• Journal of Genetic Medicine
• /
• v.1 no.1
• /
• pp.17-22
• /
• 1997

The angiotensin converting enzyme (ACE) is a key component of the renin-angiotensin system thought to be important in the pathogenesis of hypertension and cardiovascular diseases. Deletion polymorphism in the ACE gene may be a risk factor for myocardial infarction. The insertion/deletion (I/D) polymorphism of the ACE detected by PCR analysis appears to be associated with hypertension in Koreans and its nucleotide was subcloned into T-vector and its nucleotide sequences were determined. We also examined an association between hypertension and genetic variance of ACE. We identified the angiotensin I-converting enzyme genotype in 127 hypertensive and 189 normotensive Korean subjects. The distribution of ACE genotype II, ID, DD were 39.2%, 40.2%, 20.6% respectively and the frequency for ACE alleles I and D were 0.593 and 0.407, respectively in all subjects. The frequency of D allele in Korean males is higher than that of Korean females (male; 0.438 : female; 0.267), and the frequency of I allele in Korean females is higher than that of Korean males (female; 0.733 : male; 0.562). Genotype distributions of angiotensin I-converting enzyme genes in Korean normal adult population were different from that of Caucasians (P<0.001). There were no significant differences in genotype frequency between the hypertensive control group (n=127) and the normotensive group (n=189). We observed significant differences of ACE genotype distribution between the male group and the female group in total (P=0.001) and in hypertensive Korean subjects (P=0.013).

• Journal of Pharmacopuncture
• /
• v.26 no.4
• /
• pp.298-306
• /
• 2023

Objectives: Cucumis sativus L. (C. sativus) is vegetable commonly used for managing blood pressure and often consumed in combination with standard antihypertensive therapy, despite lack of scientific evidence supporting their use. Combination of herbs and standard medication could have positive or negative effects. Therefore, this study aimed to evaluate the antihypertensive activity of C. sativus and the combined effect with losartan in the hypertensive rat model induced by angiotensin II. Angiotensin II is a component of the renin-angiotensin-aldosterone system that, upon binding to its receptor, constricts blood vessels leading to elevation of blood pressure. Methods: In an antihypertensive study, rats received C. sativus orally at doses of 9, 18, 27, and 36 mg/kg (full dose); while in a combination study, animals received losartan 2.25 mg/kg combined by either with C. sativus 9 or 18 mg/kg. The standards group received losartan 2.25 mg/kg or 4.5 mg/kg (full dose). Results: Blood pressure was measured using the tail-cuff method. C. sativus significantly attenuated angiotensin II-induced hypertension as observed in groups receiving C. sativus at 9, 18, 27, and 36 mg/kg at 30 minutes after induction showed the average change (Δ) of systolic blood pressure (SBP) and diastolic blood pressure (DBP) with respect to time zero were 28.8/18.3, 24.8/15.8, 22.8/15.5, and 11.5/9.0 mmHg, respectively. Whereas the average change (Δ) of SBP and DBP in the rats receiving the combination of half doses of C. sativus and losartan were 8.8/9.0 mmHg, respectively. These diminished effects were better than a full dose of C. sativus and comparable with a full dose of losartan (6.5/7.8 mmHg). Conclusion: The present findings indicate that C. sativus dose-dependently blocks blood pressure elevation induced by angiotensin II. The combination of half dose of C. sativus and losartan has an additive effect in lowering blood pressure.

