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Journal articles on the topic 'Ca++ antagonist'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Yoneyama, Fumiya, Keisuke Satoh, and Norio Taira. "SD-3211, a new non-dihydropyridine Ca-antagonist, is as vasoselective as dihydropyrldine Ca-antagonists." Japanese Journal of Pharmacology 52 (1990): 282. http://dx.doi.org/10.1016/s0021-5198(19)55670-0.

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2

Bkaily, Ghassan, Sanaa Choufani, Levon Avedanian, et al. "Nonpeptidic antagonists of ETA and ETB receptors reverse the ET-1-induced sustained increase of cytosolic and nuclear calcium in human aortic vascular smooth muscle cellsThis article is one of a selection of papers published in the special issue (part 2 of 2) on Forefronts in Endothelin." Canadian Journal of Physiology and Pharmacology 86, no. 8 (2008): 546–56. http://dx.doi.org/10.1139/y08-048.

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Our previous work showed that ET-1 induced a concentration-dependent increase of cytosolic Ca2+ ([Ca]c) and nuclear Ca2+ ([Ca]n) in human aortic vascular smooth muscle cells (hVSMCs). In the present study, using hVSMCs and 3-dimensional confocal microscopy coupled to the Ca2+ fluorescent probe Fluo-3, we showed that peptidic antagonists of ETA and ETB receptors (BQ-123 (10−6 mol/L) and BQ-788 (10−7 mol/L), respectively) prevented, but did not reverse, ET-1-induced sustained increase of [Ca]c and [Ca]n. In contrast, nonpeptidic antagonists of ETA and ETB (respectively, BMS-182874 (10−8–10−6 mol

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3

Conway, William S., Wojciech J. Janisiewicz, Joshua D. Klein, and Carl E. Sams. "Strategy for Combining Heat Treatment, Calcium Infiltration, and Biological Control to Reduce Postharvest Decay of `Gala' Apples." HortScience 34, no. 4 (1999): 700–704. http://dx.doi.org/10.21273/hortsci.34.4.700.

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The viability of Penicillium expansum Link conidia in sporulating culture declined rapidly when exposed to 38 °C, and when conidia were exposed to 38 °C prior to inoculation of apple fruits (Malus ×domestica Borkh.), the resulting lesions were smaller than those on fruit inoculated with nonheated conidia. `Gala' apples were heated after harvest (38 °C for 4 days), pressure infiltrated with a 2% solution of CaCl2, or treated with the antagonist Pseudomonas syringae van Hall, alone or in combinations to reduce postharvest decay caused by Penicillium expansum. After up to 6 months in storage at 1

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4

Page, Stephen J., Mingyan Zhu, and Suzanne M. Appleyard. "Effects of acute and chronic nicotine on catecholamine neurons of the nucleus of the solitary tract." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 316, no. 1 (2019): R38—R49. http://dx.doi.org/10.1152/ajpregu.00344.2017.

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Nicotine is an addictive drug that has broad effects throughout the brain. One site of action is the nucleus of the solitary tract (NTS), where nicotine initiates a stress response and modulates cardiovascular and gastric function through nicotinic acetylcholine receptors (nAChRs). Catecholamine (CA) neurons in the NTS influence stress and gastric and cardiovascular reflexes, making them potential mediators of nicotine’s effects; however nicotine’s effect on these neurons is unknown. Here, we determined nicotine’s actions on NTS-CA neurons by use of patch-clamp techniques in brain slices from

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5

Gilliam, F. R., P. A. Rivas, D. J. Wendt, C. F. Starmer, and A. O. Grant. "Extracellular pH modulates block of both sodium and calcium channels by nicardipine." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 4 (1990): H1178—H1184. http://dx.doi.org/10.1152/ajpheart.1990.259.4.h1178.

