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Department of Pharmacology, Shiga University of Medical Science, Seta, Otsu, Japan (N.T., K.A., T.O.); and Toyama Institute for Cardiovascular Pharmacology Research, Azuchi-machi, Chuo-ku, Osaka, Japan (N.T.)
Discovery of the unexpected intercellular messenger and transmitter nitric oxide (NO) was the highlight of highly competitive investigations to identify the nature of endothelium-derived relaxing factor. This labile, gaseous molecule plays obligatory roles as one of the most promising physiological regulators in cardiovascular function. Its biological effects include vasodilatation, increased regional blood perfusion, lowering of systemic blood pressure, and antithrombosis and anti-atherosclerosis effects, which counteract the vascular actions of endogenous angiotensin (ANG) II. Interactions of these vasodilator and vasoconstrictor substances in the circulation have been a topic that has drawn the special interest of both cardiovascular researchers and clinicians. Therapeutic agents that inhibit the synthesis and action of ANG II are widely accepted to be essential in treating circulatory and metabolic dysfunctions, including hypertension and diabetes mellitus, and increased availability of NO is one of the most important pharmacological mechanisms underlying their beneficial actions. ANG II provokes vascular actions through various receptor subtypes (AT1, AT2, and AT4), which are differently involved in NO synthesis and actions. ANG II and its derivatives, ANG III, ANG IV, and ANG-(1-7), alter vascular contractility with different mechanisms of action in relation to NO. This review article summarizes information concerning advances in research on interactions between NO and ANG in reference to ANG receptor subtypes, radical oxygen species, particularly superoxide anions, ANG-converting enzyme inhibitors, and ANG receptor blockers in patients with cardiovascular disease, healthy individuals, and experimental animals. Interactions of ANG and endothelium-derived relaxing factor other than NO, such as prostaglandin I2 and endothelium-derived hyperpolarizing factor, are also described.
Abstract I. Introduction II. Endothelium-Derived Relaxing Factor and Angiotensin: Synthesis and Mechanisms of Action on Blood Vessels A. Nitric Oxide B. Prostaglandin I2 (Prostacyclin) C. Endothelium-Derived Hyperpolarizing Factor D. Angiotensin III. Angiotensin-Induced, Endothelium-Derived Relaxing Factor-Mediated Vasodilatation A. Angiotensin II-Induced Vasodilatation 1. In Vitro Studies. 2. Studies on Gene-Targeted Mice. 3. In Vivo Studies. 4. Involvement of Angiotensin II Receptors Other Than Angiotensin Receptor Type 2. B. Angiotensin III [Angiotensin-(2-8)]-Induced Vasodilatation C. Angiotensin-(1-7)-Induced Vasodilatation D. Angiotensin IV [Angiotensin-(3-8)]-Induced Vasodilatation IV. Radical Oxygen Species Production Stimulated by Angiotensin II V. Vasodilatation Induced by Angiotensin I-Converting Enzyme (Kininase II) Inhibitors Associated with Endothelial Nitric Oxide via Bradykinin A. Human Studies VI. Mechanisms Underlying Vasodilatation Induced by Angiotensin Receptor Type 1 Blockade VII. Interaction between Endothelial Nitric Oxide and Angiotensin II in Patients and Healthy Subjects A. Coronary Blood Flow Response B. Renovascular Response C. Forearm and Other Regional Blood Flow Responses D. Blood Pressure Response E. Other Responses VIII. Interaction between Endothelial Nitric Oxide and Angiotensin II in Experimental Animals A. Systemic Blood Pressure B. Regional Blood Flow C. Renal Vasculature 1. In Vivo Study in Rats. 2. In Vivo Study in Mice. 3. In Vivo Study in Dogs, Sheep, Pigs, and Rabbits. 4. In Vitro Study. D. Coronary Vasculature and the Heart 1. Coronary Vasculature. 2. Myocardium. E. Cerebral Vasculature F. Pulmonary Vasculature G. Mesenteric Vasculature H. Placental and Uterine Vasculatures I. Other Vasculatures J. Kidney 1. Renal Function a. Studies in rats. b. Studies in dogs and rabbits. 2. Renin. K. Other Organs and Tissues
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