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Autonomic & autacoid pharmacology, ISSN 1474-8665, 2002
Journal
Journal of cardiovascular pharmacology, ISSN 0160-2446
Journal
2010, ISBN 0470772743, xvi, 342
Some drugs which are not aimed at treating heart disease have nevertheless been found to have profound effects on heart muscle. Cardiotoxicity is one of the... 
Cardiovascular toxicology
Book
Cardiovascular toxicology, ISSN 1530-7905, 2001
Journal
Vascular pharmacology, ISSN 1537-1891, 2002
Journal
Journal of cardiovascular pharmacology and therapeutics, ISSN 1074-2484, 1996
Journal
Circulation Research, ISSN 0009-7330, 03/2015, Volume 116, Issue 6, pp. 960 - 975
Blockers of the renin–angiotensin–aldosterone system (RAAS), that is, renin inhibitors, angiotensin (Ang)-converting enzyme (ACE) inhibitors, Ang II type 1... 
remodeling | gender | aldosterone | AT2 receptor | hyperkalemia | resistant hypertension | receptor | renin | primary aldosteronism | reactive oxygen species | angiotensin | angiotensin-(1-7) | prorenin | angiotensin-(1–7) | CARDIAC & CARDIOVASCULAR SYSTEMS | BLOOD-PRESSURE RESPONSES | PLASMA-RENIN | CONVERTING ENZYME-INHIBITORS | CORONARY VASCULAR BED | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | II TYPE-2 RECEPTOR | HEMATOLOGY | MYOCARDIAL-INFARCTION | AT 2 receptor | CELL MINERALOCORTICOID RECEPTORS | SEX-DIFFERENCES | CONGESTIVE-HEART-FAILURE | Antihypertensive Agents - pharmacology | Drugs, Investigational - pharmacology | Angiotensin II Type 1 Receptor Blockers - therapeutic use | Humans | Drugs, Investigational - therapeutic use | Endothelium, Vascular - drug effects | Hypertension - drug therapy | Male | Ion Channels - physiology | Sex Chromosomes | Molecular Targeted Therapy | Gonadal Steroid Hormones - physiology | Vasoconstriction - physiology | Drug Interactions | Angiotensin-Converting Enzyme Inhibitors - therapeutic use | Hyperaldosteronism - physiopathology | Female | Hypertension - genetics | Drug Evaluation, Preclinical | Drug Resistance | Precision Medicine | Aldosterone - physiology | Endothelium, Vascular - physiopathology | Hyperaldosteronism - genetics | Mice, Transgenic | Renin-Angiotensin System - genetics | Renin-Angiotensin System - physiology | Clinical Trials as Topic | Sex Characteristics | Antihypertensive Agents - therapeutic use | Vasoconstriction - drug effects | Hyperaldosteronism - drug therapy | Hypertension - physiopathology | Mice, Knockout | Mineralocorticoid Receptor Antagonists - therapeutic use | Animals | Renin-Angiotensin System - drug effects | Mice | Therapeutic Equivalency
Journal Article
Journal of the American College of Cardiology, ISSN 0735-1097, 11/2009, Volume 54, Issue 19, pp. 1747 - 1762
Heart failure is a syndrome characterized initially by left ventricular dysfunction that triggers countermeasures aimed to restore cardiac output. These... 