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Slowing of the recovery of the Na channel from local anesthetic block at low external pH has been well described. In contrast the Ca channel has been reported not to show such an effect. Because of the absence of this response, a two-site model for the interaction of Ca antagonists with the Ca channel has been proposed. We sought to determine whether these results were a consequence of utilizing the poorly lipid-soluble Ca antagonist diltiazem as the test drug. We have measured the time constants of recovery (tau r) of Na (INa) and Ca currents (ICa) recorded from rabbit atrial myocytes during

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6

BUSHI, KIMIHIKO. "Drug interaction of digitalis and Ca antagonist." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 24, no. 1 (1993): 237–38. http://dx.doi.org/10.3999/jscpt.24.237.

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7

HIRZEL, H. "Clinical profile of a Ca++-CaM-Antagonist." Journal of Molecular and Cellular Cardiology 19 (1987): S35. http://dx.doi.org/10.1016/s0022-2828(87)80111-6.

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8

Lamouche, Stéphane, and Nobuharu Yamaguchi. "Role of PAC1 receptor in adrenal catecholamine secretion induced by PACAP and VIP in vivo." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 2 (2001): R510—R518. http://dx.doi.org/10.1152/ajpregu.2001.280.2.r510.

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The present study was conducted to investigate the functional implication of the pituitary adenylate cyclase-activating polypeptide (PACAP) type I (PAC1) receptor in the adrenal catecholamine (CA) secretion induced by either PACAP-27 or vasoactive intestinal polypeptide (VIP) in anesthetized dogs. PACAP-27, VIP, and their respective antagonists were locally infused to the left adrenal gland via the left adrenolumbar artery. Plasma CA concentrations in adrenal venous and aortic blood were determined by means of a high-performance liquid chromatograph coupled with an electrochemical detector. Ad

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9

Janisiewicz, Wojciech J., William S. Conway, D. Michael Glenn, and Carl E. Sams. "Integrating Biological Control and Calcium Treatment for Controlling Postharvest Decay of Apples." HortScience 33, no. 1 (1998): 105–9. http://dx.doi.org/10.21273/hortsci.33.1.0105.

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Two nonfungicidal postharvest treatments and N fertility were evaluated for their effectiveness, singly and in combination, in controlling decay (“blue mold”) of apple (Malus ×domestica Borkh.) by Penicillium expansum Link. The antifungal treatments were biological control using the antagonist Pseudomonas syringae van Hall (isolate ESC-11 used in BioSave-11 and BioSave-110 products), and pressure infiltration of fruit with 0.27 M CaCl2. Fruit susceptibility to decay was evaluated using fruit after 3 and 6 months of storage over 2 years. Calcium infiltration resulted in a 3-fold increase in Ca

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10

Negulescu, P. A., and T. E. Machen. "Intracellular Ca regulation during secretagogue stimulation of the parietal cell." American Journal of Physiology-Cell Physiology 254, no. 1 (1988): C130—C140. http://dx.doi.org/10.1152/ajpcell.1988.254.1.c130.

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Intracellular [Ca] ([Ca]i) was measured following secretagogue stimulation of rabbit gastric glands loaded with the Ca-sensitive dye fura-2. Glands were mounted on cover slips and placed either in a perfused cuvette (for spectrofluorimetric measurements on whole glands) or in a chamber on the stage of a microscope (for microspectrofluorimetric measurements on single parietal cells within a gland). In parietal cells resting [Ca]i = 91 nM. Either histamine or carbachol caused [Ca]i to increase (spike) rapidly (within 5 s) to greater than 425 nM by releasing Ca from an intracellular store. The tw

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11

Islam, MS, T. Akhter, and M. Matsumoto. "Asterosap, an Egg Jelly Peptide, Elevate Intracellular Ca²⁺ and Activate the Motility of Spermatozoa." Progressive Agriculture 19, no. 1 (2013): 79–88. http://dx.doi.org/10.3329/pa.v19i1.17358.

