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001-es BibID:BIBFORM101728
035-os BibID:(cikkazonosító)1465 (scopus)85123579850 (wos)000756238000001
Első szerző:Csípő Tamás
Cím:A Central Role for TRPM4 in Ca2+-Signal Amplification and Vasoconstriction / Csípő Tamás, Czikora Ágnes, Fülöp Gábor Á., Gulyás Hajnalka, Rutkai Ibolya, Tóth Enikő Pásztorné, Pórszász Róbert, Szalai Andrea, Bölcskei Kata, Helyes Zsuzsanna, Pintér Erika, Papp Zoltán, Ungvári Zoltán, Tóth Attila
Dátum:2022
ISSN:1661-6596 1422-0067
Megjegyzések:Transient receptor potential melastatin-4 (TRPM4) is activated by an increase in intracellular Ca2+ concentration and is expressed on smooth muscle cells (SMCs). It is implicated in the myogenic constriction of cerebral arteries. We hypothesized that TRPM4 has a general role in intracellular Ca2+ signal amplification in a wide range of blood vessels. TRPM4 function was tested with the TRPM4 antagonist 9-phenanthrol and the TRPM4 activator A23187 on the cardiovascular responses of the rat, in vivo and in isolated basilar, mesenteric, and skeletal muscle arteries. TRPM4 inhibition by 9-phenanthrol resulted in hypotension and a decreased heart rate in the rat. TRPM4 inhibition completely antagonized myogenic tone development and norepinephrine-evoked vasoconstriction, and depolarization (high extracellular KCl concentration) evoked vasoconstriction in a wide range of peripheral arteries. Vasorelaxation caused by TRPM4 inhibition was accompanied by a significant decrease in intracellular Ca2+ concentration, suggesting an inhibition of Ca2+ signal amplification. Immunohistochemistry confirmed TRPM4 expression in the smooth muscle cells of the peripheral arteries. Finally, TRPM4 activation by the Ca2+ ionophore A23187 was competitively inhibited by 9-phenanthrol. In summary, TRPM4 was identified as an essential Ca2+-amplifying channel in peripheral arteries, contributing to both myogenic tone and agonist responses. These results suggest an important role for TRPM4 in the circulation. The modulation of TRPM4 activity may be a therapeutic target for hypertension. Furthermore, the Ca2+ ionophore A23187 was identified as the first high-affinity (nanomolar) direct activator of TRPM4, acting on the 9-phenanthrol binding site
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Ca2+ signaling
vascular smooth muscle
blood pressure regulation
transient receptor potential melastatin-4
transient receptor potential
Megjelenés:International Journal Of Molecular Sciences. - 23 : 3 (2022), p. 1-13. -
További szerzők:Czikora Ágnes (1982-) (molekuláris biológus) Fülöp Gábor Áron (1988-) (általános orvos) Gulyás Hajnalka Rutkai Ibolya (1985-) (molekuláris biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Szalai Andrea (1968-) (analitikus) Bölcskei Kata Helyes Zsuzsanna Pintér Erika Papp Zoltán (1965-) (kardiológus, élettanász) Ungvári Zoltán Tóth Attila (1971-) (biológus)
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001-es BibID:BIBFORM043723
Első szerző:Pintér Erika
Cím:Pharmacological characterisation of the somatostatin analogue TT-232 : effects on neurogenic and non-neurogenic inflammation and neuropathic hyperalgesia / Pintér E., Helyes Zs., Németh J., Pórszász R., Pethő G., Thán M., Kéri G., Horváth A., Jakab B., Szolcsányi J.
Dátum:2002
ISSN:0028-1298
Megjegyzések:The putative anti-inflammatory and anti-nociceptive activity of the heptapeptide somatostatin analogue TT-232 ( D-Phe-Cys-Tyr- D-Thr-Lys-Cys-Thr-NH(2)) was investigated in the rat and mouse, as well as its effect on neuropathic hyperalgesia, gastric ulceration and the release of sensory neuropeptides. In the rat, carrageenin-induced paw oedema was inhibited dose dependently by TT-232 (3x2.5-20 microg/kg i.v.). Evans blue accumulation induced by intraarticular bradykinin injection (0.5 nmol in 0.1 ml) was slightly, but significantly inhibited by a single TT-232 dose (5-20 microg/kg). Cutaneous neutrophil accumulation over a 3-h period after intradermal (i.d.) injection of carrageenin (1 mg/site) or interleukin 1beta (IL-1beta, 3 pmol/site) was inhibited significantly by TT-232 (3x80 microg/kg i.v.), while diclofenac (3x10 mg/kg i.v.) elicited significant inhibition only in the IL-1beta test. In the mouse, TT-232 potently decreased oedema formation induced by 2.5% capsaicin applied topically to the ear. Mechano-nociception in the rat hind-paw during neuropathic pain induced by partial sciatic nerve injury (model of Seltzer) was measured using the Randall-Selitto test. TT-232 (5-20 microg/kg i.p. on the 7th day after the operation) dose-dependently inhibited the mechano-nociceptive hyperalgesia. In vitro release of substance P (SP), calcitonin gene-related peptide (CGRP) and somatostatin from the isolated rat trachea in response to electrical field stimulation (40 V, 0.1 ms, 10 Hz, 120 s) of its nervous elements was inhibited significantly by 500 nM TT-232. The role of G protein-coupled receptors in the effect of TT-232 was indicated by the prevention of its inhibitory action on the release of sensory neuropeptides by incubation the tissue for 1 or 6 h with pertussis toxin (100 ng/ml). The release of sensory neuropeptides to in response to electrical nerve stimulation was not inhibited by a potent tyrosine kinase inhibitor, genistein (50 microM). TT-232 (up to 5 mg/kg i.p.) did not induce mucosal lesions in either the stomach or the duodenum. These data suggest that TT-232, a somatostatin analogue devoid of endocrine effects, is a promising lead molecule in the search for novel, broad-spectrum anti-inflammatory and analgesic agents.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 366 : 2 (2002), p. 142-150. -
További szerzők:Helyes Zsuzsanna Németh József (Pécs) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Pethő Gábor Thán Márta Kéri György Horváth Anikó Jakab Balázs (Pécs) Szolcsányi János (Pécs)
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