• Korean Journal of Clinical Laboratory Science
• /
• v.43 no.2
• /
• pp.43-47
• /
• 2011

Angiotensin converting enzyme (ACE) is a vital enzyme in the renin-angiotensin-aldosterone system, and there are literature reports describing its relationship between the ACE polymorphism and muscular strength, muscular endurance and flexibility. The purpose of this study is to identify the distribution of the ACE gene polymorphism among individual golfers and the relationship between different golfers group. We analyzed the ACE gene polymorphism to study the individual differences among professional golfers (n=35), junior golfers (n=30) and general golfers (n=25). Genotype frequencies of DD, ID and II in total golfers (n=90) were 16.7%, 52.2% and 31.1% respectively. In professional golfers, the frequencies of DD, ID and II were 25.7%, 45.7% and 28.6% respectively. The frequency of DD genotype in professional golfers was higher than in junior golfers and in general golfers, but the II genotype in professional golfers was lower than in other groups. In conclusion, these data suggest that the capability and power of golf exercise are associated with the hereditary characteristics of the ACE polymorphism.

• Korean Journal of Food Science and Technology
• /
• v.46 no.3
• /
• pp.375-383
• /
• 2014

This study aimed to investigate the effects of 50% ethanol extract of ripe black raspberry (Rubus occidentalis, RBR) on hypertension in human umbilical vein endothelial cells (HUVECs) and in spontaneously hypertensive rats (SHR). Angiotensin converting enzyme (ACE) inhibition and activation of nitric oxide production by endothelial nitric oxide synthase were significantly regulated by RBR in HUVEC cells. Moreover, the SHR showed significantly higher levels of blood pressure, ACE, renin, endothelin-1, and interleukin-6 than Wistar Kyoto rats (WKY). However, treatment with captopril and RBR decreased the levels of these hypertension-related events in the SHR. The renal arteriole showed greater media thickness/lumen diameter (%) in the SHR than in the WKY. However, media thickness/lumen diameter (%) was reduced in SHR by treatment with captopril and RBR. In addition, the number of eosinophilic cardiac muscle cells was decreased in the heart muscles after treatment with captopril and RBR. Therefore, this study suggests that 50% ethanol extract of RBR may be useful for the prevention and treatment of high blood pressure.

• Childhood Kidney Diseases
• /
• v.7 no.1
• /
• pp.52-59
• /
• 2003

Purpose : The renin-angiotensin system(RAS) plays an important role in renal growth and development. We have studied the prevalence of renal anomalies and documented the association between karyotype and renal anomalies using IVP and ultrasonography. Furthermore, to investigate the impact of RAS gene polymorphism on renal anomaly in Turner syndrome, we examined the ACE I/D genotype, angiotensinogen(AGT) gene M235T, angiotensin receptor type 1(ATR) gene A1166C. Methods : Cytogenetic analysis was performed in 33 Turner syndrome patients on peripheral blood lymphocytes. Ultrasonography(US) of the kidneys and collecting system and intravenous pyelography(IVP) were perfomed in all patients. Nuclear scintigraphy{Tc 99m dimercaptosuccinic acid(DMSA) scan} was also performed for the definite renal diagnosis if indicated. And, ACE I/D genotype, angiotensinogen(AGT) gene M235T, angiotensin receptor type 1(ATR) gene A1166C were examined by PCR amplification of genomic DNA samples. Results : The prevalence of renal anolmalies in Turner syndrome was 36.4%(12/33). The Karyotype 45, X was observed in 18 of the 33 girls(54.5%), of whom 8(44.4%) had renal anomalies. Mosaic karyotypes were observed in 11(33.3%) and four(12.2%) had a non-mosaic structural aberration of the X chromosome. In this group 4(25.7%) had renal anomalies. More renal anomalies were associated with the 45, X karyotype than those with mosaic/structural abnormalities of X chromosome, but the difference was not statistically significant(P>0.05). And, there was no significant differences in the RAS gene polymorphism and allele frequencies between renal anomaly group and normal group in Turner syndrome. Conclusion : The prevalence of renal anolmalies in Turner syndrome was 36.4%. There is no significant differences in the RAS gene polymorphism and allele frequencies between the renal anomaly group and the normal group in Turner syndrome.