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Components from the outer envelopes of the egg that influence the flagellar beating and acrosome reaction of spermatozoa are regulated by ion flux across the plasma membrane. Asterosap, a sperm-activating peptide from the starfish egg jelly layer, causes a transient increase in intracellular cyclic GMP (cGMP) through the activation of the asterosap receptor, a guanylyl cyclase (GC), and causes an increase in intracellular Ca2+. Here we describe the pathway of asterosap-induced Ca2+ elevation using different Ca2+ channel antagonists. Fluo-4 AM, a cell permeable Ca2+ sensitive dye was used to de

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12

Wang, Y. X., and M. I. Kotlikoff. "Muscarinic signaling pathway for calcium release and calcium-activated chloride current in smooth muscle." American Journal of Physiology-Cell Physiology 273, no. 2 (1997): C509—C519. http://dx.doi.org/10.1152/ajpcell.1997.273.2.c509.

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We investigated the muscarinic activation of Ca(2+)-activated Cl- currents [ICl(Ca)] in voltage-clamped equine tracheal myocytes. The threshold of cytosolic free Ca2+ concentration ([Ca2+]i) required for activation of ICl(Ca) was 202 +/- 22 nM, and full activation of the current occurred at 771 +/- 31 nM. Hexahydro-sila-difenidol (M3 antagonist) inhibited the methacholine-induced phasic [Ca2+]i increase and ICl(Ca) in a concentration-dependent manner, whereas methoctramine (M2 antagonist) only slightly attenuated the [Ca2+]i increase and ICl(Ca) (14.8 and 21.4%, respectively), consistent with

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13

Rank, M. M., K. C. Murray, M. J. Stephens, J. D'Amico, M. A. Gorassini, and D. J. Bennett. "Adrenergic Receptors Modulate Motoneuron Excitability, Sensory Synaptic Transmission and Muscle Spasms After Chronic Spinal Cord Injury." Journal of Neurophysiology 105, no. 1 (2011): 410–22. http://dx.doi.org/10.1152/jn.00775.2010.

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The brain stem provides most of the noradrenaline (NA) present in the spinal cord, which functions to both increase spinal motoneuron excitability and inhibit sensory afferent transmission to motoneurons (excitatory postsynaptic potentials; EPSPs). NA increases motoneuron excitability by facilitating calcium-mediated persistent inward currents (Ca PICs) that are crucial for sustained motoneuron firing. Spinal cord transection eliminates most NA and accordingly causes an immediate loss of PICs and emergence of exaggerated EPSPs. However, with time PICs recover, and thus the exaggerated EPSPs ca

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14

Dittel, B. N., D. B. Sant'Angelo, and C. A. Janeway. "Peptide antagonists inhibit proliferation and the production of IL-4 and/or IFN-gamma in T helper 1, T helper 2, and T helper 0 clones bearing the same TCR." Journal of Immunology 158, no. 9 (1997): 4065–73. http://dx.doi.org/10.4049/jimmunol.158.9.4065.

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Abstract Engagement of a TCR by its peptide Ag bound by MHC class II molecules leads to T cell activation, resulting in proliferation and cytokine production. This agonist response can be antagonized by analogue peptides containing single amino acid substitutions. We used T cell clones isolated from a mouse transgenic for the rearranged TCR alpha- and beta-chains of the D10.G4.1 (D10) Th2 clone specific for hen egg conalbumin peptide 134-146 (CA 134-146) to characterize antagonist peptides for the D10.TCR. The D10.TCR CD4 T cell clones proliferated in a dose-dependent manner to CA 134-146, and

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15

Saha, J. K., L. V. Hryshko, R. A. Bouchard, T. Chau, and D. Bose. "Analysis of the effects of (−) and (+) isomers of the 1,4-dihydropyridine calcium channel agonist BAY k 8644 on postrest potentiation in the canine ventricular muscle." Canadian Journal of Physiology and Pharmacology 67, no. 7 (1989): 788–94. http://dx.doi.org/10.1139/y89-125.

