• Animal cells and systems
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• v.8 no.1
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• pp.41-47
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• 2004

The kallikrein-kinin system affects regulation of blood pressure, and genes encoding for the components of this system have been considered as good candidates for hypertension. To evaluate the relationship between genetic polymorphisms of candidate genes involved in this system and hypertension, we performed case-control studies using genetic markers in Korean normotensives and hypertensives, respectively. By association study, there was a marginal association with hypertension in AA genotype distribution of A1789G polymorphism in the hKLK1 gene (P=0.0754). Thus, this genetic polymorphism may weakly contribute to the susceptibility to hypertension in Koreans. We also observed that significant linkage disequilibrium exists among three polymorphic sites in the hKLK1 gene studied, suggesting that the three genetic polymorph isms can be useful as genetic markers in clinical association studies. Further studies using larger sample sizes and more genetic markers will be needed to clarify genetic influence of kallikrein-kinin system for hypertension.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.05a
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• pp.69-69
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• 2004

• 대한생식의학회:학술대회논문집
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• 2004.11a
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• pp.38-38
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• 2004

• Journal of Integrative Natural Science
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• v.10 no.2
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• pp.74-77
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• 2017

Bradykinin receptor B2 (B2R) is a GPCR protein which binds with the inflammatory mediator hormone bradkynin. Kallidin, a decapeptide, also signals through this receptor. B2R is crucial in the cross-talk between renin-angiotensin system (RAS) and the kinin-kallikrein system (KKS) and in many processes including vasodilation, edema, smooth muscle spasm and pain fiber stimulation. Thus the structural study of the receptor becomes important. We have predicted the peptide structures of Bradykinin and Kallidin from their amino acid sequences and the structures were docked with the receptor structure. The results obtained from protein-protein docking could be helpful in studying the B2R structural features and in the pathophysiology in various diseases related to it.

• Journal of Integrative Natural Science
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• v.9 no.4
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• pp.234-240
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• 2016

Bradykinin receptor B2, a GPCR protein, binds with the inflammatory mediator hormone bradkynin. It plays an important role in cross-talk between the renin-angiotensin system (RAS) and the kinin-kallikrein system (KKS). Also, it is involved in many processes including vasodilation, edema, smooth muscle spasm and pain fiber stimulation. Hence, studuying the structural features of the receptor becomes important. But the unavailability of the three dimensional structure of the protein makes the analysis difficult. Hence we have performed the homology modelling of Bradykinin receptor B2 with 5 different templates. 25 different homology models were constructed. Two best models were selected based on the model validation. The developed models could be helpful in analysing the structural features of Bradykinin receptor B2 and in pathophysiology of various disorders related to them.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.191-196
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• 1994

Captopril, an inhibitor of angiotensin converting enzyme, is also known to inhibit the degradation of bradykinin. We examined the effects of intracerebroventricular (ICV) captopril on the central pressor response to bradykinin in normotensive, 2-kidney, 1 clip Goldblatt (GHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Captopril (1 mg) and bradykinin (5 nmol) were administered into the right lateral cerebral ventricle, and blood pressure and heart rate were continuously monitored throughout the experiment. ICV captopril alone did not affect the blood pressure within 10 minutes but it significantly augmented the central pressor response to bradykinin in GHR. On the contrary, captopril was without effect on the pressor response to bradykinin in normotensive and DOCA-salt rats. These findings indicate that endogenous kinins are not critical in regulating arterial pressure in normotensive and DOCA hypertensive rats. However, in GHR, an enhanced activity of the brain kallikrein-kinin system in maintaining the high blood pressure is suggested.