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Circulation research, ISSN 0009-7330, 02/2007, Volume 100, Issue 3, pp. 342 - 353
A large body of evidence has accrued indicating that voltage-gated Ca channel subtypes, including L-, T-, N-, and P/Q-type, are present within renal vascular... 
Renal microcirculation | Mibefradil | channels | Afferent arteriole | channel blockers | Efferent arteriole | Renal disease | Voltage-dependent Ca | Efonidipine | Ca | Ca2+ channel blockers | N-TYPE | CARDIAC & CARDIOVASCULAR SYSTEMS | EFFERENT ARTERIOLES | efonidipine | SPONTANEOUSLY HYPERTENSIVE-RATS | RHO-KINASE INHIBITOR | renal microcirculation | ANGIOTENSIN-II | T-TYPE | renal disease | mibefradil | DEPENDENT CALCIUM-CHANNELS | CARDIAC L-TYPE | RENAL MICROVASCULAR CONSTRICTION | efferent arteriole | voltage-dependent Ca2+ channels | PERIPHERAL VASCULAR DISEASE | afferent arteriole | HEMATOLOGY | IN-VIVO VISUALIZATION | Arterioles - physiology | Kidney - physiology | Protein Subunits | Antihypertensive Agents - pharmacology | Kidney - blood supply | Humans | Calcium Channel Blockers - therapeutic use | Hypertension - drug therapy | Antihypertensive Agents - classification | Calcium Channels - physiology | Calcium Channels, T-Type - chemistry | Neurotransmitter Agents - secretion | Calcium Channels - drug effects | Calcium Channels, N-Type - drug effects | Cardiovascular Diseases - physiopathology | Kidney - drug effects | Calcium Channels - classification | Rats | Calcium Channels, L-Type - physiology | Antihypertensive Agents - therapeutic use | Arterioles - drug effects | Disease Progression | Antihypertensive Agents - adverse effects | Mice, Knockout | Calcium Signaling - drug effects | Diabetes Mellitus - physiopathology | Models, Biological | Calcium Channels - chemistry | Calcium Channels, T-Type - drug effects | Mice | Vasodilation - drug effects | Hydronephrosis - physiopathology | Calcium Channel Blockers - adverse effects | Calcium Signaling - physiology | Cardiovascular Diseases - drug therapy | Renal Circulation - physiology | Microcirculation - drug effects | Microcirculation - physiology | Renal Circulation - drug effects | Blood Pressure - drug effects | Calcium Channels, L-Type - chemistry | Kidney Diseases - metabolism | Calcium Channels, T-Type - physiology | Renin - secretion | Aldosterone - physiology | Kidney Diseases - drug therapy | Renin-Angiotensin System - physiology | Calcium Channel Blockers - pharmacology | Hypertension - physiopathology | Animals | Calcium Channels, L-Type - drug effects | Calcium Channels, N-Type - physiology | Calcium Channels, N-Type - chemistry
Journal Article
American journal of physiology. Lung cellular and molecular physiology, ISSN 1040-0605, 07/2013, Volume 305, Issue 2, pp. L154 - L164
Journal Article
Nature (London), ISSN 1476-4687, 2010, Volume 468, Issue 7324, pp. 696 - 700
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2018, Volume 13, Issue 12, pp. e0209363 - e0209363
One of the pathological site effects in excitotoxic activation is Zn2+ overload to postsynaptic neurons. Such an effect is considered to be equivalent to the... 
ACETYL-COA | INHIBITION | NEURONAL DEATH | MULTIDISCIPLINARY SCIENCES | ZN2+ TOXICITY | ISOCITRATE DEHYDROGENASE | NITRIC-OXIDE | CA2+ CHANNEL | GLUCOSE DEPRIVATION | NEUROTOXICITY | ACETYLCHOLINE METABOLISM | Cell Survival - drug effects | Nifedipine - pharmacology | Calcium - metabolism | Cholinergic Neurons - metabolism | Zinc - metabolism | Mitochondria - metabolism | Cholinergic Neurons - drug effects | Calcium Channel Blockers - pharmacology | Calcium Channels, N-Type - metabolism | Animals | Cations, Divalent - metabolism | Cell Line, Tumor | Neurotoxins - metabolism | Mice | Calcium Channels, L-Type - metabolism | Energy Metabolism - drug effects | Neuroblastoma - pathology | Antimitotic agents | Calcium channels | Physiological aspects | Genetic aspects | Research | Neuroblastoma | Drug therapy | Antineoplastic agents | Tricarboxylic acid cycle | Oxidative stress | Calcium antagonists | Cell culture | Dehydrogenases | Calcium | Laboratories | Toxicity | Homeostasis | Pyruvic acid | Antagonists | Dehydrogenase | Depolarization | Neurotoxicity | Mitochondria | Neurodegeneration | Calcium channel blockers | NADP-isocitrate dehydrogenase | Oxidation | NADP | Isocitrate dehydrogenase | Calcium homeostasis | Glutathione | Enzymes | Neurons | Shortages | Calcium channels (voltage-gated) | Pyruvate dehydrogenase (lipoamide) | Gene expression | Zinc | Malondialdehyde | Nifedipine | Medicine | Excitotoxicity | Calcium channels (L-type) | Axonal transport | ATP | Index Medicus
Journal Article
Investigational new drugs, ISSN 0167-6997, 02/2017, Volume 35, Issue 3, pp. 1 - 10
Introduction This was an open-label, dose escalation (3 + 3 design), Phase I study of SOR-C13 in patients with advanced tumors of epithelial origin. Primary... 
