Biomedical subjects

C Qiu

Publications and source records attributed to C Qiu.

At least 37 records · Page 2Linked to original sources

PubMed2000

Enhanced delta-opioid receptor-mediated antinociception in mu-opioid receptor-deficient mice.

Inflammatory hyperalgesia was induced in wild-type, heterozygous and mu-opioid receptor knockout mice after an intraplantar injection of complete Freund's adjuvant. micro-Opioid receptor knockout mice exhibited faster recovery from hyperalgesia as compared to heterozygous (P<0.05) and wild-type (P<0.01) mice. Naloxone restored hyperalgesia in all genotypes. Naltrindole (delta-opioid receptor-selective antagonist) partially restored the hyperalgesia only in mu-opioid receptor knockout mice (P<0.001). Nor-binaltorphimine (kappa-opioid receptor-selective antagonist) had no effect. The mu-opioid receptor-selective agonist, [D-Ala(2), MePhe(4),Gly-ol(5)]enkephalin (DAMGO), reduced the hyperalgesia in heterozygous and wild-type but not in mu-opioid receptor knockout mice while U69,593 ¿(+)-(5alpha,7alpha, 8beta)-N-methyl-N-[7-(1-pyrrolidinyl)-1-oxaspiro[4. 5]dec-8-yl]-benzeneacetamide, kappa-opioid receptor-selective¿ produced similar effects in all mice. The delta-opioid receptor-selective agonists, [D-Pen(2), D-Pen(5)]enkephalin (DPDPE) and deltorphin ([D-Ala(2)]deltrophin-II), produced significantly greater antihyperalgesia in knockout mice (P<0.05). The findings suggest that mu-opioid receptors may be involved in the persistence of inflammatory hyperalgesia and that a delta-opioid receptor-mediated compensatory mechanism in the absence of the mu-opioid receptor is activated by persistent hyperalgesia.

Analgesia↗

PubMed2000

Inner hair cell loss leads to enhanced response amplitudes in auditory cortex of unanesthetized chinchillas: evidence for increased system gain.

Carboplatin preferentially destroys inner hair cells (IHCs) in the chinchilla inner ear, while retaining a near-normal outer hair cell (OHC) population. The present study investigated the functional consequences of IHC loss on the compound action potential (CAP), inferior colliculus potential (ICP) and auditory cortex potential (ACP) recorded from chronically implanted electrodes. IHC loss led to a reduction in CAP amplitude that was roughly proportional to IHC loss. The ICP amplitude was typically reduced by IHC loss, but the magnitude of this reduction was generally less than that observed for the CAP. In contrast to the CAP and ICP, ACP amplitudes were generally not reduced following IHC loss. In some animals, the ACP amplitude remained at pre-carboplatin values despite substantial IHC loss. However, in other animals, IHC loss led to an increase ('enhancement') of ACP amplitude. ACP enhancement was greatest at 1-2 weeks post-carboplatin, returning towards baseline amplitudes at 5 weeks post-carboplatin. In other animals, the ACP remained enhanced up to 5 weeks post-carboplatin. We interpret the transient and sustained enhancement of ACP amplitude following partial IHC loss as evidence of functional reorganization occurring at or below the level of the auditory cortex. These results suggest that the gain of the central auditory pathway increases following IHC loss to compensate for the reduced input from the cochlea.

Action Potentials↗

PubMed2000

Dexamethasone worsens nitric oxide inhibition-induced hypertension and renal dysfunction.

