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Clinical and Experimental Pharmacology and Physiology, ISSN 0305-1870, 09/2007, Volume 34, Issue 9, pp. 938 - 945
SUMMARY • In the present review, we addressed studies in humans and rats to determine the role that oxidative stress may play in mediating cardiovascular... 
kidney | aopcynin | F2-isoprostanes | superoxide | tempol | molsidomine | F2‐isoprostanes | Tempol | Aopcynin | Superoxide | Molsidomine | Kidney | PHYSIOLOGY | DIMORPHISM | SPONTANEOUSLY HYPERTENSIVE-RATS | QUANTIFICATION | PROSTAGLANDIN-F2-ALPHA METABOLITE | F-2-ISOPROSTANES | IN-VIVO | PHARMACOLOGY & PHARMACY | VASODILATOR | POSTMENOPAUSAL WOMEN | PROGRESSION | Cardiovascular Diseases - prevention & control | Humans | Kidney - enzymology | NADPH Oxidases - metabolism | Nitric Oxide Synthase - antagonists & inhibitors | Hypertension - drug therapy | Male | Spin Labels | Kidney - metabolism | Cyclic N-Oxides - pharmacology | Acetophenones - pharmacology | Female | Blood Pressure - drug effects | Nitric Oxide Donors - pharmacology | Superoxide Dismutase - metabolism | NG-Nitroarginine Methyl Ester - pharmacology | Rats, Inbred SHR | Cardiovascular Diseases - etiology | Glutathione Peroxidase - metabolism | Cardiovascular Diseases - physiopathology | Kidney - drug effects | Cardiovascular Diseases - metabolism | NADPH Oxidases - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | Antioxidants - pharmacology | Hypertension - physiopathology | Hypertension - metabolism | Catalase - metabolism | Antioxidants - therapeutic use | Animals | Ascorbic Acid - pharmacology | Molsidomine - pharmacology | Sex Factors | Hypertension - complications | Nitric Oxide Synthase - metabolism | Oxidative Stress - drug effects | Nitric Oxide - metabolism | Vitamin E - pharmacology | Kidney, drug effects | NG-Nitroarginine Methyl Ester, pharmacology | Nitric Oxide Synthase, antagonists and inhibitors | Oxidative Stress, drug effects | Ascorbic Acid, pharmacology | Hypertension, drug therapy | Cardiovascular Diseases, etiology | Cardiovascular Diseases, prevention and control | Cyclic N-Oxides, pharmacology | Enzyme Inhibitors, pharmacology | Superoxide Dismutase, metabolism | Nitric Oxide Synthase, metabolism | Hypertension, physiopathology | Antioxidants, pharmacology | Kidney, metabolism | NADPH Oxidase, antagonists and inhibitors | Blood Pressure, drug effects | Catalase, metabolism | Cardiovascular Diseases, metabolism | Hypertension, metabolism | Acetophenones, pharmacology | Vitamin E, pharmacology | Antioxidants, therapeutic use | Kidney, enzymology | Nitric Oxide, metabolism | Molsidomine, pharmacology | NADPH Oxidase, metabolism | Hypertension, complications | Nitric Oxide Donors, pharmacology | Glutathione Peroxidase, metabolism | Cardiovascular Diseases, physiopathology | Hypertension | Oxidative stress | Blood pressure
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 01/2000, Volume 28, Issue 1, pp. 55 - 63
Reactive oxygen species have been shown to be involved in the mutagenicity, clastogenicity, and apoptosis of mammalian cells treated with arsenic or cadmium.... 