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Contraction of canine ventricular trabeculae were recorded at a stimulation frequency of 0.5 Hz and after rest periods of 2 and 8 min to analyze the effect of the Ca channel agonist BAY k 8644, on sarcoplasmic reticular function. Short periods of rest interposed between steady trains of stimuli caused a potentiation of the postrest beat. This is believed to be due to the mobilization of activator Ca from the sarcoplasmic reticulum (SR). Racemic BAY k 8644 and its Ca channel agonist enantiomer, (−) BAY k 8644, both produced an increase in contraction in response to a steady train of stimuli but

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16

Witte, David G., Steven C. Cassar, Jeffrey N. Masters, Timothy Esbenshade, and Arthur A. Hancock. "Use of a Fluorescent Imaging Plate Reader-Based Calcium Assay to Assess Pharmacological Differences between the Human and Rat Vanilloid Receptor." Journal of Biomolecular Screening 7, no. 5 (2002): 466–75. http://dx.doi.org/10.1177/108705702237679.

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The cloned vanilloid receptor 1 (VR1) is a ligand-gated calcium channel that is believed to be the capsaicin-activated vanilloid receptor found in native tissues, based on similarities regarding molecular mass, tissue distribution, and electrophysiological properties. Using a Fluorescent Imaging Plate Reader (FLIPR), along with Fluo-3 to signal intracellular calcium levels ([Ca++]i), rat VR1 (rVR1) and a human orthologue (hVR1) were pharmacologically characterized with various VR1 ligands. HEK-293 cells, stably expressing rVR1 or hVR1, exhibited dose-dependent increases in [Ca++]i when challen

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17

KAWAGOE, Reiko, Hiroyuki MINO, and Akira TAKEUCHI. "Effects of organic Ca antagonist, diltiazem, on neuromuscular transmission." Japanese Journal of Physiology 40, no. 3 (1990): 325–36. http://dx.doi.org/10.2170/jjphysiol.40.325.

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18

Takahashi, Kenzo, Satomi Kishi, Noriyuki Miyata, et al. "Cardiovascular effects of a novel Ca antagonist, CD-832." Japanese Journal of Pharmacology 58 (1992): 400. http://dx.doi.org/10.1016/s0021-5198(19)49693-5.

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19

BELZ, G. "Fendiline: Clinical pharmacological profile of a Ca++-CaM-antagonist." Journal of Molecular and Cellular Cardiology 19 (1987): S5. http://dx.doi.org/10.1016/s0022-2828(87)80021-4.

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20

MORICHIKA, KOH, TAKAYUKI HASHIMOTO, MASAKO KUSANO, KUNIAKI INAMI, and TAKAO KURAMOTO. "Reflux esophagitis caused by Ca antagonist in the elderly." Juntendo Medical Journal 46, no. 1 (2000): 78–83. http://dx.doi.org/10.14789/pjmj.46.78.

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21

Khan, Hidayat-Ullah, Irshad Ali, Arif-Ullah Khan, Rubina Naz, and Anwarul Hassan Gilani. "Antibacterial, antifungal, antispasmodic and Ca++antagonist effects ofCaesalpinia bonducella." Natural Product Research 25, no. 4 (2011): 444–49. http://dx.doi.org/10.1080/14786419.2010.529445.

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22

Corsano, Stefano, Giovannella Strappaghetti, Elsa Di Domenico, Livio Brasili, and Maria Teresa Picchio. "Synthesis and Ca-Antagonist Activity of Some Benzhydryl Derivatives." Archiv der Pharmazie 322, no. 12 (1989): 873–78. http://dx.doi.org/10.1002/ardp.19893221207.

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23

Utami, Mellati Dian, Ana Medawati, and Bella Pardian Nur Alifiah. "Correlation of Antihypertensive Drugs Ca-Antagonist Amlodipine with Xerostomia." PROCEEDING IMPROVE QUALITY IN DENTISTRY 1, no. 1 (2024): 138–42. http://dx.doi.org/10.18196/imunity.v1i1.22.

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Xerostomia is defined as a subjective complaint of dry mouth. Interestingly, patients complaining of dry mouth often have no objective signs of decreased salivation and their symptoms vary. May be secondary to qualitative and/or quantitative factors. changes in the composition of saliva. Normal stimulated salivary flow averages 1.5-2.0 ml/min while unstimulated salivary flow is about 0, 3-0.4 ml/min. This review aimed to determine the correlation between the Ca antagonist of the antihypertensive drug (Amlodipine) and xerostomia through a literature review conducted by researchers which was use

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24

Müller, Wolfgang, Uwe Heinemann, and Karin Berlin. "Cholecystokinin Activates CCKB-Receptor–Mediated Ca-Signaling in Hippocampal Astrocytes." Journal of Neurophysiology 78, no. 4 (1997): 1997–2001. http://dx.doi.org/10.1152/jn.1997.78.4.1997.

