By Professor Thomas Unger, Professor Bernward A. Schölkens (auth.)
Nearly thirty years in the past, in 1974, the amount on Angiotensin edited through Irvine H.Page and F. Merlin Bumpus increased the instruction manual of Experimental Pharmacology. Even after twenty years the multiplicity of its activities looks to not were absolutely came upon. to name realization to its many services is without doubt one of the reasons of this e-book. This new version of the quantity on Angiotensin makes an attempt to supply an up to date account of the data and findings accrued because the complexity of angiotensin was once so competently recognized.
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Extra info for Angiotensin Vol. II
However, ongoing large-scale clinical trials will compare ATl antagonists against ACE inhibitors, and evaluate ATl antagonists versus placebo in ACE-intolerant patients. The combination therapy of ATl receptor antagonist and ACE inhibitor will be investigated. Combined therapy is theoretically appealing and was shown, in the Randomized Evaluation Of strategies for Left Ventricular Dysfunction (RESOLVD) study (McKelvie et al. 1999) to be more beneficial than either single treatment in improving the neurohormonal balance and left ventricular remodeling.
B. ) receptors , other specific cell surface receptors, including AT2, AT4 and angiotensin (1-7), are involved in the actions of angiotensin peptides and are discussed elsewhere in this book. The major effects of angiotensin II (Jackson 2001) include vasoconstriction; enhancement of peripheral noradrenergic transmission; increased central nervous sympathetic discharge; release of aldosterone; decreased urinary Na+; increased urinary K+ excretion; migration, proliferation, and hypertrophy of vascular smooth muscle cells; hypertrophy of cardiac myocytes; proliferation and increased synthetic capacity of fibroblasts leading to increased cardiac and vascular extracellular matrix formation; release of thromboxane A2; and increased production of matrix metalloproteinases.
In addition, ANG 11 induces plasminogen activator inhibitor I (PAIl), which is involved in the fine tuning of proteolytic ECM turnover. This review focuses on the regulation of fibronectin, collagen and proteoglycan expression by ANG 11 in VSMC and blood vessels and on the modulation of ECM degradation by matrix metalloproteinases. Furthermore, the modulation of focal adhesion signaling through the convergence with ANG II-induced tyrosine phosphorylation is discussed. T. Unger et al. ), Angiotensin © Springer-Verlag Berlin Heidelberg 2004 40 J.
Angiotensin Vol. II by Professor Thomas Unger, Professor Bernward A. Schölkens (auth.)