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Systemic Lupus Erythematosus
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Maria A. Giraldo-Isaza, Bettina F. Cuneo
Calcium Channel Hypothesis: Cross reactivity of L-type calcium channels with anti-/SSA or anti-SSA/SSB antibodies has also been proposed as a mechanism altering calcium homeostasis leading to conduction abnormalities. This might also lead to pathogenic apoptosis and subsequent inflammation and fibrosis [69–73].
Striated MusclesSkeletal and Cardiac Muscles
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Within the myocyte, myofibrils are surrounded by a network of membranes, the sarcoplasmic reticulum. The sarcoplasmic reticulum in the heart is less dense and not as well developed as that in skeletal muscles. The T-tubules of the cardiac muscle are located at the Z lines, whereas they are positioned at the ends of the I-bands in skeletal muscle. Consequently, the T-tubule is linked with the terminal cisterna of the sarcoplasmic reticulum of only one sarcomere, forming a diad, rather than a triad, in the skeletal muscle. As there is less sarcoplasmic reticulum in cardiac muscle, intracellular calcium levels depend on calcium influx into the cardiac myocyte through L-type calcium channels on the sarcolemma (via activated dihydropyridine receptor), as well as its release from sarcoplasmic reticulum. The L-calcium channels open more slowly than sodium channels and remain open longer (200–300 ms). This explains why the action potential in ventricular muscle is much longer than in skeletal muscle in which the L-type calcium channels do not open. Some of this calcium causes opening of ryanodine receptors on the sarcoplasmic reticulum, and calcium diffuses out of the sarcoplasmic reticulum. All the calcium released from the sarcoplasmic reticulum, and some from the influx via the sarcolemma, binds to troponin, resulting in actin–myosin interaction and cross-bridge cycling.
Ion Channels and The Control of Uterine Contractility
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Functional voltage-gated calcium channels have been recently expressed in Xenopus oocytes injected with poly (A+)mRNA obtained from pregnant rat myometrium.16 These calcium channels possess electrophysiological and pharmacological properties similar to those recorded in isolated myometrial cells and belong to the L-type calcium channel.
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 are crucial for the contraction of all types of muscles. After influx into the cytoplasm, they interact with myofilaments and ultimately allow for interaction between myosin and actin filaments, and thus for muscle contraction. Since they are a trigger and an executor of muscle contractions, their concentration in the sarcoplasm must be strictly regulated. In striated muscles, cell membrane depolarization is a signal that initiates the cascade responsible for muscle contraction. Changes in the cell membrane potential activate and open the L-type calcium channels. Then, the local increase in Ca2+ concentration activates the ryanodine receptor, a sarcoplasmic calcium channel, which releases the next portion of calcium ions into the cytoplasm, which interacts with myofilaments.
Vasodilation in patients with calcium channel blocker poisoning treated with high-dose insulin: a comparison of amlodipine versus non-dihydropyridines
Published in Clinical Toxicology, 2022
Jon B. Cole, Samantha C. Lee, Matthew E. Prekker, Nathan M. Kunzler, Kelly A. Considine, Brian E. Driver, Michael A. Puskarich, Travis D. Olives
CCBs functionally belong to two categories: dihydropyridines (DHP) and non-dihydropyridines (non-DHP). All CCBs bind L-type calcium channels in the myocardium and smooth muscle. Non-DHPs tend to have more central myocardial effects, resulting in reduced cardiac contractility, depressed sinoatrial node activity, and slowed atrioventricular node activity in addition to decreased systemic vasodilation. DHPs, however, due to subtle binding differences of the α1c subunit of L-type calcium channels, result primarily in vasodilation and reflex tachycardia [12,13]. In both DHP and non-DHP poisoning, animal models suggest that myocardial contractility is reduced early in poisoning regardless of class, while cardiac output is relatively preserved in DHP poisoning compared to non-DHP poisoning [12]. As shock worsens in CCB poisoning, cardiac output falls regardless of CCB class [12], though reflex tachycardia with DHP poisoning is seen even in profound shock [13].
Impact of chronic medications in the perioperative period: mechanisms of action and adverse drug effects (Part I)
Published in Postgraduate Medicine, 2021
Ofelia Loani Elvir-Lazo, Paul F White, Hillenn Cruz Eng, Firuz Yumul, Raissa Chua, Roya Yumul
Calcium channel blockers (CCBs) exert their clinical effects by blocking L-type voltage-gated calcium channels found in the heart, vascular smooth muscles, and pancreas. The CCBs are primarily metabolized by cytochrome P450 CYP3A4. Non-dihydropyridines Ca-blockers (e.g. verapamil and diltiazem) have a higher selectivity for cardiac L-type calcium channel receptors and exert inhibitory effects on the sinoatrial (SA) and atrioventricular (AV) nodes, resulting in slowed cardiac conduction and reduced contractility [14]. These compounds are used to treat supraventricular tachy-dysrhythmias, hypertension, cardiac ischemia, coronary spasm, and hypertrophic cardiomyopathy. Dihydropyridine CCBs (e.g. nifedipine, isradipine, felodipine, nicardipine, nisoldipine, lacidipine, amlodipine, and levamlodipine) have higher selectivity for vascular smooth muscle receptors and are used as peripheral vasodilators to treat hypertension, post-intracranial hemorrhage associated vasospasm, migraines, and Raynaud’s phenomenon [15,16].