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Neuropathic Pain †
Published in Gary W. Jay, Chronic Pain, 2007
Work in animal models demonstrates that voltage-dependent calcium channels may also be important in modulating neuropathic transmission. Unfortunately, the currently available calcium channel blockers are cardioselective, and are not particularly effective in neuropathic pain. There appear to be at least six calcium channel subtypes, and studies with novel N-type calcium channel blockers are promising in animals (13). Preliminary studies with conotoxin (SNX-111) are positive, although the drug must be administered intrathecally.
Neuropathic Pain
Published in Mark V. Boswell, B. Eliot Cole, Weiner's Pain Management, 2005
David R. Longmire, Gary W. Jay, Mark V. Boswell
Work in animal models demonstrates that voltage-dependent calcium channels may also be important in modulating neuropathic transmission. Unfortunately, the currently available calcium channel blockers are cardioselective and are not particularly effective in neuropathic pain. There appear to be at least six calcium channel subtypes, and studies with novel N-type calcium channel blockers are promising in animals (Chaplan, 2000). Preliminary studies with conotoxin (SNX-111) are positive although the drug must be administered intrathecally.
Neuronal calcium channels blocker, ziconotide (ɷ-conotoxin MVIIA), reverses morphine withdrawal-induced memory impairments via alteration in hippocampal NMDA receptor expression in rats
Published in Toxin Reviews, 2020
Hooman Bozorgi, Ehsan Motaghi, Melika Zamani, Reza Ghavimi
Ziconotide (non-opioid/an atypical analgesic drug in human) is the synthetic form of an ω-conotoxin peptide originated from Conus magus that acts as an inhibitor of the N-type Ca2+ channels at the end of the neurons. Ziconotide routinely is applied IT for the treatment of chronic back pain (McGivern 2007). It works by blocking pain signals from the nerves to the brain (McGivern 2007). In 2004, Food and Drug Administration (FDA) approved ziconotide when administered as an infusion into the cerebrospinal fluid (McGivern 2007). Ziconotide displays neuroprotection via two pathways: (1) direct obstruction of Ca2+ entry by the N-type calcium channels and (2) reduction of Ca2+ entrance via postsynaptic NMDARs by the indirect blocking of N-type calcium channel-modulated release of the presynaptic excitatory neurotransmitters (glutamate) (Twede et al.2009). We previously reported that ziconotide attenuated signs of spontaneous and naloxone-precipitated morphine withdrawal (Bozorgi et al. 2016). It has been shown that the L-type calcium channels blocker, nimodipine, diminished morphine withdrawal severity and ameliorated memory failure (Vaseghi et al. 2014), but there is no obvious study about the effectiveness of N-type calcium channel blockers on cognitive performance. Therefore, the possibility that specific N-type calcium channel antagonists might exert improvement of memory function (may be by altering the glutamatergic transmission) during morphine withdrawal has been of interest.
The effect of an L/N-type calcium channel blocker on intradialytic blood pressure in intradialytic hypertensive patients
Published in Clinical and Experimental Hypertension, 2019
Takayasu Ito, Naoki Fujimoto, Eiji Ishikawa, Kaoru Dohi, Mika Fujimoto, Tomohiro Murata, Michiyo Kiyohara, Hideyuki Takeuchi, Sukenari Koyabu, Hiroyuki Nishimura, Toshiaki Takeuchi, Masaaki Ito
In non-dialysis patients with essential HTN, the L-type calcium channel blocker, amlodipine, increased sympathetic nerve activity and elevated the plasma norepinephrine concentration (16). In contrast, the L/N-type calcium channel blocker, cilnidipine, suppressed sympathetic activity without affecting the plasma norepinephrine concentration (14,17). Although it has been reported that cilnidipine suppressed sympathetic nerve activity in HD patients, it was unclear whether the sympathetic nerve was also suppressed, especially in HD patients with intradialytic-HTN. In the present study, patients taking cilnidipine exhibited unchanged plasma norepinephrine and epinephrine concentrations. In addition, we observed no significant effects of cilnidipine on intradialytic heart rate. These results may indicate that cilnidipine induces less sympathetic activation, if any, as compared to the L-type calcium channel blocker in intradialytic-HTN with no fluid overload. In addition, it was unclear whether alpha-blocker influenced sympathetic activation in cilnidipine group.
Role of primary care physicians in intrathecal pain management: a narrative review of the literature
Published in Postgraduate Medicine, 2018
Gladstone C. McDowell, Joseph Winchell
IT drug delivery differs from systemic administration, in which medications are distributed via the circulatory system and interact with receptors throughout the body [20]. IT administration delivers analgesic medication directly into the cerebrospinal fluid targeting spinal receptors, which allows for lower systemic exposure to achieve the same pain relief as with oral medications, thereby reducing systemically mediated adverse drug effects and drug elimination load [15,21–23]. IT drug delivery may also improve adherence and lessen concerns over aberrant drug-related behaviors such as abuse and diversion [24]. Morphine, a µ-opioid receptor agonist [25], and ziconotide, a non-opioid, selective N-type calcium channel blocker [26], are the only agents approved by the FDA to treat chronic refractory pain by the IT route.