Chronic nitric oxide (NO) inhibition with Nomega-nitro-L-arginine methyl ester (L-NAME) has previously been reported to produce systemic hypertension, renal vasoconstriction, and renal damage. In this study we investigated whether a compensatory restoration of NO synthesis occurs in chronic L-NAME hypertension and whether chronic treatment with dexamethasone (Dex) (which inhibits inducible NO synthase [iNOS]) can influence the course of the hypertension. We found that in the conscious chronically L-NAME-treated (approximately =10 mg/kg/24 h) hypertensive rats, acute systemic NOS inhibition elicited a further increase in blood pressure (BP), indicating partial restoration of NO production. Chronic Dex in a dose previously reported to inhibit iNOS (5 microg/24 h), amplified the hypertension (within 2 days), renal vasoconstriction, and reduction in glomerular filtration rate because of L-NAME. In contrast, chronic Dex alone had no effects on renal hemodynamics or BP during the first week, although by the end of week 2 a small increase in BP (approximately =10 mm Hg) was evident. These results show that BP continues to increase with chronic L-NAME despite partial restoration of NO production. An iNOS, which might be stimulated and escaped inhibition by L-NAME, may be responsible for the compensatory restoration of NO synthesis, serving to attenuate the development of hypertension and renal dysfunction.

Animals↗

PubMed2000

Association analysis of variants in the core promoter region of angiotensinogen gene with essential hypertension in Tibetan population.

OBJECTIVE: To detect the variants in the core promoter region of angiotensinogen(AGT) gene, and to analyse the relationship between the AGT gene polymorphisms and essential hypertension in Tibetan population. METHODS: This is a case-control study consisting of 103 essential hypertensive subjects and 82 normotensive controls matched by age and sex. The variants in the AGT gene core promoter region were screened by polymerase chain reaction/single strand conformation polymorphism(PCR/SSCP) and further identified by automated sequencing. The A(-6)G polymorphism was determined in DNA extracted from leucocytes by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). RESULTS: (1) There were two different electrophoresis band patterns in PCR/SSCP analysis. PCR product direct sequencing showed that the two band patterns represented the AA, AC genotypes in the (-20) site of AGT gene respectively. The distribution of A(-20)C genotype was almost identical in essential hypertensive and normotensive groups (P>0.8). The A allele frequency was very high in both groups (control: 0.9175, hypertensive: 0.9124). (2)Distribution of genotype in the (-6) site of AGT gene was much different between the patient group and control group (P<0.005). The frequency of G allele was statistically higher in the patient group than in controls (0.374 vs 0.220, P<0.025). CONCLUSION: Both Tibetan hypertensives and normotensives have higher frequency of A allele in AGT gene (-20) site. The higher frequency of G allele in the AGT gene (-6) site in Tibetan hypertension patients suggests that this allele may be the genetic susceptibility factor in the proceeding of essential hypertension in the Tibetan population.

Angiotensinogen↗

PubMed2000

[Analyses on the association of CA-repeat polymorphism and A1166-->C variant in the 3'-flanking region of AT(1)R gene with essential hypertension in Tibetans].

OBJECTIVE: To investigate whether CA-repeat polymorphism and A1166 --> C variant in the 3n-flanking region of AT(1)R gene are in association with the genetic susceptibily to essential hypertension (EH) in Tibetans. METHODS: A case-control study was carried out. Sibpair analysis and family linkage analysis were conducted. The CA-repeat polymorphism of AT &(1) R gene was identified by polymerase chain reaction(PCR) with fluorescence labeled dCTP as substrate and by semi-automatic sequence technology. The A1166 -->C variant was detected by PCR-RFLP. RESULTS: Association of AT&(1)R gene locus with EH was confirmed through the case-control study in well-characterized group of 113 Tibetan EH patients and 131 normotensives(chi(2)=26.44, P<0.001). A closer examination of this gene locus found 11 alleles from Tibetan population; allele A7 (138 bp) was more frequent in both the patients and the controls. Allele A8(140 bp) was in strong positive association with genetic susceptibility to EH in Tibetans. Frequency of allele A8 was 20.5% in EH and 7.3% in normotensives. The difference of allele frequencies between the groups was significant (chi(2)=9.64, P=0.002, OR=3.46, 95% CI 1.44-8.51). Affected sibpair analysis showed chi(2)=3.85, P=0.025; family linkage analysis gave Lod score of 0.80. No association between A1166 --> C variant in AT(1)R gene and EH in Tibetans was observed (P>0.05). CONCLUSION: The result suggests that CA-repeat polymorphism of AT(1)R gene be in association with EH in Tibetans, which implicates that AT(1)R gene may be in linkage disequilibrium with the causative genes of EH.

