Effectiveness and safety of medium- and long-term elcatonin use in the prevention and treatment of bone mass loss

Jiménez, Fernando; Albizuri, J.M. Aranburu; Alier, Jose Maria Almirall; Soto, Jorge Julian Molina; Canales, Alfredo Gracia

doi:10.1016/0011-393x(95)85007-4

Cited by 6 publications

(3 citation statements)

References 47 publications

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“…Calcitonin is a polypeptide hormone released from the thyroid gland that regulates the calcium homeostasis in vertebrates [1][2][3] and is used clinically to treat hypercalcemia [4] and osteoporosis [5][6][7]. In addition, calcitonin has been reported to relieve pain associated with postmenopausal osteoporosis [8], and to ameliorate neuropathic pain associated with lumbar spinal canal stenosis [9], diabetic neuropathy [10], reflex sympathetic dystrophy [11] and post-herpetic neuralgia [12].…”

Section: Introductionmentioning

confidence: 99%

Anti-Hyperalgesic Effects of Calcitonin on Neuropathic Pain Interacting with its Peripheral Receptors

et al. 2012

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BackgroundThe polypeptide hormone calcitonin is clinically well known for its ability to relieve neuropathic pain such as spinal canal stenosis, diabetic neuropathy and complex regional pain syndrome. Mechanisms for its analgesic effect, however, remain unclear. Here we investigated the mechanism of anti-hyperalgesic action of calcitonin in a neuropathic pain model in rats.ResultsSubcutaneous injection of elcatonin, a synthetic derivative of eel calcitonin, relieved hyperalgesia induced by chronic constriction injury (CCI). Real-time reverse transcriptase-polymerase chain reaction analysis revealed that the CCI provoked the upregulation of tetrodotoxin (TTX)-sensitive Nav.1.3 mRNA and downregulation of TTX-resistant Nav1.8 and Nav1.9 mRNA on the ipsilateral dorsal root ganglion (DRG), which would consequently increase the excitability of peripheral nerves. These changes were reversed by elcatonin. In addition, the gene expression of the calcitonin receptor and binding site of 125I-calcitonin was increased at the constricted peripheral nerve tissue but not at the DRG. The anti-hyperalgesic effect and normalization of sodium channel mRNA by elcatonin was parallel to the change of the calcitonin receptor expression. Elcatonin, however, did not affect the sensitivity of nociception or gene expression of sodium channel, while it suppressed calcitonin receptor mRNA under normal conditions.ConclusionsThese results suggest that the anti-hyperalgesic action of calcitonin on CCI rats could be attributable to the normalization of the sodium channel expression, which might be exerted by an unknown signal produced at the peripheral nerve tissue but not by DRG neurons through the activation of the calcitonin receptor. Calcitonin signals were silent in the normal condition and nerve injury may be one of triggers for conversion of a silent to an active signal.

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Section: Introductionmentioning

confidence: 99%

Anti-Hyperalgesic Effects of Calcitonin on Neuropathic Pain Interacting with its Peripheral Receptors

et al. 2012

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“…7,8) Therefore, calcitonin is used clinically to treat hypercalcemia 9) and osteoporosis. 10,11) Calcitonin also has the ability to relieve pain associated with a variety of disorders, including osteoporosis. [12][13][14][15][16] These actions are mediated by increased cAMP and intracellular Ca 2+ levels evoked by the stimulation of calcitonin receptors coupled to G proteins.…”

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confidence: 99%

Vasodilator Effects of Elcatonin, a Synthetic Eel Calcitonin, on Retinal Blood Vessels in Rats

