The effects of various peptides on the isolated pulmonary artery

Obara, Hidefumi; Kusunoki, Masato; Mori, Miyako; Mikawa, Katsuya; Iwai, Seizo

doi:10.1016/0196-9781(89)90100-9

Cited by 15 publications

(6 citation statements)

References 10 publications

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“…Specifically, NT-induced hypotension could be accounted for, at least in part, by inhibitory NT effect on noradrenaline release from rat perivascular nerve fibers (Tsuda and Masuyma, 1993), as well as by modulation of the reninangiotensin system (Kerouac et al, 1983;Rioux et al, 1982b). Interestingly, studies on isolated vascular tissue revealed no NT effects on isolated rat aortic strips (Di Paola and Richelson, 1990) and rabbit pulmonary artery (Obara et al, 1989). These findings therefore suggest that NT-induced changes in blood pressure are largely attributed to the stimulatory effects upon release of various endogenous vasoactive neuromodulators (briefly overviewed in Table 1), rather than caused by direct effects of NT on vascular smooth muscle tone.…”

Section: Blood Pressurementioning

confidence: 91%

Emerging role of neurotensin in regulation of the cardiovascular system

Osadchii

2015

European Journal of Pharmacology

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Section: Blood Pressurementioning

confidence: 91%

Emerging role of neurotensin in regulation of the cardiovascular system

Osadchii

2015

European Journal of Pharmacology

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“…VIP potently relaxes the vessels that supply the upper airways (Lundberg et al, 1981;Lung and Widdicombe, 1987;Malm et al, 1980), trachea, bronchi (Laitinen et al, 1987), and pulmonary vessels (Hamasaki et al, 1983a(Hamasaki et al, , 1983bNandiwada et al, 1985;Obara et al, 1989), and VIP-induced vasodilation is more potent in tracheal circulation than in bronchial circulation (Matran et al, 1989a(Matran et al, , 1989b. The vasodilation is reported to be independent of endothelial cells Greenberg et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…One study in rat airways using immunohistochemistry for VPAC 1 led to staining of macrophages and airway epithelium from trachea to terminal bronchioles, but not of bronchial smooth muscle or vascular smooth muscle other than infrequent staining of some intermediate-sized pulmonary veins (Ichikawa et al, 1995). A second study reported VPAC 1 -like immunoreactivity in leukocytes and vascular smooth muscle myocytes of some vessels but not in epithelial cells (Busto et al, 2000).VIP potently relaxes the vessels that supply the upper airways (Lundberg et al, 1981;Lung and Widdicombe, 1987;Malm et al, 1980), trachea, bronchi (Laitinen et al, 1987), and pulmonary vessels (Hamasaki et al, 1983a(Hamasaki et al, , 1983bNandiwada et al, 1985;Obara et al, 1989), and VIP-induced vasodilation is more potent in tracheal circulation than in bronchial circulation (Matran et al, 1989a(Matran et al, , 1989b. The vasodilation is reported to be independent of endothelial cells Greenberg et al, 1987).…”

mentioning

confidence: 99%

Expression and Distribution of Vasoactive Intestinal Polypeptide Receptor VPAC2 mRNA in Human Airways

Groneberg

Hartmann

Dinh

et al. 2001

Laboratory Investigation

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SUMMARY:Vasoactive intestinal polypeptide (VIP) is a putative neurotransmitter of the inhibitory non-adrenergic noncholinergic nervous system and influences many aspects of mammalian airway function. VIP binds to two G-protein-coupled VPAC receptors that are highly homologous structurally but distinguished by their different affinities for peptide analogues of VIP. As VIP binding sites in the respiratory tract have only been examined by ligand binding and cytochemical techniques, we studied the distribution of the mRNA that encodes the inducible receptor subtype VPAC 2 in the human respiratory tract. Northern blots demonstrated the expression of VPAC 2 mRNA in human airways and other tissues. A human-specific VPAC 2 cRNA probe was used to detect VPAC 2 mRNA expression in human lung by nonradioactive in situ hybridization. In larger airways, positive VPAC 2 mRNA signals were localized to tracheal and bronchial ciliated epithelial cells. There was also marked staining of mucous and serous cells of submucosal glands. No signals were obtained in airway and vascular smooth muscle myocytes and endothelial cells. In peripheral lung tissues, VPAC 2 mRNA expression was localized to epithelial cells of the bronchioles. Specific staining was detected in immune cells and alveolar macrophages. In summary, VPAC 2 is localized in airway epithelial, glandular, and immune cells of the lung but not in airway and vascular smooth muscle. The absence of VPAC 2 mRNA in vascular and airway smooth muscle myocytes may indicate that the effects of VIP on vasodilation and bronchodilation are mediated by VPAC 1 or undefined receptors. However, a paracrine modulation of the two most prominent effects of VIP in the respiratory tract by VPAC 2 cannot be excluded. (Lab Invest 2001, 81:749 -755).T he 28-amino acid vasoactive intestinal polypeptide (VIP) is a putative neurotransmitter or neuromodulator of the inhibitory non-adrenergic noncholinergic nervous system in mammalian airways (Maggi et al, 1995). VIP-immunoreactivity (VIP-IR) is present in cells of the tracheobronchial smooth muscle layer, in the walls of pulmonary and bronchial vessels, around submucosal glands, in the lamina propria, and in pulmonary ganglia (Dey et al, 1981;Lundberg et al, 1984). VIP-IR nerve fibers are found as branching networks in the respiratory tract (Ghatei et al, 1982) They decrease in frequency as the airways become smaller but extend to peripheral bronchioles (Lundberg et al, 1984). The pattern of VIPergic nerves largely follows that of cholinergic nerves (Laitinen et al, 1985). VIP-IR is also present in sensory nerves (Lundberg et al, 1984;Luts and Sundler, 1989).Several studies using receptor binding techniques have been performed to demonstrate the presence of VIP receptors and have shown abundant binding in different parts of the lungs Robberecht et al, 1981Robberecht et al, , 1988. Two types of VIP receptors have been cloned and characterized in the past years. They were termed the VPAC 1 receptor, formerly described as the VIP 1 receptor (Ishihara et a...

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“…Although these findings indicate that peripheral vasoconstrictor effects of CCK can be mediated via CCK 1 receptors, other studies in vitro have reported a vasorelaxant effect of the peptide, particularly in vessels from the splanchnic and pulmonary circulations (Obara et al, 1989;Sá nchez-Ferná ndez et al, 2004). In isolated mesenteric arteries the octapeptide fragment of CCK failed to alter myogenic tone (in relaxed vessels) although it did produce a CCK 2 receptor-mediated inhibition of contractions induced by transmural nerve stimulation.…”

Section: Local Actions At the Level Of The Peripheral Vasculaturementioning

confidence: 89%

CCK as a modulator of cardiovascular function

Lovick

2009

Journal of Chemical Neuroanatomy

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The effects of various peptides on the isolated pulmonary artery

Cited by 15 publications

References 10 publications

Emerging role of neurotensin in regulation of the cardiovascular system

Emerging role of neurotensin in regulation of the cardiovascular system

Expression and Distribution of Vasoactive Intestinal Polypeptide Receptor VPAC2 mRNA in Human Airways

CCK as a modulator of cardiovascular function

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