Adult↗

PubMed2000

[Chromosome localization of the dentinogenesis imperfecta type II locus].

OBJECTIVE: To scrutinize the linkage between dentinogenesis imperfecta type II and chromosome 4q21 in a Tianjin-Tanggu family. METHODS: Blood samples were collected from 13 members of the family. DNA was analyzed with 4 short tandem repeat polymorphisms markers UGATA62A11, DSP(P), SPP1 and D4S1563 Y using fluorescence-based PCR. The linkage between four markers on chromosome 4q21 and dentinogenesis imperfecta type II was tested by Lod score analysis. RESULTS: GATA62A11 and DSP(P) suggested linkage and yielded a Lod score of 1.63 at theta =0, and 1.68 at theta =0 by means of the MLINK software, respectively. Genotype and haplotype were acquired. CONCLUSION: The disease gene of the dentinogenesis imperfecta type II family is located on chromosome 4q. The result will be helpful for the further identification of the dentinogenesis imperfecta type II gene.

Chromosome Mapping↗

PubMed2000

[The function of benzol peroxide in the induction of Syrian golden hamster tongue carcinoma by chemical carcinogen].

OBJECTIVE: To testify the function of promoter(benzol peroxide) in the induced tongue carcinogenesis of Syrian golden hamster as well as the function of carcinogen (DMBA). METHODS: In this study, group 1: 20% benzoyl peroxide in acetone solution was brushed to the right tongue border of Syrian golden hamster, followed by 0.5% 7, 12-dimethybenzanthrancene(DMBA) in acetone, twice a week, lasting 20 weeks. Group 2: 0.5% 7,12-dimethybenzanthrancene(DMBA) in acetone was painted on the right tongue border of golden Syrian hamster in the manner of group 1. Group 3: 20% benzoyl peroxide in acetone solution was used with mentioned methods. RESULTS: Group 2: showed 90% (27/30) carcinogenesis-rate in tongue of Syrian golden hamster. While it was 100% (30/30) of induced tongue carcinoma and 3/30 lymph node metastasis was found in group 1. No tongue carcinogenesis was found in group 3. The former two groups had the manifestations of hyperplasia of epithelium cell, carcinoma in situ, invasive and cervical lymph node metastatic carcinoma in the process of experiment, but it was 2 weeks shorter in group 1 than that of group 2. Both groups had the same features under eye and light microscope. The samples were high-differentiated squamous cell carcinoma histologically through HE stain. CONCLUSION: This study indicated that benzoyl peroxide could increase carcinogenesis of golden hamster tongue which induced by DMBA. Consideration of promoting agent should be taken in carcinogenesis as well as carcinogen.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2000

[Association of HLA-DRB genes with Vogt-Koyanagi-Harada syndrome in a Chinese Han population].

OBJECTIVE: To investigate the molecular genetic background of VKH syndrome in Han Chinese by HLA-DRB genotyping. METHODS: HLA-DRB genotyping was performed by PCR-SSOP method, then DR4 alleles were analyzed by SSOP and RFLP methods. RESULTS: The frequency of DRB1 * 0405 was significantly higher in VKH patients than that in normal controls (80.4% vs 8.1%, Pc < 10(-7), RR = 46.7), so was the frequency of DRB1 * 15 in DRB1 * 0405 negative individuals (Pc < 0.05, RR = 6.0). On the other hand, the frequencies of DRB1 * 14 and DRB1 * 08 were significantly lower in VKH patients than that in normal controls. Comparing the clinical features between DRB1 * 0405 positive and negative VKH patients, no significant differences were found. CONCLUSIONS: (1) DRB1 * 0405 and DRB1 * 15 are closely associated with the susceptibility to VKH syndrome, DRB1 * 0405 may be the major susceptible gene and DRB1 * 15 may be the minor; (2) DRB1 * 14 and DRB1 * 08 are negatively associated with the susceptibility to VKH syndrome, suggesting that they may be the resistant genes; (3) DRB1 * 0405 is not related to the clinical features, incidence of ocular complications as well as visual prognosis.

