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Vol. 52, Issue 1, 11-34, March 2000

Molecular and Cellular Mechanisms of Angiotensin II-Mediated Cardiovascular and Renal Diseases

Shokei Kim1 and Hiroshi Iwao

Department of Pharmacology, Osaka City University Medical School, Abeno-ku, Osaka, Japan

I. Introduction
II. Classification and Biochemical Characteristics of Angiotensin Receptors
    A. AT1 Receptor
    B. AT2 Receptor
III. Molecular and Cellular Actions of Angiotensin II in Heart
    A. Molecular Characteristics of Pathological Cardiac Hypertrophy
    B. Cultured Cardiac Myocytes
    C. Neonatal versus Adult Cardiac Myocytes
    D. Cultured Cardiac Fibroblasts
    E. Effects of In Vivo Angiotensin II Infusion on Heart
    F. Effects of Angiotensin Blockade on Experimental Cardiac Diseases
        1. Spontaneously Hypertensive Rats and Other Hypertensive Models.
        2. Acute Pressure Overload Model.
        3. Myocardial Infarction.
        4. Volume Overload Model.
        5. Diabetes.
IV. Molecular and Cellular Actions of Angiotensin II in Blood Vessels
    A. Cultured Smooth Muscle Cells
    B. Cultured Endothelial Cells
    C. Effects of In Vivo Angiotensin II Infusion on Vascular Tissues
    D. Effects of Angiotensin Blockade on Experimental Vascular Diseases
        1. Hypertensive Rats.
        2. Balloon Injury.
        3. Other Models.
V. Molecular and Cellular Actions of Angiotensin II in Kidney
    A. Cultured Glomerular Cells
    B. Effects of In Vivo Angiotensin II Infusion on Kidney
    C. Effects of Angiotensin Blockade on Experimental Glomerular Diseases
VI. AT1 Receptor Antagonists versus Angiotensin-Converting Enzyme Inhibitors
    A. Pharmacological Differences
    B. Is the AT2 Receptor Beneficial or Detrimental?
    C. Combination Therapy
VII. Conclusions
Acknowledgments
References

A growing body of evidence supports the notion that angiotensin II (Ang II), the central product of the renin-angiotensin system, may play a central role not only in the etiology of hypertension but also in the pathophysiology of cardiovascular and renal diseases in humans. In this review, we focus on the role of Ang II in cardiovascular and renal diseases at the molecular and cellular levels and discuss up-to-date evidence concerning the in vitro and in vivo actions of Ang II and the pharmacological effects of angiotensin receptor antagonists in comparison with angiotensin-converting enzyme inhibitors. Ang II, via AT1 receptor, directly causes cellular phenotypic changes and cell growth, regulates the gene expression of various bioactive substances (vasoactive hormones, growth factors, extracellular matrix components, cytokines, etc.), and activates multiple intracellular signaling cascades (mitogen-activated protein kinase cascades, tyrosine kinases, various transcription factors, etc.) in cardiac myocytes and fibroblasts, vascular endothelial and smooth muscle cells, and renal mesangial cells. These actions are supposed to participate in the pathophysiology of cardiac hypertrophy and remodeling, heart failure, vascular thickening, atherosclerosis, and glomerulosclerosis. Furthermore, in vivo recent evidence suggest that the activation of mitogen-activated protein kinases and activator protein-1 by Ang II may play the key role in cardiovascular and renal diseases. However, there are still unresolved questions and controversies on the mechanism of Ang II-mediated cardiovascular and renal diseases.

1 Address for correspondence: Shokei Kim, MD, PhD, Department of Pharmacology, Osaka City University Medical School, 1-4-3 Asahimachi, Abeno, Osaka 545-8585, Japan. E-mail: kims{at}med.osaka-cu.ac.jp

0031-6997/00/5201-0011$03.00/0
PHARMACOLOGICAL REVIEWS
Copyright © 2000 by The American Society for Pharmacology and Experimental Therapeutics


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G. F. Tomaselli and D. P. Zipes
What Causes Sudden Death in Heart Failure?
Circ. Res., October 15, 2004; 95(8): 754 - 763.
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 Mol. Biol. CellHome page
B. E. Thomas and T. J. Thekkumkara
Glucose Mediates Transcriptional Repression of the Human Angiotensin Type-1 Receptor Gene: Role for a Novel Cis-acting Element
Mol. Biol. Cell, October 1, 2004; 15(10): 4347 - 4355.
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