Excision repair | Reactive oxygen species | Peroxynitrite | Hydrogen peroxide | Free radicals | Nitric oxide | nitric oxide | free radicals | OXIDATIVE STRESS | peroxynitrite | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | hydrogen peroxide | SODIUM ARSENITE | STRAND BREAKS | excision repair | CHINESE-HAMSTER CELLS | reactive oxygen species | HEAT-SHOCK RESPONSE | L-ARGININE | ENDOCRINOLOGY & METABOLISM | HYDROGEN-PEROXIDE | WELL WATER | MALIGNANT NEOPLASMS | Cadmium Chloride - toxicity | Catalase - pharmacology | Free Radical Scavengers - pharmacology | Amitrole - pharmacology | Mutagens - toxicity | Citrulline - analogs & derivatives | Reactive Oxygen Species - metabolism | Nitric Oxide Synthase - antagonists & inhibitors | Endothelium, Vascular - drug effects | Molsidomine - analogs & derivatives | Thiourea - pharmacology | Endothelium, Vascular - chemistry | Phenanthrolines - pharmacology | Chromans - pharmacology | Arsenites - toxicity | Cattle | Superoxides - metabolism | Nitric Oxide Donors - pharmacology | Superoxide Dismutase - pharmacology | N-Glycosyl Hydrolases - pharmacology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Sodium Selenite - pharmacology | Antioxidants - pharmacology | Onium Compounds - pharmacology | Hydrogen Peroxide - metabolism | Nitroarginine - pharmacology | Nitrates - metabolism | Bacterial Proteins - pharmacology | DNA-Formamidopyrimidine Glycosylase | Animals | Citrulline - pharmacology | Ditiocarb - pharmacology | Escherichia coli Proteins | Sodium Compounds - toxicity | Uric Acid - pharmacology | Molsidomine - pharmacology | Thiomalates - pharmacology | Aorta - cytology | DNA Damage | Nitric Oxide - metabolism | Thiourea - analogs & derivatives | formamidopyrimidine-DNA glycosylase | formamidopyrimidine | 3-morpholinosydnonimine | 8-oxoguanine
Journal Article
Journal of Comparative Neurology, ISSN 0021-9967, 03/2005, Volume 483, Issue 3, pp. 278 - 291
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 2000, Volume 74, Issue 6, pp. 2268 - 2277
An excess of the free radical nitric oxide (NO) is viewed as a deleterious factor involved in various CNS disorders. Numerous studies have shown that the... 
Neuroprotection | Flavonoids | Protein kinase C | Ischemia | Ginkgo biloba extract (EGb 761) | Nitric oxide | Hippocampal cells | GERBIL HIPPOCAMPUS | nitric oxide | LIPID-PEROXIDATION | hippocampal cells | BIOCHEMISTRY & MOLECULAR BIOLOGY | OXIDATIVE-METABOLISM | NEUROSCIENCES | ischemia | SIGNAL-TRANSDUCTION | neuroprotection | DOUBLE-BLIND | PLATELET-ACTIVATING-FACTOR | RAT-BRAIN | flavonoids | CEREBRAL-ISCHEMIA | SUPEROXIDE-DISMUTASE | protein kinase C | MEDIATED NEUROTOXICITY | Free Radical Scavengers - pharmacology | Nitric Oxide Donors - toxicity | Brain Ischemia - metabolism | Neurons - cytology | Molsidomine - analogs & derivatives | Phenanthridines - pharmacology | Lactones - pharmacology | Organoselenium Compounds - pharmacology | Alkaloids | Neuroprotective Agents - pharmacology | Protein Kinase C - metabolism | Estrenes - pharmacology | Pyrrolidinones - pharmacology | Flavonoids - pharmacology | Molsidomine - toxicity | Neurons - drug effects | Plant Extracts | Cells, Cultured | Enzyme Inhibitors - pharmacology | Alzheimer Disease - drug therapy | Phosphodiesterase Inhibitors - pharmacology | Rats | Calcium Channels, L-Type - physiology | Antioxidants - pharmacology | Nitrendipine - pharmacology | Azoles - pharmacology | Calcium Channel Blockers - pharmacology | Hippocampus - cytology | Rats, Sprague-Dawley | Ginkgolides | Ginkgo biloba | Nitroprusside - toxicity | Animals | Vasodilator Agents - toxicity | Signal Transduction - drug effects | Benzophenanthridines | Brain Ischemia - drug therapy | Neurons - enzymology | Alzheimer Disease - metabolism | Diterpenes | Oxidative Stress - drug effects | Nitric Oxide - metabolism | Flavonoids - chemistry | Plants, Medicinal
Journal Article
JOURNAL OF EXPERIMENTAL BIOLOGY, ISSN 0022-0949, 05/2001, Volume 204, Issue 10, pp. 1719 - 1727
Journal Article
Acta physiologica, ISSN 1748-1708, 07/2017, Volume 220, Issue 3, pp. 382 - 393
Aim: Multiple interacting pathways contribute to progression of renal and cardiac damage in chronic kidney disease followed by chronic heart failure... 
