• Journal of Community Nutrition
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• v.8 no.2
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• pp.69-75
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• 2006

Adipose tissue has now been recognized as a rich source of metabolically active molecules that include leptin and angiotensinogen (AGT), the precursor of angiotensin II (Ang II). Both of which have been implicated in the pathogenesis of metabolic alteration and hypertension associated with obesity. In this study, we examined the relationship between body mass index (BMI), adipocyte size, leptin, Ang II secretion and mRNA expression in human adipose tissue obtained from female subjects. Leptin and Ang II were analyzed using specific radioimmunoassay kits following a 48hour tissue culture. Leptin and Ang II secretion varied from 1.4 - 72.1ng/g and 0.8 - 57.3pg/g of tissue respectively. These large individual variations limit significant correlation between BMI, leptin and Ang II secretion. Ang II secretion was significantly higher in the obese than the non-obese (p < 0.05) and positively correlated with BMI. However, no difference in leptin secretion between the obese and the non-obese was observed and leptin secretion showed negative correlation with BMI. No difference in leptin and AGT mRNA expression in adipose tissue between the obese and the non-obese was observed. Although several limitations of this study, we found increased Ang II secretion in obese patients compared with non-obese patients, and positive correlation between AGT and BMI. Observed difference in AGT expression between the obese and the non-obese in this study might be of importance in relation with obesity related hypertension. (J Community Nutrition 8(2): 69-75, 2006)

• Journal of Life Science
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• v.25 no.2
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• pp.231-236
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• 2015

Angiotensin II (AngII) is an essential hormone that affects vascular physiology. For example, stimulation of vascular smooth muscle cells (VSMCs) rapidly induces vasoconstriction and results in the up-regulation of blood pressure. Chronic stimulation of VSMCs with AngII also results in hypertrophy. In this study, we confirmed an involvement of phosphatidylinositol 3-kinase (PI3K)-dependent calcium mobilization in AngII-induced generation of reactive oxygen species (ROS). Stimulation of rat aortic smooth muscle cells (RASMCs) with AngII significantly induced the generation of ROS in a dose- and time-dependent manner. AngII-induced generation of ROS was completely abolished by pharmacological inhibition of PI3K (with LY294002), but inhibition of the ERK signaling pathway had no effect. AngII-induced calcium mobilization was completely blocked by inhibition of PI3K, whereas inhibition of the ERK signaling pathway by PD98059 was ineffective. Depletion of extracellular calcium or inhibition of the L-type calcium channel by nifedipine completely blocked AngII-induced calcium mobilization. Depletion of extracellular calcium by EGTA and incubation of RASMCs with calcium-free medium both significantly blocked AngII-induced ROS generation. Inhibition of the L-type calcium channel also significantly blocked AngII-induced ROS generation. These results suggest that AngII-induced ROS generation is regulated by calcium mobilization, which, in turn, is modulated by a PI3K/L-type calcium channel signaling pathway.

• Proceedings of the Korean Society of Fisheries Technology Conference
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• 2002.10a
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• pp.193-194
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• 2002

Angiotensin I converting enzyme (ACE) inhibitor was purified from Crassostrea gigas. The ACE belongs to the class of metalloprotease. This enzyme plays an important physiological role in regulating blood pressure of the rennin-angiotensin system by converting from angiotensin I to octapeptide angiotensin II, a potent vasoconstrictor and by inactivating bradykinin, which has depressor action. (omitted)

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 1976.10a
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• pp.188.3-189
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• 1976

Angiotensin II는 peptide (octa)성 hermone으로 취급되고 있으며 강한 blood pressor activity를 나타내고있다. 이와 관련해서 근내 미생물 유래의 혈압강하성물질에 대한 관심이 높아지고 있으며 이것은 여러가지 면에서 흥미를 느끼게 하고있다. 물질을 미생물계에서 검색코저 시도하였으며 여기서 사용한 방법이 이 연구에 적용될 수 있으리라고 생각됨으로 그 방법을 여기에 발표코저 한다.

• Archives of Pharmacal Research
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• v.18 no.3
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• pp.215-216
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• 1995

• Food Science of Animal Resources
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• v.40 no.1
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• pp.106-117
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• 2020

Cellular senescence is associated with age-related vascular disorders and has been implicated in vascular dysfunctions. Here, we show that duck oil-loaded nanoemulsion (DO-NE) attenuates premature senescence of vascular smooth muscle cells (VSMCs) triggered by angiotensin II (Ang II). Compared with control nanoemulsion (NE), DO-NE significantly inhibited the activity of senescence-associated β-galactosidase, which is a biomarker of cellular senescence, in Ang II-treated VSMCs. SIRT1 protein expression was dose- and time-dependently induced in VSMCs exposed to DO-NE, but not in those exposed to NE, and SIRT1 promoter activity was also elevated. Consistently, DO-NE also dose-dependently rescued Ang II-induced repression of SIRT1 expression, indicating that SIRT1 is linked to the anti-senescence action of DO-NE in VSMCs treated with Ang II. Furthermore, the SIRT1 agonist resveratrol potentiated the effects of DO-NE on VSMCs exposed to Ang II, whereas the SIRT1 inhibitor sirtinol elicited the opposite effect. These findings indicate that DO-NE inhibits senescence by upregulating SIRT1 and thereby impedes vascular aging triggered by Ang II.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.17 no.11
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• pp.708-715
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• 2016