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Müller, Wolfgang, Uwe Heinemann, and Karin Berlin. Cholecystokinin activates CCKB-receptor–mediated Ca-signaling in hippocampal astrocytes. J. Neurophysiol. 78: 1997–2001, 1997. Cholecystokinin-8S (CCK-8S) is the most abundant neuropeptide in the mammalian cortex and the limbic system; however, its physiological functions remained largely obscure. We studied effects of CCK on astrocytic Ca signaling, which has met considerable interest as a second messenger in astrocytic-neuronal signaling, by digital ratio-imaging of Fura-2/AM loaded rat and mouse hippocampal astrocytes in dissociated culture

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25

Liu, Shi J., та Richard H. Kennedy. "α1-Adrenergic activation of L-type Ca current in rat ventricular myocytes: perforated patch-clamp recordings". American Journal of Physiology-Heart and Circulatory Physiology 274, № 6 (1998): H2203—H2207. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h2203.

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α1-Adrenergic stimulation has little effect on L-type Ca2+channel current ( I Ca,L) in adult cardiac myocytes measured using conventional whole cell voltage-clamp techniques. In this study using perforated-patch techniques, we reevaluated the effect of α1-adrenergic stimulation on I Ca,L in adult rat ventricular myocytes. Action potentials and I Ca,L were examined in the presence of 1 μM nadolol, a β-adrenergic antagonist, in myocytes internally dialyzed with Na+- and K+-free solutions (Cs+ and tetraethylammonium as substitutes). Phenylephrine (PE; 30 μM) increased the action potential duratio

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26

Newsholme, P., A. A. Adogu, M. A. Soos, and C. N. Hales. "Complement-induced Ca2+ influx in cultured fibroblasts is decreased by the calcium-channel antagonist nifedipine or by some bivalent inorganic cations." Biochemical Journal 295, no. 3 (1993): 773–79. http://dx.doi.org/10.1042/bj2950773.

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The effects of different extracellular cations or organic Ca(2+)-channel modulators on complement-induced changes in intracellular Ca2+ and cell death have been investigated in the transfected NIH-3T3 HIR 3.5 cell line, which overexpresses the human insulin receptor. Cells were incubated with mouse anti-(human insulin receptor) monoclonal antibodies before exposure to rabbit or human serum (sources of heterologous complement). Changes in intracellular Ca2+ were complement-dependent (measured by influx of 45Ca), as was cytotoxicity (monitored by leakage of lactate dehydrogenase into the culture

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27

Frerichs, Kai U., Perttu J. Lindsberg, John M. Hallenbeck, and Giora Z. Feuerstein. "Platelet-activating factor and progressive brain damage following focal brain injury." Journal of Neurosurgery 73, no. 2 (1990): 223–33. http://dx.doi.org/10.3171/jns.1990.73.2.0223.

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✓ The effects of a platelet-activating factor (PAF) antagonist on brain edema, cortical microcirculation, blood-brain barrier (BBB) disruption, and neuronal death following focal brain injury are reported. A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser was used to induce highly reproducible focal cortical lesions in anesthetized rats. Secondary brain damage in this model was characterized by progressive cortical hypoperfusion, edema, and BBB disruption in the vicinity of the hemispheroid lesion occurring acutely after injury. The histopathological evolution was followed for up to 4 days. N

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28

Tiwari-Woodruff, S. K., and T. C. Cox. "Boar sperm plasma membrane Ca(2+)-selective channels in planar lipid bilayers." American Journal of Physiology-Cell Physiology 268, no. 5 (1995): C1284—C1294. http://dx.doi.org/10.1152/ajpcell.1995.268.5.c1284.

