FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3009271397> ?p ?o ?g. }

• W3009271397 abstract "The renin-angiotensin system is activated in acute severe asthma although the mechanism for is unclear. Angiotensin II is a weak bronchoconstrictor, potentiates the effects of other bronchoconstrictors and can be formed by inflammatory proteases. In vitro, angiotensin II is a growth promoter for human airway smooth muscle cells. The insertion/deletion polymorphism of the ACE gene accounts for variation in ACE activity and the deletion allele may be more frequent in asthmatics. In view of these facts, further clarification of the role of the renin-angiotensin system in asthma is required. Aims This thesis examines the factors causing activation of the renin-angiotensin system in acute severe asthma, the role of the ACE gene polymorphism, the putative effects of angiotensin II on the action of histamine in the human airway both in vitro and in vivo, the effects of angiotensin II on rat airway smooth muscle cell growth in vivo and seeks evidence for the existence of a local renin-angiotensin system in the human lung. 1. Mechanism of Activation of the Renin-Angiotensin System in Asthma Clinical data were obtained from 40 acute asthmatic hospital admissions and correlated with plasma levels of renin and angiotensin II. The genotype for the ACE gene polymorphism was determined in this group, a group of 20 non-asthmatic acute medical hospital admissions and 78 healthy volunteers to allow comparison of allele frequencies and correlation with both ACE activity and angiotensin II levels. Plasma renin and angiotensin II were elevated in some, but not all of the acute asthmatics and no correlation was found with any of the parameters measured. The DD homozygote for the ACE gene polymorphism had the highest ACE activity in all groups measured. There was a non-significant trend towards an increased frequency of the deletion allele in asthmatics compared with normal controls. An unexpected finding was the increased ACE activity for the DD and ID genotypes found in acute hospital admissions compared with healthy controls. The clinical significance of this is uncertain. 2. Effect of Angiotensin II on Histamine-Induced Bronchoconstriction The effect of angiotensin II on histamine-induced contraction of human bronchial rings in vitro was examined by constructing concentration-response curves to histamine (10-9M - 3x10-4M) in the presence and absence of sub-threshold doses of angiotensin II (10-7M - 10-6M). This was also studied in vivo in 8 asthmatic volunteers who had histamine bronchial provocation testing in a double-blinded fashion in the presence of infusions of placebo (5% dextrose) and angiotensin II (1 and 2 ng/kg/min). Angiotensin II in subthreshold doses for contraction of airway smooth muscle had no effect on histamine-induced bronchoconstriction in the human airway neither in vitro nor in vivo. 3. Effect of Angiotensin II on Remodelling of Rat Airway & Vasculature The effect of endogenous activation of the renin-angiotensin system by dietary sodium restriction and subcutaneous infusion of angiotensin II on the rat airways was compared to the mesenteric vasculature. DNA synthesis was measured by infusing the thymidine analogue bromo-2'-deoxyuridine subcutaneously then revealing those cells undergoing DNA synthesis using immunocytochemistry. Changes in the volume of the airway tissues were measured morphometrically. Endogenous activation of the renin-angiotensin system in rats known to increase arterial medial DNA synthesis results in increased renin mRNA expression in the renal juxta-glomerular cells with increased plasma aldosterone and plasma renin activity and manor insignificant variations in blood pressure. However, no change was seen m DNA synthesis or morphometry of the airways. Similarly, infusion of angiotensin II for two weeks in rats causes a rise in blood pressure and suppresses renal juxta-glomerular renin mRNA expression with a nonsignificant suppression of plasma renin activity. DNA synthesis increased in the mesenteric arterial media and there was a non-significant tendency towards the artery wall being thicker. No difference was found in DNA synthesis or morphometry of the airways. 4. Evidence for a Local Renin-Angiotensin System in the Human Lung Samples of normal human lung were obtained from thoracotomy specimens and were examined by immunocytochemistry for renin and ACE, and by in situ hybridisation and Northern blotting for renin mRNA, angiotensinogen mRNA, ACE mRNA and AT1 receptor mRNA. In situ angiotensin II receptor localisation and autoradiography were also performed. In human lung, ACE was identified in vascular endothelium however, no other components of the renin-angiotensin system could be found. In control rat lung tissue, angiotensin II receptors appeared to be present. Conclusion The renin-angiotensin system is activated in some acute asthmatics but the mechanism for this remains unclear." @default.
