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001-es BibID:	BIBFORM013279
Első szerző:	Horváth Gabriella
Cím:	Mice deficient in pituitary adenylate cyclase activating polypeptide display increased sensitivity to renal oxidative stress in vitro / Gabriella Horvath, Laszlo Mark, Reka Brubel, Peter Szakaly, Boglarka Racz, Peter Kiss, Andrea Tamas, Zsuzsanna Helyes, Andrea Lubics, Hitoshi Hashimoto, Akemichi Baba, Norihito Shintani, Gergely Furjes, Jozsef Nemeth, Dora Reglodi
Dátum:	2010
Megjegyzések:	Pituitary adenylate cyclase activating polypeptide (PACAP) is a multifunctional neuropeptide, showingwidespread occurrence in the nervous system and also in peripheral organs. The neuroprotective effectsof PACAP are well-established in different neuronal systems against noxious stimuli in vitro and in vivo.Recently, its general cytoprotective actions have been recognized, including renoprotective effects. However,the effect of endogenous PACAP in the kidneys is not known. The main aim of the present studywas to investigate whether the lack of this endogenous neuropeptide influences survival of kidney cellsagainst oxidative stress. First, we determined the presence of endogenous PACAP from mouse kidneyhomogenates by mass spectrometry and PACAP-like immunoreactivity by radioimmunoassay. Second,primary cultures were isolated from wild type and PACAP deficient mice and cell viability was assessedfollowing oxidative stress induced by 0.5, 1.5 and 3mM H2O2. Our mass spectrometry and radioimmunoassayresults show that PACAP is endogenously present in the kidney. The main part of our studyrevealed that the sensitivity of cells from PACAP deficient mice was increased to oxidative stress: bothafter 2 or 4 h of exposure, cell viability was significantly reduced compared to that from control wild typemice. This increased sensitivity of kidneys from PACAP deficient mice could be counteracted by exogenouslygiven PACAP38. These results show, for the first time, that endogenous PACAP protects againstoxidative stress in the kidney, and that PACAP may act as a stress sensor in renal cells. These findingsfurther support the general cytoprotective nature of this neuropeptide.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Cell viability Oxidative stress PACAP knockout mice Renoprotection
Megjelenés:	Neuroscience Letters. - 469 : 1 (2010), p. 70-74. -
További szerzők:	Márk László (1956-) (belgyógyász, kardiológus) Brubel Réka Szakály Péter Rácz Boglárka Kiss Péter Tamás Andrea (Idegtudomány) (Pécs) Helyes Zsuzsanna Lubics Andrea (Pécs) Hashimoto, Hitoshi Baba, Akemichi Shintani Norihito Fürjes Gergely Németh József (1954-) (vegyész, analitikus) Reglődi Dóra (Idegtudományok)
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001-es BibID:	BIBFORM043852
035-os BibID:	PMID:7715824
Első szerző:	Pórszász Róbert (farmakológus, klinikai farmakológus)
Cím:	Antidromic vasodilatation in the striated muscle and its sensitivity to resiniferatoxin in the rat / Róbert Pórszász, János Szolcsányi
Dátum:	1994
ISSN:	0304-3940
Megjegyzések:	Antidromic stimulation at the L4-L5 dorsal roots elicited a blood flow increase in ipsilateral muscles of lower extremities in rats measured by laser-Doppler flowmetry. Stimulation with 0.5 Hz; 20 V; 0.5 ms; 50 impulses was much less effective in muscle (18.9 +/- 6.4 area under the curve (%); mean +/- S.E.) than in the glabrous skin (80.5 +/- 8.25; P < 0.001). No significant difference was seen at 10 Hz (51.6 +/- 10.6 muscle; 60.6 +/- 17.3 skin). In the muscle the latency period of the response was long (37.4 +/- 3.1 s; mean +/- S.E.) at 0.5 Hz stimulation and was much shorter (8.8 +/- 0.8 s) at the higher frequency of 10 Hz, unlike in the skin where latency values at both frequencies were similar (9.7 +/- 0.8 s and 8.9 +/- 0.9 s, respectively). Antidromic vasodilatation in the muscle and the skin was abolished by resiniferatoxin (RTX) in an i.v. dose of 1.0 microgram/kg. These results provide a direct evidence for the existence of antidromic vasodilatation in striated muscle and suggest a mediating role for capsaicin/RTX sensitive afferents.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Neuroscience Letters 182 : 2 (1994), p. 267-270. -
További szerzők:	Szolcsányi János (Pécs)
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