• Childhood Kidney Diseases
• /
• v.4 no.2
• /
• pp.127-135
• /
• 2000

Purpose: Cyclosporine(CsA) is a potent immunosuppressant but the use of CsA is associated with various side effects, especially nephrotoxicity. In tile kidney, salt depletion activates tile renin-angiotensin-aldosteron(RAS) system and accentuates chronic CsA nephropathy. We postulate that angiotensin converting enzyme inhibitors(ACEI) can prevent chronic CsA nephropathy, since ACEI may inhibit this cascades. This study was aimed to assess the effect of ACEI on chronic cyclosporin nephropathy in salt depleted rats. Methods: 36 Fischer-344 rats were divided into 6 goups. Group I received normal salt diet(NSD). Group II received a low salt diet(LSD). Group III received CsA with a NSD. Group IV received CsA with a LSD. Group V received NSD+CsA with ACEI. Group VI received LSD+CsA with ACEI. Rats were sacrificed after six weeks and the glomerular filtration rate(GFR), serum sodium, potassium and whole blood cyclosporine levels were measured. Renal tissues me sampled for the observation of histological changes. Results: No differences in blood CsA level & serum sodium were found between groups during the course of this experiment. Serum potassium in group VI was significantly increased compared with group IV and V (P<0.05). In groups treated with CsA only and in those where CsA was combined with ACEI, GFR was found to be significantly more decreased in LSD than NSD, and GFR in group V was significantly decreased in comparison with group III (P<0.05). Renal histologic lesions associated with CsA which consisted of cortical interstitial fibrosis, tubular atrophy and hyalinization of arterioles were more severe in tile LSD group. But, no differences were observed between tile groups treated with CsA and ACEI, and the groups treated with only CsA. Conclusion: Salt depletion associated with the activation of the RAS system accentuated chronic CsA nephrotoxicity, but, ACEI could not reduce the functional and morphological changes of salt depleted kidneys, in which nephropathy can be exacerbated in spite of the blocking of the angiotensin II pathway. further studies are required to elucidate whether Am ameliorated the effect of salt-depleted CsA nephrotoxicity upon the effective renal blood flow.

• Journal of Preventive Medicine and Public Health
• /
• v.53 no.6
• /
• pp.476-486
• /
• 2020

Objectives: The objective of this study was to estimate the risk of lung cancer in relation to angiotensin II receptor blocker (ARB) use among patients with hypertension from the Korean National Health Insurance Service-National Health Screening Cohort. Methods: We conducted a retrospective cohort study of patients with hypertension who started to take antihypertensive medications and had a treatment period of at least 6 months. We calculated the weighted hazard ratios (HRs) and their 95% confidence intervals (CIs) of lung cancer associated with ARB use compared with calcium channel blocker (CCB) use using inverse probability treatment weighting. Results: Among a total of 60 469 subjects with a median follow-up time of 7.8 years, 476 cases of lung cancer were identified. ARB use had a protective effect on lung cancer compared with CCB use (HR, 0.75; 95% CI, 0.59 to 0.96). Consistent findings were found in analyses considering patients who changed or discontinued their medication (HR, 0.50; 95% CI, 0.32 to 0.77), as well as for women (HR, 0.56; 95% CI, 0.34 to 0.93), patients without chronic obstructive pulmonary disease (HR, 0.75; 95% CI, 0.56 to 1.00), never-smokers (HR, 0.64; 95% CI, 0.42 to 0.99), and non-drinkers (HR, 0.69; 95% CI, 0.49 to 0.97). In analyses with different comparison antihypertensive medications, the overall protective effects of ARBs on lung cancer risk remained consistent. Conclusions: The results of the present study suggest that ARBs could decrease the risk of lung cancer. More evidence is needed to establish the causal effect of ARBs on the incidence of lung cancer.

