Matches in SemOpenAlex for { <https://semopenalex.org/work/W2893149089> ?p ?o ?g. }
Showing items 1 to 65 of
65
with 100 items per page.
- W2893149089 abstract "Essential hypertension is an increase in the systemic arterial blood pressureWithout an apparent cause. Hypertension affects about 25% of the world population.According to a study conducted in urban areas, the prevalence of systolic andDiastolic hypertension in india is 40.9% and 29.3%, respectively (das,sanyal, &Basu, 2005). In india, hypertension is the predominant risk factor for coronary arteryDisease (cad) in all ethnic groups. Therefore, understanding the pathophysiology ofHypertension is important. More than 90% of hypertensive individuals suffer fromEssential hypertension. It shows an earlier onset in men, than in women. The factorsLinked to essential hypertension are age, obesity, smoking and stress. A strongGenetic predisposition is also suggested. Blood pressure is mainly under the controlOf blood volume and peripheral resistance, determined predominantly by theArterioles. It is influenced by hormones as well as by the local factors. Nitric oxide(no), a second messenger of immense importance in the maintenance of bloodPressure is a vasodilator, which brings down the peripheral resistance.No is synonymous with endothelial derived relaxing factor (katzung, 2004).It acts via the heme moiety of guanylyl cyclase to produce cyclic guanosine monophosphate(cgmp). This reduces the levels of cytosolic ca++ and alsoPhosphorylates myosin light chain kinase(mlck). No decreases the activity ofPlatelets and neutralizes free radicals. Thus, it plays a major role in preventingAtherosclerosis. It prevents binding of leucocytes to the endothelium and decreasesInflammation. Hence, it is considered as an important factor in preventingHypertension. There is a close link between the level of available no and bloodPressure. Various studies suggest that, the factors influencing the levels of no willHave an important role in the pathophysiology and susceptibility to essentialHypertension.The main source of circulating no is the endothelium, where it is producedFrom the amino acid l-arginine by the action of endothelial nitric oxide synthase(enos). This is a constitutive enzyme with its gene (enos/nos3) on chromosome7. Nos is a heme protein that exists in its inactive form as a monomer, but dimerizesBefore action. No is produced by the neurons too, where neuronal nitric oxideSynthase (nnos/ nos1), another constitutive enzyme, is responsible for itsProduction. Inducible nitric oxide synthase (inos/nos2) on chromosome 17 isInduced mostly during inflammation. It is responsible for the harmful effects of theGas. It is expressed in macrophages, smooth muscle cells and hepatocytes and isResponsible for pathological vaso-relaxation. The enos is membrane bound, whileThe other two are present in soluble form. No is removed from circulation mostly byReaction with free radicals, such as superoxide. The balance between the productionAnd removal of no is very important with regard to hypertension .Because enos is the major enzyme responsible for nitric oxide production,Variation in its expression and activity can be linked to hypertension. It has beenFound that, a g to t polymorphism in the exon 7 region leading to a change fromGlutamate at 298 position to aspartate decreases the expression of the enzyme, butHas no effect on the activity (kato et al., 1999). Another study has suggested that,Such a change causes the enzyme to undergo selective proteolysis (hingorani, 2003).In intron 4 of nos3, there can be four 27 bp repeats (allele ‘a’) or five (allele‘b’). Presence of allele ‘a’, rather than the wild-type allele ‘b’, though shows anIncrease in the expression of the enzyme, reduces its activity (kato et al. 1999). ThePromoter region t to c polymorphism has also been shown to reduce the expressionOf the enzyme. The association of these polymorphisms to hypertension has beenControversial. Whereas, the g to t polymorphism has been associated withHypertension in many ethnic groups (miyamoto et al., 1998), including the indianPopulation (srivastava k, narang r, sreenivas v, das s and das n ,2008), theAssociation of the other two polymorphisms has been more controversial (hingorani,2003; kato et al., 1999). Few studies have been conducted on asians, especiallyThose living in india, regarding these polymorphisms.Hence, it is proposed to study the association of serum no level and enosIntron4 polymorphism in essential hypertension." @default.