heart failure | chronic kidney disease | fibrosis | inflammation | renin–angiotensin system | FOLLISTATIN-LIKE 1 | PHYSIOLOGY | MYOCARDIAL-INFARCTION | HEART-FAILURE | INJURY | ANGIOTENSIN-ALDOSTERONE SYSTEM | DAMAGE | INHIBITION | CARDIORENAL SYNDROME | CHRONIC KIDNEY-DISEASE | HYPERTENSIVE-RATS | renin-angiotensin system | Metoprolol - pharmacology | Angiotensin II Type 1 Receptor Blockers - therapeutic use | Rats, Inbred Lew | Male | Spin Labels | Angiotensin II Type 1 Receptor Blockers - pharmacology | Sympatholytics - therapeutic use | Coronary Vessels | Kidney Function Tests | Pyrrolidines - pharmacology | Pyrrolidines - therapeutic use | Cyclic N-Oxides - therapeutic use | Ligation | Thiocarbamates - pharmacology | Nephrectomy | Cyclic N-Oxides - pharmacology | Sympatholytics - pharmacology | Nitric Oxide Donors - therapeutic use | Nitric Oxide Donors - pharmacology | Drug Evaluation, Preclinical | Drug Therapy, Combination | Disease Models, Animal | NF-kappa B - antagonists & inhibitors | Kidney - drug effects | Losartan - pharmacology | Thiocarbamates - therapeutic use | Metoprolol - therapeutic use | Antioxidants - pharmacology | Cardio-Renal Syndrome - drug therapy | Antioxidants - therapeutic use | Animals | Molsidomine - therapeutic use | Fibrosis | Losartan - therapeutic use | Molsidomine - pharmacology | Heart - drug effects | Heart failure | Heart beat | Chronic kidney failure | Angiotensin | Superoxide | Drug therapy, Combination | Gene expression | Heart | NF-κB protein | Renal function | Metoprolol | Coronary artery | Tempol | Superoxide dismutase | Connective tissue growth factor | Coronary artery disease | Heart rate | Angiotensin AT1 receptors | Rodents | Xenografts | Blood pressure | Receptor mechanisms | Angiotensin II | Heart diseases | Structure-function relationships | Index Medicus
Journal Article
European Journal of Pharmacology, ISSN 0014-2999, 03/2012, Volume 679, Issue 1-3, pp. 40 - 50
We previously reported that both nitric oxide (NO) generated from NO synthase by bombesin and NO generated from SIN-1 (NO donor) activate the brain... 
S-Nitrosylation | Brain | Adrenomedullary outflow | Bombesin | Cyclooxygenase-1 | Nitric oxide | POTASSIUM CHANNELS | NITRIC-OXIDE SYNTHASE | SYMPATHETIC PREGANGLIONIC NEURONS | THORACIC SPINAL-CORD | DORSAL VAGAL COMPLEX | PARAVENTRICULAR NUCLEUS | PLASMA NORADRENALINE | PHARMACOLOGY & PHARMACY | GASTRIC-ACID SECRETION | CENTRAL-NERVOUS-SYSTEM | THROMBOXANE A | 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - administration & dosage | Cysteine - analogs & derivatives | Oxadiazoles - administration & dosage | Rats, Wistar | Injections, Intraventricular | Imidazoles - administration & dosage | Male | Molsidomine - analogs & derivatives | Molsidomine - administration & dosage | S-Nitrosothiols - metabolism | Bombesin - administration & dosage | Dose-Response Relationship, Drug | Quinoxalines - pharmacology | Bombesin - pharmacology | Oxadiazoles - pharmacology | Dithiothreitol - administration & dosage | Sulfhydryl Reagents - administration & dosage | Ethylmaleimide - pharmacology | Adrenal Medulla - drug effects | Cysteine - metabolism | Nitric Oxide Donors - pharmacology | Dithiothreitol - pharmacology | Quinoxalines - administration & dosage | Rats | Imidazoles - pharmacology | Catecholamines - blood | Benzoates - administration & dosage | Brain - drug effects | Nitric Oxide Donors - administration & dosage | Paraventricular Hypothalamic Nucleus - drug effects | Adrenal Medulla - secretion | Animals | Bombesin - antagonists & inhibitors | 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology | Molsidomine - pharmacology | Paraventricular Hypothalamic Nucleus - metabolism | Benzoates - pharmacology | Molsidomine - antagonists & inhibitors | Sulfhydryl Reagents - pharmacology | Ethylmaleimide - administration & dosage | Nitrogen oxide | Cysteine | Catecholamines | Neuropeptides | Cells | Thromboxanes | Thiols | Neurons | Adrenal medulla | Thromboxane A2 | Hypothalamus | Paraventricular nucleus | Guanylate cyclase | Nitric-oxide synthase | Dithiothreitol | N-Ethylmaleimide
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 04/2010, Volume 113, Issue 2, pp. 363 - 373
Journal Article