Bradykinin stimulates prostaglandin E<sub>2</sub> production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa <i>in vitro</i>

Morrissey, N. K.; Bellenger, C. R.; Baird, Alan W.

doi:10.2746/042516408x293556

Cited by 16 publications

(13 citation statements)

References 39 publications

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“…Recently, it was demonstrated that BK stimulates COX enzymes in gastric mucosal cells [35]. Therefore, it was suggested that COX-1 is a significant pathway for basal PGE 2 production, whereas in another study B 1 and B 2 receptors synergistically potentiated IL-1-and TNF-α-induced PGE 2 biosynthesis by a mechanism involving the increased expression of COX-2 in osteoblasts [36].…”

Section: Discussionmentioning

confidence: 98%

The Role of Inflammation and COX-Derived Prostanoids in the Effects of Bradykinin on Isolated Rat Aorta and Urinary Bladder

et al. 2011

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Bradykinin, a vasoactive peptide, increases during inflammation and induces the formation of prostaglandins through specific receptor activation. Two types of receptors mediate the biological effects of bradykinin, B(1) and B(2) receptors. Although B(2) receptors are present in most tissues, B(1) receptors are expressed after inflammatory stimuli or tissue injury. Bradykinin has a high affinity for B(2) and a low affinity for B(1) receptors, whereas the opposite occurs for des-Arg(9)-bradykinin. Recently, it has been reported that nonsteroidal anti-inflammatory drugs have different inhibitory activities on cyclooxygenase isozymes, COX-1, COX-2, and COX-3. In the present study, we have investigated the contributions of different COX isozyme inhibitions and inflammation on bradykinin-induced effects of isolated rat aorta and urinary bladder smooth muscle contractions. Male Sprague-Dawley rats weighing 200-250 g were used in the study. The vasodilatory responses to bradykinin (1 nM-1 μM) were studied on isolated rat aorta rings contracted with norepinephrine (0.1 μM) following incubation with dipyrone (100, 700, and 2,000 μM). The relaxant responses of dipyrone (100, 700, and 2,000 μM) were also compared on the isolated rat urinary bladder contracted with bradykinin (n = 8). A bacterial lipopolysaccharide was used for the induction of inflammation (n = 8). The levels of PGE(2), PGF(1α), TXB(2), nitric oxide synthase (NOS), IL-10, and TNF-α were all determined in both the plasma and the perfusate of the aorta preparations (n = 5). The vasodilatory activities of bradykinin and des-Arg9-bradykinin were significantly increased upon the inhibition of COX-3 (dipyrone at 100 μM). These effects disappeared in the inflamed group. PGE(2), PGF1α, and TXB(2) were significantly high, but NOS activity was low in the aorta perfusate after the inhibition of COX-3. Dipyrone showed the relaxant activity of the urinary bladder contracted with bradykinin. The vasodilatory activity of des-Arg(9)-bradykinin was in the inflamed group but not in the non-inflamed group. Bradykinin did not contract urinary bladder in inflamed group. The results suggest that COX-induced products may play an important role in the bradykinin-induced rat aortic smooth muscle relaxations.

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Section: Discussionmentioning

confidence: 98%

The Role of Inflammation and COX-Derived Prostanoids in the Effects of Bradykinin on Isolated Rat Aorta and Urinary Bladder

et al. 2011

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“…[31][32][33][34][35][36] Bradykinin stimulates cyclooxygenase activity through both kinin B1 and B2 receptors. [31][32][33][34][35][36] Bradykinin stimulates cyclooxygenase activity through both kinin B1 and B2 receptors.…”

Section: Role Of Cox-2mentioning

confidence: 99%

COX-2 Mediated Induction of Endothelium-independent Contraction to Bradykinin in Endotoxin-treated Porcine Coronary Artery

Kim

Zhao

et al. 2014

Journal of Cardiovascular Pharmacology

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This study examined the vascular effects of bradykinin in health and vascular inflammation comparing responses of isolated pig coronary arteries in the absence and presence of endotoxins. Bradykinin induced contractions in lipopolysaccharide-treated, but not untreated, arterial rings without endothelium. The B2-receptor antagonist HOE140, but not the B1-receptor inhibitor SSR240612, blocked these endothelium-independent contractions in response to bradykinin. The bradykinin-induced contractions were blocked by indomethacin, celecoxib, and terbogrel but not valeryl salicylate, AH6809, AL 8810, or RO1138452. They were attenuated by N-(p-amylcinnamoyl) anthranilic acid, and by diethyldithiocarbamate plus tiron but not by L-NAME. Quantitative reverse-transcription polymerase chain reaction revealed significant upregulations of messenger RNA expressions of B1 receptors, COX-2, and thromboxane A synthase 1 (TBXAS1) following lipopolysaccharide incubation but not of B2 receptors or COX-1. The present data demonstrate that bradykinin induces contractions mediated by the COX-2 pathway in endotoxin-treated pig coronary arteries. These results support differential roles of bradykinin in health and disease.

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“…Secretomotor neurons in the submucosal plexus are the final common motor pathways from the integrative networks of the enteric nervous system to the intestinal secretory glands. They transmit the signals for autonomic minute-tominute regulation of mucosal secretion and liquidity of the intestinal contents in concert with submucosal vasodilation and increased blood flow in support of the stimulated secretion [24][25][26][27] . Enhanced mucosal secretion, after elevation of excitability in secretomotor neurons, increases the liquidity of the luminal contents and might lead to neurogenic secretory diarrhea.…”

Section: Bk Stimulates CLmentioning

confidence: 99%

Neurophysiological mechanisms of bradykinin-evoked mucosal chloride secretion in guinea pig small intestine

Zhao

et al. 2016

WJGP

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Bradykinin stimulates prostaglandin E₂ production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa in vitro

Cited by 16 publications

References 39 publications

The Role of Inflammation and COX-Derived Prostanoids in the Effects of Bradykinin on Isolated Rat Aorta and Urinary Bladder

The Role of Inflammation and COX-Derived Prostanoids in the Effects of Bradykinin on Isolated Rat Aorta and Urinary Bladder

COX-2 Mediated Induction of Endothelium-independent Contraction to Bradykinin in Endotoxin-treated Porcine Coronary Artery

Neurophysiological mechanisms of bradykinin-evoked mucosal chloride secretion in guinea pig small intestine

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Bradykinin stimulates prostaglandin E2 production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa in vitro

Cited by 16 publications

References 39 publications

The Role of Inflammation and COX-Derived Prostanoids in the Effects of Bradykinin on Isolated Rat Aorta and Urinary Bladder

The Role of Inflammation and COX-Derived Prostanoids in the Effects of Bradykinin on Isolated Rat Aorta and Urinary Bladder

COX-2 Mediated Induction of Endothelium-independent Contraction to Bradykinin in Endotoxin-treated Porcine Coronary Artery

Neurophysiological mechanisms of bradykinin-evoked mucosal chloride secretion in guinea pig small intestine

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Bradykinin stimulates prostaglandin E₂ production and cyclooxygenase activity in equine nonglandular and glandular gastric mucosa in vitro