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Entry of Ca2+ through Ca2+ channels is thought to trigger the acrosome reaction of spermatozoa during fertilization. Antagonists of the L-type Ca2+ channel are known to prevent the intracellular Ca2+ (Ca2+) increase and inhibit acrosomal exocytosis in mammalian sperm. Planar bilayer recordings were used to study Ca2- channels incorporated from partially purified boar sperm plasma membranes. With symmetrical 50 mM NaCl and 100 mM BaCl2 on the cis side, single-channel events consistent with Ba2+ flux from cis to trans were observed. These channels were activated by the dihydropyridine agonist (+

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29

Kasai, H., T. Aosaki та J. Fukuda. "Presynaptic Ca-antagonist ω-conotoxin irreversibly blocks N-type Ca-channels in chick sensory neurons". Neuroscience Research Supplements 4, № 3 (1987): 228–35. http://dx.doi.org/10.1016/s0921-8696(87)80021-x.

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Kasai, H., T. Aosaki та J. Fukuda. "Presynaptic Ca-antagonist ω-conotoxin irreversibly blocks N-type Ca-channels in chick sensory neurons". Neuroscience Research 4, № 3 (1987): 228–35. http://dx.doi.org/10.1016/0168-0102(87)90014-9.

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31

POTT, L., and P. LIPP. "Dual effect of the Ca++ calmodulin antagonist fendiline on Ca current in single cardiac cells." Journal of Molecular and Cellular Cardiology 19 (1987): S75. http://dx.doi.org/10.1016/s0022-2828(87)80233-x.

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32

Almaraz, L., M. T. Perez-Garcia, A. Gomez-Nino, and C. Gonzalez. "Mechanisms of alpha2-adrenoceptor-mediated inhibition in rabbit carotid body." American Journal of Physiology-Cell Physiology 272, no. 2 (1997): C628—C637. http://dx.doi.org/10.1152/ajpcell.1997.272.2.c628.

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We have used the in vitro preparation of the intact carotid body (CB) and isolated chemoreceptor cells to elucidate the distribution and function of alpha2-adrenoreceptors. The significance of the study lies in the fact that norepinephrine (NE), being the neurotransmitter of the sympathetic innervation to the CB, is also abundant in chemoreceptor cells. In intact CB whose catecholamine (CA) deposits had been labeled by prior incubation with the CA precursor [3H]tyrosine, the alpha2-antagonist yohimbine (10 microM) potentiated the low-PO2 (33 and 60 mmHg)-induced release of [3H]CA by 100 and 53

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33

Crossley, I., T. Whalley, and M. Whitaker. "Guanosine 5'-thiotriphosphate may stimulate phosphoinositide messenger production in sea urchin eggs by a different route than the fertilizing sperm." Cell Regulation 2, no. 2 (1991): 121–33. http://dx.doi.org/10.1091/mbc.2.2.121.

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We show that microinjecting guanosine-5'-thiotriphosphate (GTP gamma S) into unfertilized sea urchin eggs generates an intracellular free calcium concentration [( Ca]i) transient apparently identical in magnitude and duration to the calcium transient that activates the egg at fertilization. The GTP gamma S-induced transient is blocked by prior microinjection of the inositol trisphosphate (InsP3) antagonist heparin. GTP gamma S injection also causes stimulation of the egg's Na+/H+ antiporter via protein kinase C, even in the absence of a [Ca]i increase. These data suggest that GTP gamma S acts

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Konteatis, Z. D., S. J. Siciliano, G. Van Riper, et al. "Development of C5a receptor antagonists. Differential loss of functional responses." Journal of Immunology 153, no. 9 (1994): 4200–4205. http://dx.doi.org/10.4049/jimmunol.153.9.4200.