adrenergic receptor | beta-blockers | heart failure | sympathomimetic inotropes | sympatholytics | sympathetic nervous system | CARDIAC-INSUFFICIENCY BISOPROLOL | OBSTRUCTIVE SLEEP-APNEA | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | AUTONOMIC FUNCTION | RANDOMIZED CONTROLLED-TRIAL | DILATED CARDIOMYOPATHY | LEFT-VENTRICULAR DYSFUNCTION | BETA-BLOCKADE | POSITIVE AIRWAY PRESSURE | BETA-ADRENERGIC RECEPTOR | Receptors, Adrenergic, alpha-1 - metabolism | Sympathetic Nervous System - drug effects | Humans | Heart Failure - physiopathology | Adrenergic alpha-Antagonists - therapeutic use | Receptors, Adrenergic, beta-2 - drug effects | Sympathetic Nervous System - physiopathology | Sympatholytics - therapeutic use | Cardiotonic Agents - therapeutic use | Receptors, Adrenergic - genetics | Parasympathetic Nervous System - physiopathology | Digoxin - therapeutic use | Adrenergic beta-Antagonists - therapeutic use | Sympathomimetics - therapeutic use | Receptors, Adrenergic, alpha-1 - drug effects | Heart Failure - genetics | Heart Failure - metabolism | Receptors, Adrenergic, beta-2 - metabolism | Heart Failure - drug therapy | Polymorphism, Genetic | Randomized Controlled Trials as Topic | Parasympathetic Nervous System - drug effects | Exercise Tolerance | Renin-Angiotensin System - drug effects | Hemodynamics - drug effects | Proteins | Confidence intervals | Heart rate | Heart failure | Heart attacks | Rodents | Mortality | Hospitalization | Kinases | Beta blockers
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2016, Volume 311, Issue 4, pp. H871 - H880
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of... 
Heart failure | Brain | Sympathetic activity | Hypothalamic paraventricular nucleus | Mitogen-activated protein kinase | Subfornical organ | Endoplasmic reticulum stress | heart failure | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | INDUCED PHOSPHORYLATION | MYOCARDIAL-INFARCTION | ER STRESS | subfornical organ | KINASE | RATS | sympathetic activity | KAPPA-B | brain | endoplasmic reticulum stress | hypothalamic paraventricular nucleus | mitogen-activated protein kinase | UNFOLDED PROTEIN RESPONSE | PERIPHERAL VASCULAR DISEASE | UP-REGULATION | Cholagogues and Choleretics - pharmacology | Tumor Necrosis Factor-alpha - genetics | Heart Failure - physiopathology | Male | NF-KappaB Inhibitor alpha - genetics | Peptidyl-Dipeptidase A - drug effects | Interleukin-1beta - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Activating Transcription Factor 6 - genetics | Subfornical Organ - drug effects | Brain - metabolism | Heat-Shock Proteins - genetics | Inflammation - metabolism | Receptor, Angiotensin, Type 1 - genetics | Cyclooxygenase 2 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Signal Transduction | Rats | Cyclooxygenase 2 - drug effects | Heart Failure - metabolism | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Tumor Necrosis Factor-alpha - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Endoplasmic Reticulum Stress | Paraventricular Hypothalamic Nucleus - metabolism | Infusions, Intraventricular | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Interleukin-1beta - drug effects | Sympathetic Nervous System - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | X-Box Binding Protein 1 - drug effects | Sympathetic Nervous System - metabolism | Transcription Factor RelA - genetics | Activating Transcription Factor 6 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Taurochenodeoxycholic Acid - pharmacology | Peptidyl-Dipeptidase A - genetics | Renin-Angiotensin System | Receptor, Angiotensin, Type 1 - drug effects | RNA, Messenger - drug effects | Subfornical Organ - metabolism | Heat-Shock Proteins - drug effects | Activating Transcription Factor 4 - genetics | Activating Transcription Factor 4 - drug effects | NF-KappaB Inhibitor alpha - drug effects | Paraventricular Hypothalamic Nucleus - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Transcription Factor RelA - drug effects | X-Box Binding Protein 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Cellular signal transduction | Endoplasmic reticulum | Health aspects | Mitogen-activated protein kinases | Cardiovascular Neurohormonal Regulation
Journal Article
Current vascular pharmacology, ISSN 1570-1611, 2003
Journal
New drugs annual, cardiovascular drugs, ISSN 0742-387X, 1983
Journal
Journal of the National Cancer Institute, ISSN 0027-8874, 2012, Volume 104, Issue 2, pp. 93 - 113
With the advent of targeted agents for the treatment of renal cell carcinoma (RCC), overall survival has improved, and patients are being treated continuously... 
