Halothane Decreases the Release of Neuropeptide Y and 3,4-Dihydroxyphenylglycol from Superfused Segments of Dog Pulmonary Artery

Rorie, Duane K.; Hunter, Larry W.; Lunn, Jeffrey J.

doi:10.1097/00000542-199010000-00019

Cited by 3 publications

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“…In our preliminary experiments, we also found that halothane markedly suppressed the pressor effect of DPI. Halothane has been shown to inhibit sympathetic nervous transmission at several levels Larach et al, 1987;Rorie et al, 1990). Halothane was also found to alter endothelium-dependent vasodilatation (Muldoon et al, 1988;Blaise, 1991), and to abolish the pressor responses of other NO synthase inhibitors, namely N-nitro-L-arginine (L-NNA) and its methyl ester (L-NAME) (Wang et al, 1991a;Pang et al, 1992).…”

Section: Introducdon Methodsmentioning

confidence: 99%

“…The results suggest that the inhibitory effect of halothane on the pressor response to DPI is primarily due to the suppression of sympathetic activation rather than inhibition of endothelium-dependent vasodilatation. Halothane has been shown to depress activities of the sympathetic nervous system at different levels (1) areas of the central nervous system controlling sympathetic nerve activity (Price et al, 1963;Millar et al, 1969;Larach et al, 1987;Bazil & Minneman, 1989), (2) sympathetic ganglia (Skovsted et al, 1969;Christ, 1977;Bosnjak et al, 1982;Seagard et al, 1982), and (3) sympathetic nerve endings located in the walls of blood vessels (Muldoon et al, 1975;Lunn & Rorie, 1984;Rorie et al, 1990). In addition, a small component of non-specific inhibition by halothane may also be responsible for its effect on the pressor response to DPI.…”

Section: Effects Of Anaesthetics On Dpi-induced Map Responsementioning

confidence: 99%

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Halothane inhibits the pressor effect of diphenyleneiodonium

Wang¹,

Pang²

1993

British J Pharmacology

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1 We have recently found that diphenyleneiodonium (DPI), a novel inhibitor of nitric oxide (NO) synthase, causes pressor and tachycardic responses in pentobarbitone-but not halothane-anaesthetized rats. The present study investigated the mechanism by which halothane suppresses the pressor response of DPI. The effects of halothane on the pressor response of DPI were also compared with those of other anaesthetic agents.2 In conscious rats, i.v. bolus injections of DPI (0.025 -1.6 mg kg-') caused dose-dependent increases in mean arterial pressure (MAP), with EDm of 0.07 ± 0.01 mg kg-' and maximal rise of MAP (Emax) of 59 ± 2 mmHg. While ketamine potentiated E,,, without altering the EDm and pentobarbitone increased the ED^, without changing Emax of the pressor response to DPI, chloralose, urethane and ethanol displaced the curve to the right and potentiated E,,.a. In contrast, halothane (0.5-1.25%) dosedependently and non-competitively reduced the pressor responses to DPI. 3 Intravenous bolus injection of a single dose of DPI (1.6 mg kg-') caused immediate and large increases in plasma noradrenaline and adrenaline, as well as MAP in conscious rats. Halothane (1.25%) almost completely inhibited these increases. 4 The results suggest that DPI causes a pressor response in conscious rats by activating the sympathetic nervous system and halothane abolishes this pressor response by inhibiting activities of the sympathetic nervous system. The results also show that influences of anaesthetics must be taken into consideration when evaluating pressor response of vasoactive agents.

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Section: Introducdon Methodsmentioning

confidence: 99%

Section: Effects Of Anaesthetics On Dpi-induced Map Responsementioning

confidence: 99%

Halothane inhibits the pressor effect of diphenyleneiodonium

Wang¹,

Pang²

1993

British J Pharmacology

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“…Besides the classical transmitters, NPY seems to play a role in motor behaviour. NPY (Tatemoto et al, 1982) coexists and is coreleased with noradrenaline from sympathetic nerve endings (Lundberg and Hokfelt, 1983;Everitt and Hokfelt, 1989) during major activation of the sympathetic nervous system (Rorie et al, 1990). Centrally administered NPY suppresses locomotor activity in a dose-related (and reversible) manner (Heilig and Murison, 1987), and induces EEG changes characteristic of sedation (Fuxe et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Effects of Repeated Sensory Stimulation (Electro‐acupuncture) and Physical Exercise (Running) on Open‐field Behaviour and Concentrations of Neuropeptides in the Hippocampus in WKY and SHR rats

Bucinskaite

Theodorsson

Crumpton

et al. 1996

Eur J of Neuroscience

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The effects of repeated sensory stimulation (electro-acupuncture) and physical exercise (running) on open-field behaviour and on hippocampal concentrations of neuropeptide Y, neurokinin A, substance P, galanin and vasoactive intestinal peptide (VIP)-like immunoreactivities were studied in WKY (wistar-Kyoto) and SHR (spontaneously hypertensive) rats. Significantly higher concentrations of substance P-like immunoreactivity, neurokinin A-like immunoreactivity and neuropeptide Y-like immunoreactivity were found in the hippocampus immediately after 3 weeks of treatment (electro-acupuncture and running), but not 1 week after the last (tenth) changes in neuropeptide concentrations were similar in the two rat strains. Open-field behaviour was significantly reduced during the treatment period in both strains. There were significant negative correlations between behaviour and neuropeptide concentrations in SHR rats, suggesting interdependency with sympathetic activity. It is proposed that the effects of electro-acupuncture and physical exercise in rats are related to increases in neuropeptide Y, neurokinin A and substance P in the hippocampus.

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