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Abstract C5a is a 74-amino acid glycoprotein generated on activation of the C system. The responses evoked by C5a, both in vitro and in vivo, and its association with inflammatory diseases, suggest that a receptor antagonist would be of considerable therapeutic importance. However, efforts at generating antagonists have so far been unsuccessful. Structure/activity studies of the C terminus of C5a have generated peptide analogues with nanomolar affinities, but all of these retain strong agonist properties. We now report hexapeptides of the form NMePhe-Lys-Pro-dCha-X-dArg in which increasing aro

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35

Taner, C. Burcin, Sandra R. Severson, Patricia J. M. Best, Amir Lerman, and Virginia M. Miller. "Treatment with endothelin-receptor antagonists increases NOS activity in hypercholesterolemia." Journal of Applied Physiology 90, no. 3 (2001): 816–20. http://dx.doi.org/10.1152/jappl.2001.90.3.816.

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In experimental hypercholesterolemia, endothelium-dependent relaxations decrease, as does endothelial immunoreactivity for nitric oxide (NO) synthase (NOS; eNOS) in coronary arteries. Systemic levels of NO also decrease with concomitant elevations in systemic circulating levels of endothelin (ET)-1. Chronic treatment of hypercholesterolemic pigs with ET-receptor antagonists increases circulating NO and improves endothelium-dependent relaxations. Mechanisms causing these increases are not known. Therefore, experiments were designed to test the hypothesis that chronic administration of ET-recept

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36

KUMAGAI, YUJI. "Phase I study of a new Ca antagonist, SN305(lacidipine)." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 22, no. 1 (1991): 49–50. http://dx.doi.org/10.3999/jscpt.22.49.

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37

ISHIKAWA, TOMOKO. "Drug interaction of digitalis and Ca antagonist (NZ-105,verapamil)." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 23, no. 1 (1992): 117–18. http://dx.doi.org/10.3999/jscpt.23.117.

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38

HASHIMOTO, YASUAKI. "Effects of Dihydropyridine system Ca antagonist on pharmacokinetics of Digoxin." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 27, no. 1 (1996): 245–46. http://dx.doi.org/10.3999/jscpt.27.245.

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39

Karasawa, Akira, Kazuhiro Kubo, Katsuichi Shuto, and Nobuhiro Nakamizo. "Antianginal effects of KW 3049, a new dihydropyridine Ca-antagonist." Japanese Journal of Pharmacology 39 (1985): 291. http://dx.doi.org/10.1016/s0021-5198(19)63745-5.

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40

SALIMBENI, A. "LR-A/113 binding affinity profile for Ca-antagonist sites." Pharmacological Research 26 (September 1992): 175. http://dx.doi.org/10.1016/1043-6618(92)91059-p.

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41

Park, Eun Jung, Jihyun Je, Theodomir Dusabimana, et al. "Mineralocorticoid Receptor Antagonism Attenuates Multiple Organ Failure after Renal Ischemia and Reperfusion in Mice." International Journal of Molecular Sciences 24, no. 4 (2023): 3413. http://dx.doi.org/10.3390/ijms24043413.

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Renal ischemia reperfusion (IR) injury is a major cause of acute kidney injury (AKI) that is often complicated by multiple organ failure of the liver and intestine. The mineralocorticoid receptor (MR) is activated in patients with renal failure associated with glomerular and tubular damage. We thus investigated whether canrenoic acid (CA), a mineralocorticoid receptor (MR) antagonist, protects against AKI-induced hepatic and intestinal injury, suggesting the underlying mechanisms. Mice were divided into five groups: sham mice, mice subjected to renal IR, and mice pretreated with canrenoic acid

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Cai, Rong, and Caroline Ajo-Franklin. "Towards Sensing of Breast Cancer Biomarkers: Engineering Glucose Dehydrogenase As an Estrogenic Regulated Protein." ECS Meeting Abstracts MA2022-02, no. 61 (2022): 2227. http://dx.doi.org/10.1149/ma2022-02612227mtgabs.

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Breast cancer is the second leading cause of cancer-related death in women. Approximately 50% of mortalities arise from estrogen receptor (ER)-positive tumors.[1] The major therapeutics for breast cancer are estrogen antagonists, like tamoxifen. Closely monitoring the antagonist in a patient would increase the efficacy of endocrine therapeutics while alleviating side effects during treatment. However, existing methods such as routine immunohistochemistry cannot effectively monitor estrogen antagonists because of their low throughput and high cost. To address these issues, we have devised a bio

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Valdivia, H. H., and R. Coronado. "Internal and external effects of dihydropyridines in the calcium channel of skeletal muscle." Journal of General Physiology 95, no. 1 (1990): 1–27. http://dx.doi.org/10.1085/jgp.95.1.1.

