Enhanced Bradykinin-Stimulated Prostaglandin Release in the Acutely Inflamed Guinea Pig Gallbladder Is Due to New Synthesis of Cyclooxygenase 1 and Prostacyclin Synthase

Bogar, Linda; Bartula, L.; Parkman, Henry P.; Myers, Stuart I.

doi:10.1006/jsre.1999.5612

Cited by 25 publications

(18 citation statements)

References 24 publications

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“…(30)(31)(32) In 1993, we provided the first report that insulin at physiologic amounts stimulated the synthesis of the prostanoid in endothelial cells. (33) 3.…”

Section: Inhibition Of Platelet Aggregationmentioning

confidence: 98%

The role of insulin as an antithrombotic humoral factor

Chakraborty

Sinha

2003

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Insulin is well known for its essential role in carbohydrate metabolism: insulin deficiency results in the development of diabetes mellitus. It has been known for many years that people with diabetes mellitus are predisposed to develop thrombotic diseases including myocardial infarction. It was thought that the thrombus formation was the consequence of impaired carbohydrate metabolism. In recent years, it has become apparent that insulin is capable of ameliorating several pathophysiological events, leading to the inhibition and dissolution of the formed thrombus in the system. These insulin-induced events include inhibition of platelet aggregation by prompting the synthesis of NO in platelet and prostacyclin in endothelial cells. Furthermore, insulin upregulates prostacyclin receptors and downregulates alpha(2) adrenergic receptor in platelets, thereby amplifying the inhibition of platelet aggregation. Insulin also releases tissue plasminogen activator, a potent thrombolytic enzyme, from the platelet membrane which dissolves the formed thrombus leading to the resumption of normal blood circulation. In effect, insulin could be an essential tool in the control of thrombotic disorders.

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“…(30)(31)(32) In 1993, we provided the first report that insulin at physiologic amounts stimulated the synthesis of the prostanoid in endothelial cells. (33) 3.…”

Section: Inhibition Of Platelet Aggregationmentioning

confidence: 98%

The role of insulin as an antithrombotic humoral factor

Chakraborty

Sinha

2003

BioEssays

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“…It was also known that the contractile response of normal rat bladder to B 2 receptor agonists can be blocked by COX inhibitors [16]. Several studies revealed that inflammation modulates the effects of bradykinin [6,17,18]. It was demonstrated that the contractile response to BK could not be reduced by COX inhibitors in inflamed bladder [6].…”

Section: Introductionmentioning

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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“…The activation of B 2 receptor leads to transduction of various signaling pathways, and most of the final released substances are cytokines and other inflammatory mediators, such as eicosanoids [72][73][74][75][76]. Activation of B 2 receptors induces a rapid release of eicosanoids, and a late release of prostaglandin E2 [77], probably by up-regulation of COX-2 [78].…”

Section: Inflammationmentioning

confidence: 99%