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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)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM100043
035-os BibID:	(WoS)000749267000001 (Scopus)85123922388
Első szerző:	Phan, Thieu X.
Cím:	TRPV1 in arteries enables a rapid myogenic tone / Phan Thieu X., Ton Hoai T., Gulyás Hajnalka, Pórszász Róbert, Tóth Attila, Russo Rebekah, Kay Matthew W., Sahibzada Niaz, Ahern Gerard P.
Dátum:	2022
ISSN:	0022-3751 1469-7793
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Journal Of Physiology-London. - 600 : 7 (2022), p. 1651-1666. -
További szerzők:	Ton, Hoai T. Gulyás Hajnalka Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Tóth Attila (1971-) (biológus) Russo, Rebekah Kay, Matthew W. Sahibzada, Niaz Ahern, Gerard P.
Pályázati támogatás:	OTKA-116940 OTKA GINOP-2.3.2-15-2016-00043 GINOP GINOP-2.3.2-15-2016-00050 GINOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM093229
035-os BibID:	(WoS)000575298800001 (Scopus)85092112476
Első szerző:	Phan, Thieu X.
Cím:	TRPV1 expressed throughout the arterial circulation regulates vasoconstriction and blood pressure / Thieu X. Phan, Hoai T. Ton, Hajnalka Gulyás, Róbert Pórszász, Attila Tóth, Rebekah Russo, Matthew W. Kay, Niaz Sahibzada, Gerard P. Ahern
Dátum:	2020
ISSN:	0022-3751 1469-7793
Megjegyzések:	The functional roles of the capsaicin receptor, TRPV1, outside of sensory nerves are unclear. We mapped TRPV1 in the mouse circulation, revealing extensive expression in the smooth muscle of resistance arterioles supplying skeletal muscle, heart and adipose tissue. Activation of TRPV1 in vascular myocytes constricted arteries, reduced coronary flow in isolated hearts and increased systemic blood pressure. These functional effects were retained after sensory nerve ablation, indicating specific signalling by arterial TRPV1. TRPV1 mediated the vasoconstrictive and blood pressure responses to the endogenous inflammatory lipid lysophosphatidic acid. These results show that TRPV1 in arteriolar myocytes modulates regional blood flow and systemic blood pressure, and suggest that TRPV1 may be a target of vasoactive inflammatory mediators. The capsaicin receptor, TRPV1, is a key ion channel involved in inflammatory pain signalling. Although mainly studied in sensory nerves, there are reports of TRPV1 expression in isolated segments of the vasculature, but whether the channel localizes to vascular endothelium or smooth muscle is controversial and the distribution and functional roles of TRPV1 in arteries remain unknown. We mapped functional TRPV1 expression throughout the mouse arterial circulation. Analysis of reporter mouse lines TRPV1(PLAP-nlacZ)and TRPV1-Cre:tdTomato combined with Ca(2+)imaging revealed specific localization of TRPV1 to smooth muscle of terminal arterioles in the heart, adipose tissue and skeletal muscle. Capsaicin evoked inward currents (current density similar to 10% of sensory neurons) and raised intracellular Ca(2+)levels in arterial smooth muscle cells, constricted arteriolesex vivoandin vivoand increased systemic blood pressure in mice and rats. Further, capsaicin markedly and dose-dependently reduced coronary flow. Pharmacological and/or genetic disruption of TRPV1 abolished all these effects of capsaicin as well as vasoconstriction triggered by lysophosphatidic acid, a bioactive lipid generated by platelets and atherogenic plaques. Notably, ablation of sensory nerves did not affect the responses to capsaicin revealing a vascular smooth muscle-restricted signalling mechanism. Moreover, unlike in sensory nerves, TRPV1 function in arteries was resistant to activity-induced desensitization. Thus, TRPV1 activation in vascular myocytes enables a persistent depolarizing current, leading to constriction of coronary, skeletal muscle and adipose arterioles and a sustained increase in systemic blood pressure.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk TRPV1 blood pressure capsaicin lysophosphatidic acid vascular smooth muscle
Megjelenés:	Journal of Physiology. - 598 : 24 (2020), p. 5639-5659. -
További szerzők:	Ton, Hoai T. Gulyás Hajnalka Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Tóth Attila (1971-) (biológus) Russo, Rebekah Kay, Matthew W. Niaz, Sahibzada Ahern, Gerard P.
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