• W3009271397 created "2020-03-13" @default.
• W3009271397 creator A5007103580 @default.
• W3009271397 date "1999-01-01" @default.
• W3009271397 modified "2023-09-24" @default.
• W3009271397 title "Investigations on the Role of the Renin-Angiotensin System in Asthma" @default.
• W3009271397 hasPublicationYear "1999" @default.
• W3009271397 type Work @default.
• W3009271397 sameAs 3009271397 @default.
• W3009271397 citedByCount "0" @default.
• W3009271397 crossrefType "dissertation" @default.
• W3009271397 hasAuthorship W3009271397A5007103580 @default.
• W3009271397 hasConcept C126322002 @default.
• W3009271397 hasConcept C134018914 @default.
• W3009271397 hasConcept C170493617 @default.
• W3009271397 hasConcept C198710026 @default.
• W3009271397 hasConcept C27016395 @default.
• W3009271397 hasConcept C2776042228 @default.
• W3009271397 hasConcept C2779591629 @default.
• W3009271397 hasConcept C2908929049 @default.
• W3009271397 hasConcept C71924100 @default.
• W3009271397 hasConcept C84393581 @default.
• W3009271397 hasConceptScore W3009271397C126322002 @default.
• W3009271397 hasConceptScore W3009271397C134018914 @default.
• W3009271397 hasConceptScore W3009271397C170493617 @default.
• W3009271397 hasConceptScore W3009271397C198710026 @default.
• W3009271397 hasConceptScore W3009271397C27016395 @default.
• W3009271397 hasConceptScore W3009271397C2776042228 @default.
• W3009271397 hasConceptScore W3009271397C2779591629 @default.
• W3009271397 hasConceptScore W3009271397C2908929049 @default.
• W3009271397 hasConceptScore W3009271397C71924100 @default.
• W3009271397 hasConceptScore W3009271397C84393581 @default.
• W3009271397 hasLocation W30092713971 @default.
• W3009271397 hasOpenAccess W3009271397 @default.
• W3009271397 hasPrimaryLocation W30092713971 @default.
• W3009271397 hasRelatedWork W1964696346 @default.
• W3009271397 hasRelatedWork W1967185381 @default.
• W3009271397 hasRelatedWork W1970204455 @default.
• W3009271397 hasRelatedWork W1974659437 @default.
• W3009271397 hasRelatedWork W1984027129 @default.
• W3009271397 hasRelatedWork W1998333770 @default.
• W3009271397 hasRelatedWork W2002305140 @default.
• W3009271397 hasRelatedWork W2015820511 @default.
• W3009271397 hasRelatedWork W2015914453 @default.
• W3009271397 hasRelatedWork W2071983459 @default.
• W3009271397 hasRelatedWork W2091337477 @default.
• W3009271397 hasRelatedWork W2151204220 @default.
• W3009271397 hasRelatedWork W2154221900 @default.
• W3009271397 hasRelatedWork W2166444611 @default.
• W3009271397 hasRelatedWork W2172217338 @default.
• W3009271397 hasRelatedWork W2189396410 @default.
• W3009271397 hasRelatedWork W2254622074 @default.
• W3009271397 hasRelatedWork W2320021182 @default.
• W3009271397 hasRelatedWork W2327780757 @default.
• W3009271397 hasRelatedWork W2368704906 @default.
• W3009271397 isParatext "false" @default.
• W3009271397 isRetracted "false" @default.
• W3009271397 magId "3009271397" @default.
• W3009271397 workType "dissertation" @default.