Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 9772541

[The decrease of gastric mucosal blood flow in obstructive jaundice under stress].

N Yang·W Xu·J Duan
View original source ↗Export metadata ↓

Abstract

OBJECTIVE: To investigate the cause of decrease of gastric mucosal blood flow (GMBF) in obstructive jaundice under stress. METHODS: With common bile duct ligation (CBDL) in Wistar rats under cold restraint stress, GMBF and the content of Endothelin-1, Angiotensin-II, H2, alpha 1 receptor in gastric mucosa were measured. Before stress anti-ET-1 serum, Enalapril, Cimentidine and Phetolamins were administrated, and the change of GMBF was studied. RESULTS: GMBF was significantly decreased in CBDL in stress than those in control subjects. The content of ET1 and Ang-II was significantly increaced, the density of H2 and alpha 1 receptor was significantly decreased. Before stress antagonist was administrated, and GMBF was significantly increased. CONCLUSION: GMBF was decreased by increased ET, Ang-II and decreased H2, alpha 1 receptor in CBDL, under stress. Antagonist improved gastric mucosal blood flow. They had protection from gastric mucosa.

Explore related subjects

Angiotensin IIAnimalsCholestasisCold TemperatureEndothelin-1Gastric MucosaMaleRatsRats, WistarReceptors, Histamine H2Regional Blood FlowStomach UlcerStress, PhysiologicalEnglish AbstractJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

N Yang, W Xu, J Duan. 1997. [The decrease of gastric mucosal blood flow in obstructive jaundice under stress].. https://pubmed.ncbi.nlm.nih.gov/9772541/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2000

Calcineurin blockade prevents cardiac mitogen-activated protein kinase activation and hypertrophy in renovascular hypertension.

Chronic stimulation of the renin-angiotensin system induces an elevation of blood pressure and the development of cardiac hypertrophy via the actions of its effector, angiotensin II. In cardiomyocytes, mitogen-activated protein kinases as well as protein kinase C isoforms have been shown to be important in the transduction of trophic signals. The Ca(2+)/calmodulin-dependent phosphatase calcineurin has also been suggested to play a role in cardiac growth. In the present report, we investigate possible cross-talks between calcineurin, protein kinase C, and mitogen-activated protein kinase pathways in controlling angiotensin II-induced hypertrophy. Angiotensin II-stimulated cardiomyocytes and mice with angiotensin II-dependent renovascular hypertension were treated with the calcineurin inhibitor cyclosporin A. Calcineurin, protein kinase C, and mitogen-activated protein kinase activations were determined. We show that cyclosporin A blocks angiotensin II-induced mitogen-activated protein kinase activation in cultured primary cardiomyocytes and in the heart of hypertensive mice. Cyclosporin A also inhibits specific protein kinase C isoforms. In vivo, cyclosporin A prevents the development of cardiac hypertrophy, and this effect appears to be independent of hemodynamic changes. These data suggest cross-talks between the calcineurin pathway, the protein kinase C, and the mitogen-activated protein kinase signaling cascades in transducing angiotensin II-mediated stimuli in cardiomyocytes and could provide the basis for an integrated model of cardiac hypertrophy.

Angiotensin II↗
PubMed2000

Observation of the ultrastructure and synaptic relationships of angiotensin II-like immunoreactive neurons in the rat area postrema.

The ultrastructure and synaptic relationships of the angiotensin II-containing neurons in the area postrema of the rat were studied by immunocytochemistry using the avidin-biotin-complex-DAB method, and also using silver-gold intensification following the DAB reaction. At the light microscopic level, the angiotensin II-like immunoreactive neurons were observed within the area postrema, especially in the upper region. At the electron microscopic level, the angiotensin II-like immunoreactive cell bodies were observed as having a round, unindented nucleus. The nuclei of these neurons were not immunostained. The angiotensin II-like immunoreactive axon terminals often contained a few dense core vesicles in addition to many small clear synaptic vesicles. Numerous axon terminals were found to make synapses on immunonegative dendrites; they were also found to make synapses on angiotensin II-like immunoreactive dendrites. Many angiotensin II-like immunoreactive dendrites received synapses from immunonegative axon terminals. Although angiotensin II-like immunoreactive cell bodies were sometimes postsynaptic to immunoreactive axon terminals, they did not receive synapses from immunonegative axon terminals. These results provide solid morphological evidence of AP endogenous angiotensin II and confirm that in spite of circulating angiotensin II, the local neurons in the AP may also play an important role in angiotensin II-induced cardiovascular regulation.

Angiotensin II↗
PubMed2000

Angiotensin II type 1 receptor antagonists. Why do some of them produce insurmountable inhibition?

Chinese hamster ovary (CHO) cells expressing human recombinant angiotensin II type 1 (AT(1)) receptors offer a useful experimental system in which antagonist binding and inhibition of AT-induced inositol mono-, bis-, and trisphosphate accumulation can be measured under identical experimental conditions. The major conclusions of the current work are: All investigated AT(1) antagonists are competitive with respect to AT. They bind to a common or overlapping binding site on the receptor in a mutually exclusive way. Reduction of the maximal angiotensin II response, i.e. insurmountable inhibition, is observed only when the cells are preincubated with candesartan, EXP3174, or irbesartan and is strictly related to the dissociation rate of the antagonist-receptor complex. On the other hand, inhibition by losartan is fully surmountable by AT, and its dissociation is very rapid. With respect to the binding kinetics, the antagonist-receptor complex can adopt a fast and a slow reversible state. The equilibrium between both states, which is dependent upon the nature of the antagonists, determines the extent of insurmountable inhibition. Consequently, the dissociation rate of the different antagonists correlates with the amount of insurmountable inhibition. In addition to the relatively slow dissociation of candesartan, reassociation to the receptor, which is measurable in CHO-AT(1) cells, likely contributes to its long-lasting blood pressure lowering effect in vivo.

Angiotensin II↗