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The agonist effect of the dihydropyridine (DHP) (-)Bay K 8644 and the inhibitory effects of nine antagonist DHPs were studied at a constant membrane potential of 0 mV in Ca channels of skeletal muscle transverse tubules incorporated into planar lipid bilayers. Four phenylalkylamines (verapamil, D600, D575, and D890) and d-cis-diltiazem were also tested. In Ca channels activated by 1 microM Bay K 8644, the antagonists nifedipine, nitrendipine, PN200-110, nimodipine, and pure enantiomer antagonists (+)nimodipine, (-)nimodipine, (+)Bay K 8644, inhibited activity in the concentration range of 10 n

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Goyal, Ravi, Ashwani Mittal, Nina Chu, Lubo Zhang та Lawrence D. Longo. "α1-Adrenergic receptor subtype function in fetal and adult cerebral arteries". American Journal of Physiology-Heart and Circulatory Physiology 298, № 6 (2010): H1797—H1806. http://dx.doi.org/10.1152/ajpheart.00112.2010.

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In the developing fetus, cerebral artery (CA) contractility demonstrates significant functional differences from that of the adult. This may be a consequence of differential activities of α1-adrenergic receptor (α1-AR) subtypes. Thus we tested the hypothesis that maturational differences in adrenergic-mediated CA contractility are, in part, a consequence of differential expression and/or activities of α1-AR subtypes. In CA from fetal (∼140 days) and nonpregnant adult sheep, we used wire myography and imaging, with simultaneous measurement of tension and intracellular Ca2+ concentration ([Ca2+]

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SUDO, TOSHIAKI. "Effect of diltiazem on the pharmacodynamics of Ca antagonist, MPC-1304." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 22, no. 1 (1991): 43–44. http://dx.doi.org/10.3999/jscpt.22.43.

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TSUKIYAMA, KYUICHIRO. "Effects of Ca antagonist Lacidipine on circulatory dynamics in essential hypertension." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 24, no. 1 (1993): 139–40. http://dx.doi.org/10.3999/jscpt.24.139.

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Asano, T., and H. Hidaka. "Intracellular Ca++ antagonist, HA1004: pharmacological properties different from those of nicardipine." Journal of Pharmacology and Experimental Therapeutics 233, no. 2 (1985): 454–58. https://doi.org/10.1016/s0022-3565(25)21253-8.

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Kubo, Kazuhiro, Akira Karasawa, Katsuichi Shuto, and Nobuhiro Nakamizo. "Antihypertensive effects of a novel dihydropyridine-type Ca antagonist, KW-3049." Japanese Journal of Pharmacology 39 (1985): 217. http://dx.doi.org/10.1016/s0021-5198(19)63599-7.

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Shehyan, G. G., A. A. Yalymov, V. S. Zadionchenko, and S. I. Varentsov. "Application of lercanidipine in the treatment of hypertension." CardioSomatics 5, no. 2 (2014): 46–50. http://dx.doi.org/10.26442/cs45099.

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The article presents data from clinical trials that have examined the efficacy and safety of modern calcium antagonist (CA) III generation of lercanidipine. The results of studies show that treatment with lercanidipine leads to a marked reduction in systolic and diastolic blood pressure without significant effect on heart rate. Unique pharmacokinetic characteristics of the drug provide its excellent efficacy and safety, good tolerability, convenience, acceptance and high adherence CA data in patients with hypertension. Additional properties of lercanidipine allow us to recommend the use of the

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Kojima, Toshiyuki, Yuji Imaizumi, and Minoru Watanabe. "Effect of Ca antagonist and calmodulin inhibitor on Ca-dependent K channels in isolated smooth muscle cells." Japanese Journal of Pharmacology 40 (1986): 242. http://dx.doi.org/10.1016/s0021-5198(19)59471-9.

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