Adult↗

PubMed1999

Optimizing vascular gene transfer of plasminogen activator inhibitor 1.

The vessel wall fibrinolytic system plays an important role in maintaining the arterial phenotype and in regulating the arterial response to injury. Plasminogen activator inhibitor type 1 (PAI-1) regulates tissue fibrinolysis and is expressed in arterial tissue; however, its biological role remains uncertain. To help elucidate the role of PAI-1 in the artery wall, and to begin to clarify whether manipulation of vascular PAI-1 expression might be a target for gene therapy, we used adenoviral vectors to increase expression of rat PAI-1 in rat carotid arteries. Infusion of an adenoviral vector in which PAI-1 expression was driven by a promoter derived from the Rous sarcoma virus (RSV) did not increase PAI-1 expression above endogenous levels. To improve PAI-1 expression, we modified the vector by (1) truncating the 3' untranslated region of PAI-1 to increase the mRNA half-life, (2) substituting the SRalpha or the cytomegalovirus (CMV) promoter for the RSV promoter, (3) including an intron in the expression cassette, and (4) altering the direction of transcription of the transgene cassette. The optimal expression vector, revealed by in vitro studies, contained the CMV promoter, an intron, and a truncated PAI-1 mRNA. This vector increased PAI-1 expression by 30-fold over control levels in vitro and by 1.6 to 2-fold over endogenous levels in vivo. This vector will be useful for elucidating the role of PAI-1 in arterial pathobiology. Because genes that are important in maintaining the vascular phenotype are likely to be expressed in the vasculature, the technical issues of how to increase in vivo expression of endogenous genes are highly relevant to the development of genetic therapies for vascular disease.

Adenoviruses, Human↗

PubMed1999

Genetic immunization of mice with DNA encoding the 23 kDa transmembrane surface protein of Schistosoma japonicum (Sj23) induces antigen-specific immunoglobulin G antibodies.

The 23 kDa transmembrane surface protein of schistosomes is of recognized interest in studies of immune responsiveness in schistosomiasis. To examine the immunogenicity of the 23 kDa antigen of Schistosoma japonicum, Sj23, when delivered by genetic immunization, mice were immunized using a DNA construct containing the Sj23 cDNA under the control of a CMV promotor. Serological analysis of peripheral blood from immunized mice demonstrated that this construct was able to induce the production of antigen-specific IgG antibodies that recognized a schistosome antigen of 23 kDa in Western blots. Despite inducing antigen-specific antibodies, the Sj23 DNA vaccine was unable to confer protection in immunized mice subjected to challenge with S.japonicum cercariae. Appropriate engineering of the unique structure of the Sj23 kDa transmembrane protein of schistosomes may provide a novel vehicle for expressing foreign epitopes from other infectious agents or, possibly, cancer antigens, anchored to the surface of transfected cells.

Animals↗

PubMed1999

Endothelin and angiotensin mediate most glomerular responses to nitric oxide inhibition.