Oncology | TRPV6 | Sor-C13 | Calcium channel | SURVIVAL | CELLS | CAT1 | BREAST-CANCER | RECEPTOR POTENTIAL CHANNELS | PLASMA | PROSTATE-CANCER | TARGETS | PHARMACOLOGY & PHARMACY | EXPRESSION | Neoplasms - metabolism | TRPV Cation Channels - pharmacokinetics | Calcium Channel Blockers - adverse effects | Humans | Middle Aged | Peptides - pharmacokinetics | Calcium Channel Blockers - therapeutic use | Male | Alanine Transaminase - blood | Antineoplastic Agents - therapeutic use | Hypocalcemia - chemically induced | Antineoplastic Agents - adverse effects | TRPV Cation Channels - antagonists & inhibitors | Hypokalemia - chemically induced | TRPV Cation Channels - pharmacology | Adult | Female | Antineoplastic Agents - pharmacokinetics | Antineoplastic Agents - pharmacology | Keratin-18 - blood | Calcium Channels - genetics | Headache - chemically induced | TRPV Cation Channels - therapeutic use | Treatment Outcome | Calcium Channel Blockers - pharmacology | TRPV Cation Channels - genetics | Neoplasms - drug therapy | Peptides - pharmacology | Maximum Tolerated Dose | TRPV Cation Channels - adverse effects | RNA, Messenger - blood | Aspartate Aminotransferases - blood | Urticaria - chemically induced | Aged | Calcium Channel Blockers - pharmacokinetics | Peptides - adverse effects | Peptides - therapeutic use | Antimitotic agents | Calcium channels | Physiological aspects | Genetic aspects | Research | Drug therapy | Antineoplastic agents | Tumors | Headache | Terminology | Calcium | Toxicity | Criteria | Anticancer properties | Infusion | Reduction | Fibrillation | Vitamin D | Quality | Hypokalemia | Supplementation | Pancreas | Drug dosages | Hypocalcemia | Alanine | Pharmacodynamics | Anemia | Urticaria | Pharmacology | Patients | Studies | Alanine transaminase | Antitumor activity | Aspartate aminotransferase | Solid tumors | Pharmacokinetics | Index Medicus | Phase I Studies
Journal Article
The Journal of neuroscience, ISSN 1529-2401, 2004, Volume 24, Issue 26, pp. 5922 - 5930
We used a model system in which dopaminergic (DA) neurons from embryonic rat mesencephalon undergo spontaneous and selective degeneration as they develop in... 
Excitability | GDNF | Sodium | Channel | Trophic | Dopaminergic | TYROSINE-HYDROXYLASE | POTASSIUM CHANNELS | NEUROTROPHIC FACTOR | channel | trophic | NEUROSCIENCES | sodium | CYCLIC-AMP | excitability | CALCIUM-CHANNELS | SIGNALING PATHWAY | MEMBRANE-PROPERTIES | CENTRAL-NERVOUS-SYSTEM | dopaminergic | SMALL-CONDUCTANCE | PARKINSONS-DISEASE | Mesencephalon - cytology | Sodium-Potassium-Exchanging ATPase - physiology | Rats, Wistar | Apoptosis - drug effects | gamma-Aminobutyric Acid - metabolism | Cells, Cultured - cytology | Neurons - cytology | Sodium Channels - physiology | Apamin - pharmacology | Nerve Growth Factors - pharmacology | Neuroprotective Agents - pharmacology | Glial Cell Line-Derived Neurotrophic Factor | Ion Transport - drug effects | Neurons - metabolism | Aspirin - pharmacology | Tetrodotoxin - pharmacology | Neurons - drug effects | Dopamine - metabolism | Ouabain - pharmacology | Potassium Channel Blockers - pharmacology | Sodium - pharmacology | Cells, Cultured - drug effects | Nerve Tissue Proteins - physiology | Nifedipine - pharmacology | Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors | Biological Transport, Active - drug effects | Rats | Sodium Channel Blockers - pharmacology | Sodium Channels - drug effects | Calcium Channel Blockers - pharmacology | Nerve Tissue Proteins - drug effects | Veratridine - pharmacology | Scorpion Venoms - pharmacology | Animals | Calcium Channels, T-Type - drug effects | Serotonin - metabolism | Calcium Channel Agonists - pharmacology | Cells, Cultured - metabolism | Potassium Channels, Calcium-Activated - antagonists & inhibitors | Ion Channel Gating | Sodium - physiology | Tetrodotoxin | Neuroprotective Agents | Veratridine | Mesencephalon | Neurons and Cognition | Ouabain | Calcium Channel Agonists | Calcium Channels, T-Type | Potassium Channels, Calcium-Activated | Life Sciences | Biological Transport, Active | Sodium-Potassium-Exchanging ATPase | Ion Transport | Potassium Channel Blockers | gamma-Aminobutyric Acid | Aspirin | Apamin | Dopamine | Serotonin | Neurons | Sodium Channels | Cells, Cultured | Nerve Tissue Proteins | Nifedipine | Scorpion Venoms | Calcium Channel Blockers | Nerve Growth Factors | Sodium Channel Blockers | Apoptosis | Plasticity | Development | Repair
Journal Article
11.