TYROSINE KINASE INHIBITORS | CONTROLLED-TRIAL | INTERFERON-ALPHA | SUNITINIB TREATMENT | CANCER-PATIENTS | VENOUS THROMBOEMBOLISM | ONCOLOGY | HEART-FAILURE | DOUBLE-BLIND | EXPANDED ACCESS PROGRAM | ENDOTHELIAL GROWTH-FACTOR | Niacinamide - analogs & derivatives | Hypothyroidism - chemically induced | Pneumonia - therapy | Anorexia - therapy | Humans | Drug Eruptions - therapy | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Kidney Neoplasms - metabolism | Phenylurea Compounds | Antineoplastic Agents - administration & dosage | Protein Kinase Inhibitors - adverse effects | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Weight Loss - drug effects | Benzenesulfonates - adverse effects | Bevacizumab | TOR Serine-Threonine Kinases - antagonists & inhibitors | Pyridines - adverse effects | Antineoplastic Agents - adverse effects | Pneumonia - chemically induced | Pyrroles - adverse effects | Antineoplastic Agents - pharmacology | Carcinoma, Renal Cell - drug therapy | Everolimus | Hypothyroidism - therapy | Wound Healing - drug effects | Molecular Targeted Therapy - methods | Sirolimus - adverse effects | Antibodies, Monoclonal, Humanized - adverse effects | Sirolimus - analogs & derivatives | Europe | Gastrointestinal Tract - drug effects | Cardiovascular System - drug effects | Evidence-Based Medicine | Carcinoma, Renal Cell - metabolism | Indoles - adverse effects | Pyrimidines - adverse effects | Sulfonamides - adverse effects | Anorexia - chemically induced | Kidney Neoplasms - drug therapy | Protein-Tyrosine Kinases - antagonists & inhibitors | Antimitotic agents | Drugs | Complications and side effects | Care and treatment | Adverse and side effects | Carcinoma, Renal cell | Research | Drug therapy | Antineoplastic agents
Journal Article
New cardiovascular drugs, ISSN 0891-3692, 1985
Journal
ACS Nano, ISSN 1936-0851, 02/2013, Volume 7, Issue 2, pp. 994 - 1005
Journal Article
Circulation Research, ISSN 0009-7330, 01/2017, Volume 120, Issue 1, pp. 229 - 243
The statins have been used for 30 years to prevent coronary artery disease and stroke. Their primary mechanism of action is the lowering of serum cholesterol... 
hydroxymethylglutaryl-CoA reductase inhibitors | rho-associated kinases | cardiovascular diseases | cholesterol, LDL | vascular diseases | CARDIAC & CARDIOVASCULAR SYSTEMS | CoA reductase inhibitors | ACTIVATED RECEPTOR-GAMMA | HIGH-DOSE ATORVASTATIN | NITRIC-OXIDE SYNTHASE | RHO-KINASE-ACTIVITY | HMG-COA REDUCTASE | hydroxymethylglutaryl | ACUTE CORONARY SYNDROMES | RANDOMIZED CONTROLLED-TRIAL | VASCULAR SMOOTH-MUSCLE | HUMAN ENDOTHELIAL-CELLS | LDL | cholesterol | PERIPHERAL VASCULAR DISEASE | PLACEBO-CONTROLLED TRIAL | HEMATOLOGY | Cardiovascular Diseases - physiopathology | Cardiovascular Diseases - drug therapy | Humans | Cholesterol, LDL - antagonists & inhibitors | Cardiovascular System - drug effects | Cardiovascular Diseases - genetics | Cholesterol, LDL - genetics | Cardiovascular System - physiopathology | Animals | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use | Clinical Trials as Topic - methods | Genetic Pleiotropy - genetics | Lipoproteins (low density) | Cell culture | GTP-binding protein | Reactive oxygen species | Liver | Cardiovascular disease | Post-translation | Heart diseases | Plaques | Statins | Cardiovascular system | NADPH-diaphorase | Cytokines | Coronary artery | Adenine | Inflammation | Low density lipoprotein | Cholesterol | Nitric-oxide synthase | Rho-associated kinase | Intermediates | Pleiotropy | Molecular modelling | Arteriosclerosis | Nitric oxide | Fibrosis | Hypertrophy
Journal Article