Mori

Suzawa

Sakamoto

et al. 2015

Biological & Pharmaceutical Bulletin

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The aim of this study was to examine the effects of elcatonin, a synthetic derivative of eel calcitonin, on rat retinal blood vessels, and to determine how diabetes affects the retinal vascular responses. Ocular fundus images were captured with an original high-resolution digital fundus camera in vivo. The retinal vascular responses were evaluated by measuring the diameter of retinal blood vessels contained in the digital images. Both systemic blood pressure and heart rate were continuously recorded. Elcatonin increased the diameter of retinal blood vessels but decreased mean blood pressure in a dose-dependent manner, whereas it had no significant effect on heart rate. A diminished retinal vasodilator response and significant pressor response to elcatonin were observed in rats injected intravenously with N G -nitro-L-arginine methyl ester, a nitric oxide (NO) synthase inhibitor. Intravitreal injection of indomethacin, a non-selective cyclooxygenase (COX) inhibitor, and SQ22536, an adenylyl cyclase inhibitor, markedly attenuated the vasodilator effects of elcatonin on retinal blood vessels. The retinal vasodilator responses to elcatonin were unaffected 2 weeks after the induction of diabetes by a combination of streptozotocin treatment and D-glucose feeding. These results suggest that elcatonin dilates rat retinal blood vessels via NO-and COX-dependent mechanisms and that the adenylyl cyclase-adenosine 3′,5′-cyclic monophosphate system plays a major role in the vasodilator mechanisms. The retinal vasodilatory effects of elcatonin seem to be preserved at early stages of diabetes.Key words adenylyl cyclase; cyclooxygenase; nitric oxide; prostaglandin; retinal blood vessel Diabetic retinopathy is a leading cause of blindness in industrialized countries and is the most common complication of diabetes. Tight control of blood glucose levels decreases the risk of diabetic retinopathy onset and progression; however, additional effective treatments are still needed. The narrowing of retinal blood vessels and reduction in retinal blood flow are associated with the onset of diabetic retinopathy, and the impairment of retinal circulation contributes to the pathogenesis of the disease.1-4) Therefore, one strategy for preventing the disease or reducing its severity is to improve the impaired retinal circulation.Our previous studies demonstrated that adenosine 3′,5′-cyclic monophosphate (cAMP)-elevating agents dilate retinal blood vessels more effectively than peripheral resistance vessels.5,6) For example, prostaglandin (PG) I 2 and forskolin (an activator of adenylyl cyclase), which elevate intracellular cAMP levels, dilate retinal arterioles at doses much lower than that required to decrease systemic blood pressure. 5) A cAMP analog decreased systemic blood pressure less than that by an analog of guanosine 3′,5′-cyclic monophosphate (cGMP), though they produced a comparable vasodilation of retinal blood vessels. 6) These results suggested that cAMPelevating agents could be effective drugs for improving retinal circulation.Ca...

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“…Calcitonin, a polypeptide hormone secreted from the parafollicular (C) cells of the mammalian thyroid gland into general circulation [1,2], regulates blood calcium concentration and bone metabolism by acting on osteoclasts [1,3,4] and is used clinically to treat hypercalcemia [5] and osteoporosis [6–8]. In addition, calcitonin has been used to relieve pain associated with a variety of disorders, including postmenopausal osteoporosis [9], rheumatoid arthritis [10], metastatic cancer [11], reflex sympathetic dystrophy [12], and knee osteoarthritis [13].…”

Section: Introductionmentioning

confidence: 99%

Calcitonin ameliorates enhanced arterial contractility after chronic constriction injury of the sciatic nerve in rats

Yoshimura

Ito

Takeda

et al. 2011

Fundamemntal Clinical Pharma

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In addition to its regulatory effect on bone mass, calcitonin has been shown to relieve pain and alleviate peripheral circulatory disturbance in patients with Raynaud's syndrome and complex regional pain syndrome. In the present study, we investigated whether calcitonin ameliorates diminished blood flow and enhanced arterial contraction in response to noradrenaline in chronic constriction injury (CCI) of the sciatic nerve in rats. Following surgically induced CCI, laser Doppler flowmetry studies showed a significant decrease in plantar skin blood flow of the ipsilateral hind paw compared to the contralateral side. A subcutaneous bolus injection of elcatonin (20 U/kg), a synthetic derivative of eel calcitonin, significantly improved decreased skin blood flow in the ipsilateral side. In vitro analysis of plantar arteries isolated from the ipsilateral hind paw 7-13 days after the CCI procedure showed higher sensitivity to noradrenaline than the plantar arteries from the contralateral side. Elcatonin (0.1-10 nm) significantly reduced noradrenaline-induced contraction in the arteries of the ipsilateral side, whereas it had little effect on those of the contralateral side. These results suggest that calcitonin selectively ameliorates enhanced arterial contractility in CCI neuropathic rats, thus leading to its alleviating effect on peripheral circulatory disturbance.

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Effectiveness and safety of medium- and long-term elcatonin use in the prevention and treatment of bone mass loss

Cited by 6 publications

References 47 publications

Anti-Hyperalgesic Effects of Calcitonin on Neuropathic Pain Interacting with its Peripheral Receptors

Anti-Hyperalgesic Effects of Calcitonin on Neuropathic Pain Interacting with its Peripheral Receptors

Vasodilator Effects of Elcatonin, a Synthetic Eel Calcitonin, on Retinal Blood Vessels in Rats

Calcitonin ameliorates enhanced arterial contractility after chronic constriction injury of the sciatic nerve in rats

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