This study examined the effects of an extract of Dendropanax morbifera on blood pressure, Angiotensin II, Angiotensin Converting Enzyme, Aldosterone, and lipid levels of spontaneously hypertensive rats. The groups were as follows: Control group, Hypertension control group, Water extract treated group, Ethanol extract treated group, n- hexane fraction treated group, Ethyl acetate fraction treated group, n- butanol fraction treated group, and Water fraction treated group. The blood pressure, and Angiotensin II, and Angiotensin Converting Enzyme, and Aldosterone levels were lower in the Ethyl acetate fraction treated group than in the hypertension control group. The change in blood pressure was lower in the Water extract treated group, Ethyl acetate fraction treated group, Ethanol extract treated group, n- hexane fraction treated group, and n- butanol fraction treated group than the hypertension control group. The concentration of Angiotensin II was lower in the Ethyl acetate fraction treated group, Ethanol extract treated group, n- hexane fraction treated group, and n- butanol fraction treated group than the hypertension control group(p<0.05). The level of Angiotensin Converting Enzyme was lower in the Ethyl acetate fraction treated group, Ethanol extract treated group, n- hexane fraction treated group, and n- butanol fraction treated group than the hypertension control group. The concentration of Aldosterone was lower in the Ethyl acetate fraction treated group, and n- butanol fraction treated group than the hypertension control group(p<0.05). In addition, the concentration lower in the Water extract treated group, Ethanol extract treated group, n- hexane fraction treated group than the hypertension control group. Overall, the effect of the Dendropanax morbifera extracts might be useful as anti-hypertensive, and functional food agents.

• The Korean Journal of Physiology
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• v.25 no.1
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• pp.61-67
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• 1991

In order to determine possible relationships between the renin-angiotensin system and nephron heterogeneity, we compared the response of renin release and the angiotensin-converting enzyme (ACE) activity from different areas of the rat kidney. We used the renal cortical slices from the capsular surface to the juxtamedullary junction. Slices from outer one-third of the cortex were designated as outer cortical slices (OC), middle one-third as midcortical slices (MC), and inner one-third as inner cortical slices (IC). The renal renin content markedly decreased from OC and MC to IC. The basal lenin release was higher in OC than in MC or IC. On the contrary the percent change of renin release in response to L-isoproterenol was significantly higher in MC than in OC or IC. By TMB-8, the renin release in MC by $231{\pm}21%$ was higher than OC by $171{\pm}19%$ or IC by $$162{\pm}19. Angiotensin II suppressed renin release in OC and MC by $68{\pm}2,\;71{\pm}4%$ respectively, but only $40{\pm}7%$ in IC. The ACE activity was higher in IC than in OC, MC, medulla and papilla. The present data indicate that renin content and basal lenin release gradulally decreased from outer (OC) to inner (IC) cortex. The renin release in response to beta-adrenergic agonist, L-isoproterenol and intracellular calcium antagonist, TMB-8 were higher in MC than in OC and IC, but angiotensin II suppressed renin release less in IC than in OC and MC. It is suggested that juxtaglomerular cells of outer, mid-and inner cortices show a difference in renin release response to the stimuli.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.5
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• pp.467-472
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• 2015

Histone deacetylase (HDAC) has been recognized as a potentially useful therapeutic target for cardiovascular disorders. However, the effect of the HDAC inhibitor, trichostatin A (TSA), on vasoreactivity and hypertension remains unknown. We performed aortic coarctation at the inter-renal level in rats in order to create a hypertensive rat model. Hypertension induced by abdominal aortic coarctation was significantly suppressed by chronic treatment with TSA (0.5 mg/kg/day for 7 days). Nicotinamide adenine dinucleotide phosphate-driven reactive oxygen species production was also reduced in the aortas of TSA-treated aortic coarctation rats. The vasoconstriction induced by angiotensin II (Ang II, 100 nM) was inhibited by TSA in both endothelium-intact and endothelium-denuded rat aortas, suggesting that TSA has mainly acted in vascular smooth muscle cells (VSMCs). In cultured rat aortic VSMCs, Ang II increased p66shc phosphorylation, which was inhibited by the Ang II receptor type I ($AT_1R$) inhibitor, valsartan ($10{\mu}M$), but not by the $AT_2R$ inhibitor, PD123319. TSA ($1{\sim}10{\mu}M$) inhibited Ang II-induced p66shc phosphorylation in VSMCs and in HEK293T cells expressing $AT_1R$. Taken together, these results suggest that TSA treatment inhibited vasoconstriction and hypertension via inhibition of Ang II-induced phosphorylation of p66shc through $AT_1R$.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.201-207
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• 1998

To evaluate the possibility that the ginseng saponins could be developed as an anti-arteriosclerotic agent, we examined the inhibitory effects of ginseng saponins (total saponin[TS], panaxatriol[PT], panaxadiol[PD]) on the expression of c-fos mRNA and the proliferation of cultured rat aortic vascular smooth muscle cells (VSMCs) stimulated by angiotensin II (Ang II). TS and PT (1.0 mg/ml) suppressed c-fos mRNA induction in VSMCs stimulated by $10^{-5}$ M Ang II. The order of inhibitory potency was PT>TS. Ginseng saponins ($0.01{\sim}1.0$ mg/ml) inhibited the proliferation of VSMCs stimulated by Ang II in a concentration dependent manner, the inhibitory potency was TS＞PT＞PD at $0.1{\sim}1.0$ mg/ml. These results suggest that ginseng saponins may suppress Ang II-stimulated proliferation of aortic VSMCs which can be seen in atherosclerosis, hypertension and restenosis.