55-69

      3. Role of Contractile Agonists in Growth Regulation of Vascular Smooth Muscle Cells

         • Gary K. Owens

         Pages 71-79

      4. Calcium Dependent Regulation of Vascular Smooth Muscle Contraction

         • Robert S. Moreland, Jacqueline Cilea, Suzanne Moreland

         Pages 81-94

      5. Calcium-Regulated Protein Kinases Low Km cGMP Phosphodiesterases: Targets for Novel Antihypertensive Therapy

         • Paul J. Silver, Edward D. Pagani, Wayne R. Cumiskey, Ronald L. Dundore, Alex L. Harris, King C. Lee et al.

         Pages 95-105

3. Cardiac Muscle

   1. Membrane Mechanisms

      1. Molecular Aspects of Voltage-Dependent Ion Channels

         • Robert L. Barchi

         Pages 107-117

      2. Regulation of Ionic Channels by G Proteins

         • A. M. Brown, A. Yatani, G. Kirsch, A. M. J. VanDongen, B. Schubert, J. Codina et al.

         Pages 119-134

   2. Intracellular Mechanisms

      1. Excitation-Contraction Coupling in the Heart

         • Harry A. Fozzard

         Pages 135-142

      2. Regulation of Human Cardiac Myosin Heavy Chain Gene Expression by Thyroid Hormone

         • E. Morkin, J. G. Edwards, R. W. Tsika, J. J. Bahl, I. L. Flink

         Pages 143-147

      3. Regulation of Cardiac Muscle Function in the Hypertensive Heart

         • Edward G. Lakatta

         Pages 149-173

      4. Left Ventricular Hypertrophy: Dissociation of Structural and Functional Effects by Therapy

         • Edward D. Frohlich

         Pages 175-190

      5. Ca/CaM-Stimulated and cGMP-Specific Phosphodiesterases in Vascular and Non-Vascular Tissues

         • H. S. Ahn, M. Foster, M. Cable, B. J. R. Pitts, E. J. Sybertz

         Pages 191-197

      6. Hemodynamic Response of Conscious Rats and Dogs to the Protein Kinase C Inhibitor Staurosporine

         • R. Allan Buchholz, Ronald L. Dundore, Paul J. Silver

         Pages 199-204

      7. Effects of Bufalin on Renal Venous Outflow, Urine Flow and Natriuresis in the Anesthetized Dog

         • D. Eliades, M. B. Pamnani, B. T. Swindall, F. J. Haddy

         Pages 205-210

      8. Role of Phosphatidylinositol Turnover in the Contraction of the Rat Aorta

         • Evangeline D. Motley, Robert R. Ruffolo Jr., Douglas W. P. Hay, Andrew J. Nichols

         Pages 211-216

      9. Reduced Aortic and Arteriolar Growth by Captopril in Normotensive and Renal Hypertensive Rats

         • Duo H. Wang, Russell L. Prewitt

         Pages 217-221

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.

• Calcium
• Lipid
• Pathogene
• cardiovascular
• development
• enzymes
• hypertension
• lead

• Bockus Research Institute, The Graduate Hospital and Department of Physiology, The University of Pennsylvania, Philadelphia, USA

  Robert H. Cox

Policies and ethics