- W2893149089 created "2018-10-05" @default.
- W2893149089 creator A5035757661 @default.
- W2893149089 date "2011-04-01" @default.
- W2893149089 modified "2023-09-24" @default.
- W2893149089 title "Serum Nitric Oxide Level and Endothelial NitricOxide Synthase Gene INTRON4 VNTR Polymorphism inEssential Hypertension." @default.
- W2893149089 hasPublicationYear "2011" @default.
- W2893149089 type Work @default.
- W2893149089 sameAs 2893149089 @default.
- W2893149089 citedByCount "0" @default.
- W2893149089 crossrefType "dissertation" @default.
- W2893149089 hasAuthorship W2893149089A5035757661 @default.
- W2893149089 hasConcept C120770815 @default.
- W2893149089 hasConcept C126322002 @default.
- W2893149089 hasConcept C134018914 @default.
- W2893149089 hasConcept C164705383 @default.
- W2893149089 hasConcept C2777097880 @default.
- W2893149089 hasConcept C2780972559 @default.
- W2893149089 hasConcept C2780994212 @default.
- W2893149089 hasConcept C2908647359 @default.
- W2893149089 hasConcept C519581460 @default.
- W2893149089 hasConcept C57190642 @default.
- W2893149089 hasConcept C71924100 @default.
- W2893149089 hasConcept C84393581 @default.
- W2893149089 hasConcept C99454951 @default.
- W2893149089 hasConceptScore W2893149089C120770815 @default.
- W2893149089 hasConceptScore W2893149089C126322002 @default.
- W2893149089 hasConceptScore W2893149089C134018914 @default.
- W2893149089 hasConceptScore W2893149089C164705383 @default.
- W2893149089 hasConceptScore W2893149089C2777097880 @default.
- W2893149089 hasConceptScore W2893149089C2780972559 @default.
- W2893149089 hasConceptScore W2893149089C2780994212 @default.
- W2893149089 hasConceptScore W2893149089C2908647359 @default.
- W2893149089 hasConceptScore W2893149089C519581460 @default.
- W2893149089 hasConceptScore W2893149089C57190642 @default.
- W2893149089 hasConceptScore W2893149089C71924100 @default.
- W2893149089 hasConceptScore W2893149089C84393581 @default.
- W2893149089 hasConceptScore W2893149089C99454951 @default.
- W2893149089 hasLocation W28931490891 @default.
- W2893149089 hasOpenAccess W2893149089 @default.
- W2893149089 hasPrimaryLocation W28931490891 @default.
- W2893149089 hasRelatedWork W1593364036 @default.
- W2893149089 hasRelatedWork W1969798110 @default.
- W2893149089 hasRelatedWork W1995012658 @default.
- W2893149089 hasRelatedWork W1997961649 @default.
- W2893149089 hasRelatedWork W2021184274 @default.
- W2893149089 hasRelatedWork W2055843480 @default.
- W2893149089 hasRelatedWork W2092509134 @default.
- W2893149089 hasRelatedWork W2093217834 @default.
- W2893149089 hasRelatedWork W2109157494 @default.
- W2893149089 hasRelatedWork W2116550659 @default.
- W2893149089 hasRelatedWork W2148645037 @default.
- W2893149089 hasRelatedWork W2318984587 @default.
- W2893149089 hasRelatedWork W2331943600 @default.
- W2893149089 hasRelatedWork W2333829132 @default.
- W2893149089 hasRelatedWork W2416380388 @default.
- W2893149089 hasRelatedWork W2743159965 @default.
- W2893149089 hasRelatedWork W2794328684 @default.
- W2893149089 hasRelatedWork W2981112971 @default.
- W2893149089 hasRelatedWork W37971958 @default.
- W2893149089 hasRelatedWork W771308944 @default.
- W2893149089 isParatext "false" @default.
- W2893149089 isRetracted "false" @default.
- W2893149089 magId "2893149089" @default.
- W2893149089 workType "dissertation" @default.