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Abnormalities of the Calcium Pump in Primary Hypertension
Published in Antonio Coca, Ricardo P. Garay, Ionic Transport in Hypertension: New Perspectives, 2019
Alejandro De la Sierra, Javier Sobrino, Antonio Coca
Contraction of the smooth muscle cells begins with the opening of voltage-operated and receptor-operated calcium channels, located in the cell membrane and in the sarcoplasmic reticulum. All this results in the increase of free cytosolic Ca2+ content. Calcium acts on the contractile proteins of the smooth muscle (actin and myosin) that change their spatial conformation, interacting with each other to cause the cell contraction.
Pharmacological Treatment Approaches
Published in Andrea Kohn Maikovich-Fong, Handbook of Psychosocial Interventions for Chronic Pain, 2019
Catherine G. Derington, David K. Choi, Katy E. Trinkley
Once the central nervous system receives a pain signal, several receptors can modulate how the body processes and perceives the signal, including calcium, opioid, glutamate, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl-D-aspartate (NMDA), gamma-aminobutyric acid (GABA), sodium, serotonin, and norepinephrine receptors. Calcium channels at the end of nerves stimulate the release of specific neurotransmitters to act on other nerves. The binding of opioids to opioid receptors prevents the nerve from continuing pain transmission by blocking calcium channel action. The binding of glutamate to glutamate, AMPA, and NMDA receptors excites nerves and stimulates the nerve to continue pain processing. Conversely, blocking sodium channels and/or promoting the action of GABA, serotonin, and norepinephrine inhibit the transmission and processing of pain signals.
Basic pharmacology of cardiac drugs
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
While there are calcium channels in all types of muscle, those in skeletal muscle do not play a major role in triggering contraction. Organic calcium channel antagonists therefore tend to exhibit clinical effects only on cardiac and smooth muscle. Furthermore, there are major differences between calcium antagonists in terms of their relative selectivity for myocardium and for vascular smooth muscle. For example, on a scale that rates verapamil as having roughly equal effects on both muscle types, diltiazem exhibits approximately nine times more effect on vascular smooth muscle than on myocardium, nifedipine approximately twenty times more vascular selectivity, and felodipine (another dihydropyridine) is over one hundred times more vascular-selective.
The effect of the calcium channel blocker nimodipine on hippocampal BDNF/Ach levels in rats with experimental cognitive impairment
Published in Neurological Research, 2023
Atilla Topcu, Sinan Saral, Aykut Ozturk, Ozlem Saral, Ali Koray Kaya
Calcium channels are responsible for numerous functions in the central nervous system. A previous study showed that calcium channels mediate experimentally induced neurodegeneration [24]. Nimodipine is a dihydropyridine-derivative calcium channel blocker used in aneurysmal subarachnoid hemorrhage due to the vasoselectivity it exhibits in the cerebral vessels [25,26]. Previous experimental studies have confirmed the neuroprotective effects of nimodipine [27,28]. Koskimaki et al. revealed that nimodipine is capable of somehow activating synaptic plasticity in experimentally induced brain trauma [29]. That study revealed the effect of nimodipine on the BDNF-TrkB signaling pathway. It may thus be concluded that nimodipine administration may be beneficial in reversing impaired cognitive function through its regulatory effects on the BDNF-TrkB and CREB signaling pathways [30].
Solanaceae glycoalkaloids: α-solanine and α-chaconine modify the cardioinhibitory activity of verapamil
Published in Pharmaceutical Biology, 2022
Szymon Chowański, Magdalena Winkiel, Monika Szymczak-Cendlak, Paweł Marciniak, Dominika Mańczak, Karolina Walkowiak-Nowicka, Marta Spochacz, Sabino A. Bufo, Laura Scrano, Zbigniew Adamski
Calcium ions play a crucial role in muscle contractions, and therefore, L-type calcium channels that move Ca2+ ions inward and trigger calcium release from the sarcoplasmic reticulum by activating the ryanodine receptor 2 (Striessnig et al. 2014) are just as important. Dysregulation of L-type Ca2+ channels is the basis of numerous cardiac disorders; therefore, they are also a common target in various therapies for cardiovascular diseases. L-type Ca2+ channel blockers, such as verapamil, are commonly used to treat hypertension, myocardial ischaemia, and arrhythmias (Limpitikul et al. 2018). The so-called α1 subunit forms the core of voltage-sensitive L-type Ca2+ channels. It associates with other subunits (β, α2δ, γ) to form heterooligomeric complexes. The β and α2/δ subunits are tightly but not covalently bound to the α1 subunit and modulate the biophysical properties and trafficking of the α1 subunit to the membrane (Bodi et al. 2005). The presence of L-type Ca2+ channels were also confirmed in the myocardium of Drosophila melanogaster (Limpitikul et al. 2018) and Musca domestica (Grabner et al. 1994). This tissue builds the dorsal vessel of the insect, traditionally called the heart. Even if not anatomically, the insect heart functionally and developmentally resembles the embryonic vertebrate heart. Thus, it offers an attractive alternative for studies conducted on mammals. Furthermore, many analyses can be performed in vivo without the need to sacrifice the test animal (Limpitikul et al. 2018).
Current and promising therapeutic options for Dravet syndrome
Published in Expert Opinion on Pharmacotherapy, 2022
Antonella Riva, Gianluca D’Onofrio, Elisabetta Amadori, Domenico Tripodi, Ganna Balagura, Valentina Iurilli, Maria Stella Vari, Alberto Verrotti, Pasquale Striano
Another drug repurposed for its possible anti-seizure effect is verapamil, a voltage-gated calcium channel blocker that can offer interesting results [53,54]. Nevertheless, current evidence is set at small case series and sporadic cases description. Starting from 2009, Iannetti et al. [55] described the case of two girls with DS treated with add-on verapamil from a starting dose of 1 mg/kg/day up to a target dose of 1.5 mg/kg/day. Both girls experienced a prompt response in controlling SE, myoclonic jerks, and focal onset and primarily generalized seizures, although in one girl, the therapeutic effect blurred after 13 months of treatment. No AE, except for a slight subclinical increase of phenytoin plasma levels, was observed during treatment. Later, Nicita and colleagues [56] enrolled 7 patients with DRE of different aetiologies (including 4 patients with DS) to be treated with add-on verapamil up to 14 months. Results directly pointed toward better seizure control for those patients with genetically determined DS, but once again all seizure types were well controlled for a maximum of 13 months. No AEs were reported. Hence, further observational studies will be needed to dissect the real efficacy of this calcium channel blocker over epileptic channelopathies.