Aggressive role of vasopressin in development of different gastric lesions in rats

László, Ferenc; Karácsony, G; Pávó, Imre; Varga, Csaba; Rojik, I.

doi:10.1016/0014-2999(94)90052-3

Cited by 31 publications

(9 citation statements)

References 35 publications

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“…An increase of vasopressin content has previously been observed in the gastric mucosa 1 h after indomethacin treatment, whereas the plasma vasopressin level remained unchanged. In addition, the vasopressin V 1 receptor antagonist as well as vasopressin deficiency protected the gastric mucosa against indomethacin‐induced injury 16 . The source of vasopressin in the current studies is not known, but studies on isolated vascular mesenteric, pulmonary, aortic and renal endothelial tissue have shown such cells to be capable of releasing vasopressin 21 …”

Section: Discussionmentioning

confidence: 80%

“…In the present study, the role of NO in the modulation of the early phase of jejunal microvascular plasma leakage, as a measure of acute intestinal inflammation, has been evaluated in the rat following indomethacin administration. In previous studies, endogenous vasopressin was shown to be an aggressive factor involved in gastric mucosal damage provoked by indomethacin 16 and in the early phase of microvascular injury in the bowel during sepsis 17 . In our present work using the vasopressin pressor (V 1 ) receptor antagonist, d(CH 2 ) 5 Tyr(Me)AVP, 18 we have investigated the interactions between endogenous vasopressin with constitutively formed NO in the early phase following indomethacin administration that lead to intestinal microvascular injury.…”

Section: Introductionmentioning

confidence: 98%

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Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

László

Whittle

1998

J of Gastro and Hepatol

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The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, NG‐nitro‐L‐arginine methyl ester (L‐NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L‐NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L‐NAME (2–10 mg/kg, s.c.), significant dose‐dependent plasma leakage occurred in the jejunum. Pretreatment with L‐arginine (300 mg/kg s.c.) 15 min prior to L‐NAME prevented these changes in microvascular permeability. Moreover, pretreatment with the vasopressin pressor‐receptor antagonist, d(CH2)5Tyr(Me)AVP (0.01– 0.2 μg/kg, s.c.) dose‐dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving vasopressin in the rat jejunum. This suggests a protective role of NO, formed by constitutive NO synthase, counteracting effectively the deleterious actions of endogenous vasopressin.

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Section: Discussionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 98%

Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

László

Whittle

1998

J of Gastro and Hepatol

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“…There are many additional works relating exogenous testosterone with an improvement in the ability to increase the number of receptors of endogenous vasopressin, an important aggressive factor of gastrointestinal mucosa, 27,28) 1154…”

Section: Resultsmentioning

confidence: 99%

Antiulcerogenic Activity of Four Extracts Obtained from the Bark Wood of <i>Quassia amara</i> L. (Simaroubaceae)

Toma

Gracioso

Andrade³

et al. 2002

Biological & Pharmaceutical Bulletin

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Gastric ulcers are among the most important diseases in the world. The gastric mucosa is continuously exposed to potentially injurious agents such as acid, pepsin, bile acids, food ingredients, bacterial products, and drugs. 1) These agents have been implicated in the pathogeneses of gastric ulcer, such as an increase in gastric acid and pepsin secretion, a decrease in gastric blood flow, the suppression of endogenous generation of prostaglandins, inhibition of mucosal growth and cell proliferation, and alteration of gastric mobility.2)The current therapy for this disease continues to have, as one of its major goals, the control of Helicobacter pylori as well as H ϩ /K ϩ -ATPase, acid secretion and a subsequent reversal of mucosal damage and inflammation. 3)Many pharmaceutical products have been employed for the treatment of gastroduodenal ulcer and peptic disease, and for decreasing mortality and morbidity rates, but they are not completely effective and produce many adverse effects. Moreover, these pharmaceutical products are too expensive. 4)Plant extracts are some of the most attractive sources of new drugs and have been shown to produce promising results for the treatment of gastric ulcer. 5)Simaroubaceae is a large botanical family with pantropical distribution; only a few representatives occur in temperate regions. Quassia amara L., a representative of this family, is a neotropical forest shrub or small tree reputed in traditional medicine to have good effect on stomach diseases, especially gastric ulcers. In Brazil, this species is found in a region from the border with Guiana to the state of Maranhão. It is popularly known in Latin American as "Amargo", "Hombre Grande", "Simaruba", "Pau Quassia", "Murubá", "Murupá" and "Quina de Caiena". 6)This plant is a source of several compounds which include both b-carbonile and cantin-6 alkaloids, as well as, primarily, the bitter components known as quassinoids, a group of substances belonging to the terpens class. Antimalarial, antifeedant and antifertility pharmacological activities are atributted to these quassinoids. 7)In considering the use of this plant in Brazilian folk medicine and the several chemical substances isolated and identified from Quassia amara bark, we have performed a study of the antiulcerogenic effects for four different extracts of this species using standard rodent models of induced gastric ulcer. Quassia amara L., a neotropical forest shrub of the Simaroubaceae family, is widely used in Caribbean folk medicine and in some northern states of Brazil for the treatment of gastric ulcers. This plant is a source of numerous compounds including both b b-carbonile and cantin-6 alkaloids as well as, primarily, the bitter compounds known as quassinoids. We analyzed the possible antiulcerogenic activities of four extracts of different polarities: 70% ethanol (70% EtOH), 100% EtOH, 100% dichloromethane (DCM), and 100% hexane (HEX) obtained from Quassia amara bark. All extracts, administered at doses of 5000 mg/kg orally and 1000 mg/kg intraperitonea...

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“…The potential benefits of low-dose vasopressin include restoration of vasomotor tone and preservation of renal blood flow and urine output 3 . High-dose vasopressin may compromise organ blood distribution and tissue perfusion due to excessive vasoconstriction: reduction in splanchnic blood flow 14 , aggravation of gastric lesions in stressed rats 15 or reduction in gastric mucosal hyperaemia 16 in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Terlipressin Infusion in Catecholamine-resistant Shock

Jolley

Keulenaer

Potter

et al. 2003

Anaesth Intensive Care

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Catecholamine-resistant shock is not uncommon in intensive care. Bolus dose terlipressin (a vasopressin analogue) has been used successfully in this setting allowing cessation of other vasopressor agents. The relative vasopressin deficiency in combination with the restoration of the vascular tone (by blocking adenosine triphosphate potassiumsensitive channels) by exogenous vasopressin may be the explanation of these beneficial effects. We describe a case report where the use of a continuous terlipressin infusion was associated with a dramatic improvement. To our knowledge there have been no previous reports of the use of terlipressin by continuous infusion for the treatment of catecholamine-resistant shock.

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Aggressive role of vasopressin in development of different gastric lesions in rats

Cited by 31 publications

References 35 publications

Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

Antiulcerogenic Activity of Four Extracts Obtained from the Bark Wood of <i>Quassia amara</i> L. (Simaroubaceae)

Terlipressin Infusion in Catecholamine-resistant Shock

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