BACKGROUND: Endothelin (ET) and angiotensin mediate glomerular responses to systemic nitric oxide (NO) inhibition. Acute systemic NO synthase (NOS) inhibition in the rat causes marked increases in both preglomerular (RA) and efferent arteriolar (RE) resistances and a fall in the glomerular capillary ultrafiltration coefficient (Kf). In contrast, local intrarenal NOS inhibition increases RA, but has no effect on RE while producing a similar Kf lowering effect as seen with systemic NOS inhibition. These studies were designed to assess whether the increase in RE during systemic NOS inhibition is mediated by endogenous ET and whether angiotensin II (Ang II) also contributes. METHODS: Micropuncture measurements were made before and during acute systemic NOS inhibition with N-monomethyl L-arginine (NMA) alone, NMA + the nonpeptide ETA and ETB receptor antagonist, bosentan, NMA + the Ang II type 1 receptor blocker, losartan, and NMA during combined bosentan and losartan. RESULTS: The falls in single nephron glomerular filtration rate (SNGFR) and glomerular plasma flow seen with systemic NOS inhibition were prevented by concomitant administration of bosentan and losartan alone and in combination. The increases in systemic blood pressure (BP), glomerular BP (PGC), RA, and RE and the reduction in Kf seen with systemic NOS inhibition were attenuated by either bosentan or losartan. An attenuation in the elevation in total renal vascular resistance seen with systemic NOS inhibition was also observed with bosentan. Combined ET and Ang II type 1 blockade completely prevented the increase in systemic BP, PGC, and RE and the fall in Kf with systemic NOS inhibition, leaving only a very attenuated rise in RA. CONCLUSIONS: These findings suggest that endogenous ET and Ang II partially mediate the glomerular hemodynamic responses (including the increased RE) to acute systemic NOS inhibition. The actions of ET and Ang II are mainly additive, and almost all of the vasoconstrictor responses to acute NOS inhibition are prevented when both vasoconstrictor systems are blocked.

Angiotensin II↗

PubMed1999

Screening and treatment of diabetic nephropathy by primary care physicians.

OBJECTIVE: To describe the practices of Indiana primary care physicians related to diabetic nephropathy screening and management. DESIGN: Cross-sectional, observational. SETTING: The state of Indiana. PARTICIPANTS: Active primary care physicians (defined as general internists, family practitioners, and general practitioners) in Indiana who provided care for diabetic patients at the time of the survey (n = 1,018) MEASUREMENTS AND MAIN RESULTS: Practice patterns relevant to microalbuminuria and overt albuminuria screening and management were assessed along two dimensions: the percentage of patients to whom the practices were applied and the frequency with which the practices were performed. Of 1,141 physicians who responded to the survey, 1,018 were eligible for analysis. Eighty-six percent of physicians reported screening more than half of their patients with type 1 diabetes for overt albuminuria, as did 82% of physicians for their patients with type 2 diabetes. Only 17% of physicians indicated performing microalbuminuria testing on more than half of their type 1 patients. Angiotensin-converting enzyme inhibitor agents were used frequently to treat abnormal urinary albumin excretion when hypertension was present, but less often when hypertension was absent. Physician specialty, year of graduation from medical school, practice location, and familiarity with the results of the Diabetes Control and Complications Trial were significant predictors of screening and treatment practice patterns. CONCLUSIONS: Primary care physicians report practices that allow them to detect overt albuminuria but not microalbuminuria. Angiotensin-converting enzyme inhibitors are frequently used by physicians who test for microalbuminuria, but efforts to increase the detection of early renal damage are needed so that these agents and other therapeutic strategies may be employed at the earliest opportunity.

Clinical Competence↗

PubMed1999

Mibefradil prevents L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats.