• Journal of Pharmacopuncture
• /
• v.22 no.2
• /
• pp.95-101
• /
• 2019

Objectives: Angiotensin II (AngII), a major product of renin-angiotensin system (RAS) has important role in induction of hypertension and antihypertensive effect of several medicinal plant was mediated by effect on this agent. Therefore, this study examined the possible effect of hydroalcoholic extract of Crocus sativus (C. sativus) on hypertension induced by AngII. Methods: Six groups (n = 6) of rats were used as follow: 1) Control, 2) AngII (300 ng/kg), 3) Losartan (Los, 10 mg/kg) + AngII and 4-6) C. sativus extract (10, 20 & 40 mg/kg,) + AngII. The femoral artery and vein were cannulated for recording cardiovascular parameters and drugs administration, respectively. All drugs were injected intravenously (i.v). Los and all doses of C. sativus injected 10 min before AngII. Systolic blood pressure (SBP), mean arterial blood pressure (MAP) and heart rate (HR) were recorded throughout the experiment and those peak changes (${\Delta}$) were calculated and compared to control and AngII. Results: AngII significantly increased ${\Delta}MAP$, ${\Delta}SBP$ and ${\Delta}HR$ than control (P < 0. 01 to P < 0.001) and these increments were significantly attenuated by Los. All doses of C. sativus significantly reduced peak ${\Delta}MAP$, ${\Delta}SBP$, and ${\Delta}HR$ than AngII group (P < 0. 05 to P < 0.001). In addition, peak ${\Delta}MAP$, ${\Delta}SBP$ in doses 10 and 20 were significant than Los + AngII group (P<0.05 to P< 0.01) but in dose 40 only MAP was significant (P<0.05). Peak ${\Delta}HR$ in all doses of C sativus was not significant than Los+ AngII. Conclusion: Regarding the improving effect of the C. sativus extract on AngII induced hypertension, it seems that this ameliorating effect partly mediated through inhibition of RAS.

• Environmental Analysis Health and Toxicology
• /
• v.20 no.4 s.51
• /
• pp.303-309
• /
• 2005

Essential hypertension has been considered as multifactorial disease resulted from the interaction of both environmental and genetic factors. The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure homeostasis. Recently, a homologue of angiotensin I converting enzyme, ACE2 has been focused on as a candidate gene of essential hypertension in the experiments using animal model and human being. In this study, we carried out an association study in order to clarify the relationship between the A 1075G polymorphism in the ACE2 gene and essential hypertension in Korean subjects. Because this polymorphism is located on human chromosome X, the statistical analysis for each gender was performed separately. There were no significant differences in allele distribution of the A 1075G polymorphism in the ACE2 gene between normotensives and hypertensives in the both gender groups, respectively. However, this polymorphism was significantly associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) values in only female groups (P< 0.05). Thus, these results may suggest the probable role of ACE2 gene in the inter-individual susceptibility of female group to blood pressure variability.

• YAKHAK HOEJI
• /
• v.43 no.6
• /
• pp.843-850
• /
• 1999

We investigated whether endothelium-derived NO and endothelin-1 might result enhanced vasoconstriction induced by administration of norepinephrien (NE) at the early stage of one-kidney, one-clip (1K1C) renal hypertensive rats. We also studied the relation ship of renin-angiotensin system (RAS) using rat aorta in this hypothesis. L-NMMA (30$\mu$M) and L-NAME(30${\mu}M$) enhanced vasoconstriction induced by NE in thoracic aorta of control rats. However angiotensin converting enzyme (ACE) inhibitor didn't. The aorta of 1KIC rats showed a singnificantly exaggerated contractile response to NE as compared with control rats. Rub-bing the endothelium abolished this difference. Ach and SNP-induced vasorelaxation show no significant difference between 1KIC and control rats. The treatment of phosphoramidon (10${\mu}M$) and oral administration of captopril (0.05, w/v%) abolished the exaggerated contractile response to NE at early stage of 1KIC rats. These results suggest that the increase of contractile response at the early phase in 1KIC rat is partially involved in the activation of ACE.