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Non Adrenergic, Noncholinergic Innervation of Gastrointestinal Vessels
Published in Geoffrey Burnstock, Susan G. Griffith, Nonadrenergic Innervation of Blood Vessels, 2019
Annica B. Dahlström, Ola Nilsson, Ove Lundgren, Håkan Ahlman
Evidence for the hypothesis that VIP may be the transmitter substance acting on the vascular smooth muscle (Figure 3) in the suggested reflex arch have been given by Sjöqvist and collaborators.97 They observed that mechanical activation, electrical field stimulation, or close intra-arterial infusions of 5-HT increased the release of VIP into the venous effluent concomitantly with vasodilatation.95,97,98 Furthermore, tetrodotoxin inhibited both the release of VIP and the vasodilatation.98 An inhibition of both VIP release and hyperemia was also obtained after administration of apamin, a polypeptide isolated from bee venom.91,97 Since apamin does not antagonize the VIP effect on vascular smooth muscle either in vivo or in vitro, it was proposed that apamin acts via presynaptic inhibition of VIP release.97 Also the chemically induced postprandial hyperemia seems to operate via release of VIP.89
Cellular targets and molecular activity mechanisms of bee venom in cancer: recent trends and developments
Published in Toxin Reviews, 2022
Ayşegül Varol, Serap Sezen, Dilhan Evcimen, Atefeh Zarepour, Gönül Ulus, Ali Zarrabi, Gamal Badr, Sevgi Durna Daştan, Asya Gülistan Orbayoğlu, Zeliha Selamoğlu, Mehmet Varol
Apamin is another anti-inflammatory peptide of bee venom that acts by inhibiting COX-2 and phospholipase A2 (Lee et al. 2020b). In addition to its anti-inflammatory effect, apamin may exhibit anti-oxidative and anti-apoptotic activities in animal models of many inflammatory disorders such as gouty arthritis (Mohammadi-Rad et al. 2019), multiple sclerosis (Kim et al. 2017), chronic liver disease (Bae et al. 2013), acute pancreatitis (Kim et al. 2012), and atherosclerosis (Koburova et al. 1985). Another is Adolapin, which has an anti-inflammatory effect by protecting prostaglandin synthesis through suppression of cyclooxygenase-2 (COX-2) (Ali 2012). The other important component of bee venom is sulfur contain components, which are found in the main amino acids like cysteine and methionine in bee venom. They could promote the release of cortisol, which acts as an anti-inflammatory and anti-arthritic agent (Bellik 2015). The two main enzymes of bee venom, hyaluronidase and phospholipase, can stimulate immunoglobulin E and immune responses in susceptible individuals, and hyaluronidase may also exhibit anti-inflammatory, immunomodulatory, and anti-cancer activities (Lokeshwar and Selzer 2009, Cichocka-Jarosz 2012, Mcatee et al. 2014). The other enzyme of bee venom with anti-inflammatory, immunomodulatory and anti-cancer activities is phospholipase A2, which is involved in the production of fatty acids and lysophospholipids depending on calcium ions (Almunia et al. 2013, Lee and Bae 2016b).
Why do platelets express K+ channels?
Published in Platelets, 2021
Joy R Wright, Martyn P. Mahaut-Smith
The presence of Ca2+-dependent K+ channels in platelets was originally suggested from suspension measurements of membrane potential using the fluorescent indicator diSC3(5) [9,11,12]. The Ca2+ ionophore A23187 evoked a large hyperpolarization (a shift to a more negative membrane potential) that required external Ca2+ and was blocked by quinine, charybdotoxin (CTX), but not by apamin or tetraethylammonium [9], which are characteristics of KCa3.1 rather than small or large conductance Ca2+-gated K+ channels. There is some evidence for small conductance, apamin-sensitive KCa channels from Rb+ flux experiments [19]; however, these were not observed in whole-cell patch clamp recordings [10]. Direct electrophysiological studies in the platelet concluded that the channels are not active at resting levels of intracellular Ca2+ and reversibly stimulated by physiological increases in Ca2+, including repetitive transient Ca2+ spikes. Activation of this channel will therefore lead to membrane hyperpolarization toward the K+ equilibrium potential (~-90 mV) during agonist-evoked calcium signaling [10]. This agrees with the Ca2+-dependent activation characteristics of the channel in erythrocytes and leukocytes [24–26]. The threshold for stimulation by Ca2+ is approximately 200–300 nM, and maximal activation occurs at ~1 μM [Ca2]i. This dependence upon physiologically relevant levels of cytosolic Ca2+ has allowed the KCa currents to be used extensively in whole-cell patch recordings of megakaryocytes to investigate the mechanisms of Ca2+ oscillations [27].
Activation of SK3 channel plays a pivotal role in modulation of trigeminal neuralgia
Published in Neurological Research, 2021
Jiaomei Zhao, Yue Zhang, Xiangbo Liu, Yong Rao, Jia Fu, Lu Hua, Cehua Ou
Several previous studies have shown that increased SK channels expressions were detected when exposed to noxious stimuli, which suggested that the SK channels were closely related to pain transmission pathways [19,20]. Apamin is a highly SK channel-selective bee venom peptide that contains 18 amino acids. The sensitivity of SK channel subtypes to Apamin is determined by asparagine and aspartic acid residues in SK [21]. As a type of SK channel blocker, Apamin can increase the firing frequency of neurons, while the spontaneous discharge of damaged nerves is closely related to long-lasting pain feeling [22].