OBJECTIVE: To determine the potential renal protective effects of a novel calcium channel blocker mibefradil in chronic renal failure. METHOD: We compared the long-term effects of mibefradil with an angiotensin-converting enzyme inhibitor cilazapril on blood pressure, proteinuria, renal function and histological alterations in N-nitro-L-arginine methylester (L-NAME)-treated spontaneously hypertensive rats (SHR). Three groups of SHR were studied for 45 days: group 1 (n = 14), treated with L-NAME only (50 mg/l in the drinking water); group 2 (n = 15) L-NAME plus co-treatment with mibefradil (30 mg/kg per day); group 3 (n = 15), L-NAME plus co-treatment with cilazapril (10 mg/kg per day). RESULTS: Both mibefradil and cilazapril attenuated the increased systolic blood pressure, and prevented the development of proteinuria and the decreased creatinine clearance (Ccr) seen at day 42 in the group treated with L-NAME alone. Notably, mibefradil had similar effects to cilazapril on proteinuria and Ccr, despite a reduced antihypertensive effect All animals receiving mibefradil co-treatment remained alive throughout the experiment, whereas the mortality rate was 43% in SHR treated with L-NAME alone. Both mibefradil and cilazapril completely prevented renal structural damage as assessed by scoring glomerular, tubulo-interstitial and vascular lesions. CONCLUSIONS: Our data show that mibefradil prevented the development of hypertension and proteinuria, renal functional impairment and nephrosclerosis, and also improved animal survival. The renal protective effects of mibefradil were at least equivalent to those of an ACE inhibitor in this animal model of chronic renal failure.

Animals↗

PubMed1999

Effects of nonpeptide endothelin receptor antagonists in rats with reduced renal mass.

This study was set up to evaluate the long-term effects of nonpeptide endothelin (ET) antagonists in rats with renal mass reduction (RMR). In the first series of experiments, rats were administered bosentan (100 mg/kg/day) or the angiotensin-converting enzyme inhibitor cilazapril (10 mg/kg/day) for 14 weeks beginning 24 h after RMR. As expected, cilazapril completely prevented the development of hypertension, proteinuria, and renal structural damage. In contrast, bosentan had no influence on the development of proteinuria and renal structural damage, although it had a moderate antihypertensive effect and improved creatinine clearance. A second set of experiments was performed to assess whether Ro 48-5695, a very potent ET antagonist optimized from bosentan, could prevent the development of renal damage and reverse established renal damage. Rats received Ro 48-5695 (30 mg/kg/day) beginning either 24 h (prevention) before for 8 weeks, or 4 weeks (reversal) after RMR. Ro 48-5695 attenuated the hypertension and the decline of creatinine clearance when treatment was started at 24 h, but not when started at 4 weeks. Ro 48-5695 had no effect on proteinuria. These observations suggest that ET-receptor activation does not play a major role in the progression of glomerular sclerosis in this model of chronic renal failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1999

Protective effects of endothelin receptor antagonists in dogs with aortic cross-clamping.

Endothelin (ET) may play an important role in the pathogenesis of vasoconstriction and acute renal failure after aortic cross-clamping (ACC). However, the relative contribution of the ET(A) and ET(B) receptors to the physiopathology of ischemic acute renal failure is poorly understood. This study was carried out to evaluate the potential protective effect of a selective ET(A) antagonist versus combined ET(A)/ET(B) antagonist on altered systemic, pulmonary, and renal hemodynamics induced by cross-clamping the suprarenal aorta for 1 h, followed by 2-h reperfusion. Studies were performed in three groups of anesthetized mongrel dogs. After baseline measurements, treatment (3 mg/kg i.v. bolus + 3 mg/kg/h infusion) with either a selective ET(A) antagonist, Ro 61-1790 (n = 5), or a combined ET(A)/ET(B) antagonist, bosentan (n = 5) or vehicle (n = 8) was initiated 5 min before ACC. There were marked increases in total peripheral (TPR), pulmonary (PVR), and renal (RVR) vascular resistances, and significant decreases in cardiac output (CO) and glomerular filtration rate (GFR) and tubular sodium reabsorption after ACC in the vehicle group. Both Ro 61-1790 and bosentan prevented the marked increases in TPR, PRV, and RVR, and attenuated the declines in CO, GFR, and tubular sodium reabsorption. We concluded that the profound systemic, pulmonary, and renal vasoconstriction, as well as the impairments in glomerular and tubular functions associated with ACC, is mostly ET mediated and that the ET(A) receptor activation makes a major contribution to the ET-mediated impairments of hemodynamics and renal function after ACC.

Acute Kidney Injury↗

PubMed1999

Renal vascular and biochemical responses to systemic renin inhibition in dogs at low renal perfusion pressure.

Renin is produced by the kidney and secreted into the systemic circulation. However, its biochemical and physiological role of regulating renal blood flow with changing renal perfusion pressure (RPP) is not fully understood. In this study, the function of the intrarenal renin for production of angiotensin (Ang) I and maintenance of vascular tone was evaluated in dogs under normal conditions and when the kidney was perfused at low RPP. The dog left kidney was perfused first at normal (100 mm Hg) and then at low (30 mm Hg) RPP in the presence or absence of the renin inhibitor ciprokiren (3 mg/kg, i.v.). Both hemodynamic and biochemical parameters were measured. Lowering RPP markedly reduced left renal blood flow and elevated left renal vascular resistance. These effects were prevented by ciprokiren, which blocked the intrarenal production of Ang I. Lowering RPP increased the renal venous/ arterial ratio from 1.4+/-0.1 to 3.6+/-0.3 for plasma renin activity and from 2.4+/-0.2 to 9.8+/-1.1 for Ang I, but did not change the venous/arterial ratio for Ang II. The net renal venous conversion rate of Ang I to Ang II decreased from 0.22 to 0.09 after RPP was lowered, whereas the conversion rate in arterial blood was 1.35 and did not decrease significantly. Our results demonstrated the importance of intrarenal renin-angiotensin system for Ang I production and for the maintenance of the vascular tone, especially at low RPP. Our study also shows the limited capacity for Ang I conversion in the renal vasculature in vivo.

Angiotensin I↗

PubMed1999

Gene polymorphisms of the renin-angiotensin system in essential hypertension.

OBJECTIVE: To determine whether angiotensin-converting enzyme (ACE) gene, angiotensinogen (AGT) gene and angiotensin II receptor 1 (AT1R) gene are implicated in Chinese essential hypertension (EH). METHODS: The case-control and haplotype-based haplotype relative risk (HHRR) study consisted of 169 essential hypertensive subjects (HT), 152 normotensive controls (NT) and 62 families. The polymorphisms of insertion/deletion (I/D) allele of ACE gene and the microsatellite allele of AT1R gene were determined in DNA extracted from peripheral blood leukocytes by polymerase chain reaction (PCR). The variants of AGT gene were screened by PCR-single strand conformation polymorphism (PCR-SSCP) analysis and further identified by cloning and sequencing. RESULTS: The significant association between EH and D allele of ACE gene was found (P < 0.05). The difference of the microsatellite allele distribution of AT1R gene between HT and NT groups was statistically significant (P < 0.005). By contrast, the distribution of A-20C genotype of AGT gene was almost identical in HT and NT groups. No significant linkage disequilibrium was observed between A-20C and M235T in AGT gene. CONCLUSIONS: D allele of ACE gene might correlate with a predisposing factor for EH. The microsatellite allele of AT1R gene might be linkage disequilibrium with an unidentified variant that contributes to the development of EH. A-20C of AGT gene is not a major genetic determinant of EH.

Adult↗

PubMed1999

Angiotensin I-converting enzyme gene polymorphism in Chinese patients with obstructive sleep apnea syndrome.

OBJECTIVE: To investigate the relationship of an insertion/deletion (I/D) polymorphism of the angiotension-converting enzyme (ACE) gene to obstructive sleep apnea syndrome (OSAS) patients and the control subjects. METHODS: Genomic DNA was extracted from blood samples and amplified by polymerase chain reaction (PCR). PCR primers flanked the polymorphic region in intro 16 of the ACE gene. RESULTS: OSAS patients had significantly higher frequencies of I/I genotype and insertion allele of the ACE gene as compared with the control subjects in Chinese population. The OSAS patients with I/I genotype had significantly longer apnea time, lower minimum SaO2 and greater AHI than the OSAS patients with I/D genotype. CONCLUSION: These results indicate that the I/I genotype and I allele are a risk factor for OSAS in Chinese.

Adult↗