Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of RP-HPLC-purified fractions of fish waste hydrolysates issued from three fish industries was tested on guinea pig ileum in order to examine the presence of opioid molecules. The evaluation of anti-hypertensive activities of whole hydrolysates and fractions were also tested, monitoring the ability of the fraction to inhibit the activity of angiotensin I-converting enzyme involved in hypertension regulation. Sardine autolysate and cod head hydrolysate powder (50 microg) were able to inhibit near 30% of ACE activity, whereas 50 microg of shrimp hydrolysate allows the inhibition of 57% of ACE activity. HPLC fractionation of cod head hydrolysate and sardine autolysate was necessary to evidence biological activity, whereas HPLC separation of shrimp hydrolysate exhibited low biological activity fractions. Further studies are necessary to characterise bioactive molecules from cod head alcalase hydrolysate and from sardine autolysate.
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PMID:HPLC preparation of fish waste hydrolysate fractions. Effect on guinea pig ileum and ACE activity. 1193 78

The change in plasma level of dipeptide, Val-Tyr (VY), with in vitro angiotensin I-converting enzyme inhibitory activity was investigated after a single oral administration of a VY-drink at doses of 0, 6 or 12 mg given to mild hypertensive subjects. During this protocol for up to 24 h after the intake, patient/subject blood pressure (BP) was measured for a 15 min period at designated times (0, 1, 2, 4, 8, 24 h) with the individual supine. Based on the VY determination, the maximal increment of plasma VY level was observed over the second hour postprandially (12 mg-dose; 2041+/-148 fmol/ml-plasma). In addition, the plasma VY level increased with the VY dosage. However, no marked BP change was observed with the increase of plasma VY level, suggesting that VY did not exert an acute hypotensive effect. The area under the curve at 12 mg-dose was estimated to be 8644+/-420 fmol x h/ml-plasma, comparable to that in normotensive subjects. This finding suggests that absorption of VY would not be influenced by a complaint of hypertension.
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PMID:Absorption of Val-Tyr with in vitro angiotensin I-converting enzyme inhibitory activity into the circulating blood system of mild hypertensive subjects. 1223 Jan 25

The genetic factors that contribute to the development of coronary artery disease (CAD) are poorly understood. It is likely that multiple genes that act independently or synergistically contribute to the development of CAD and the outcome. Recently, an insertion/deletion (I/D) polymorphism of the human angiotensin I-converting enzyme (ACE) gene, a major component of the reninangiotensin system (RAS), was identified. The association of the ACE gene D allele with essential hypertension and CAD has been reported in the African-American, Chinese, and Japanese populations. However, other studies have failed to detect such an association. It has been suggested that these inconsistencies may be due to the difference in backgrounds of the population characteristics. In the present study, we investigated the I/D polymorphism of the ACE gene in 103 subjects of both sexes, consisting of 59 normal controls and 44 patients with hypertension. The allele and genotype frequency were significantly different between the hypertensive and control groups (p < 0.01). Among the three ACE I/D variants, the DD genotype was associated with the highest value of the mean systolic blood pressure [SBP] and mean diastolic blood pressure [DBP] (p = < 0.05) in men, but not in women. In the overall population, the mean SBP and DBP was highest in DD subjects, intermediate in I/D subjects, and the least in II subjects
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PMID:Association between angiotensin I-converting enzyme gene polymorphism and hypertension in selected individuals of the Bangladeshi population. 1229 7

Here we report the utility of a molecular epidemiologic approach for common, polygenic diseases. Since 1992, the angiotensin I-converting enzyme (ACE) deletion/deletion (D/D) genotype has been linked to several cardiovascular diseases, including diabetic nephropathy. Earlier, the ACE D/D genotype had been associated with excess tissue ACE activity. We have observed an association of the ACE D/D genotype with a large number of common diseases, including chronic renal failure due to non-insulin-dependent diabetes mellitus or hypertension, hypertensive peripheral vascular disease, and emphysema [chronic obstructive pulmonary disease (COPD)]. ACE inhibitors have been in clinical use since 1977 and have a well-known safety record. Armed with the knowledge that ACE overactivity was associated with their disease, we gave what was intended to be a tissue ACE-inhibitory dose of a hydrophobic ACE inhibitor to 800 Caucasian and African-American male patients with hypertension and 200 Caucasian and African-American male patients with chronic renal failure, over a period of 3 years. We here report their outcomes, which include those of two patients with end-stage hypertensive peripheral vascular disease and one patient with end-stage emphysema (COPD). As a group, the outcomes are superior to what is available in the literature. This experience suggests the power of pharmacogenomics to improve clinical outcomes for common diseases safely, quickly, and inexpensively, if effective drugs already exist.
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PMID:From pharmacogenomics to improved patient outcomes: angiotensin I-converting enzyme as an example. 1239 47

With the use of in vitro receptor autoradiography, this study aims at determining whether the higher level of kinin B(2) receptor density in the spinal cord of the spontaneously hypertensive rat (SHR) is secondary to arterial hypertension and whether chronic treatment with angiotensin I-converting enzyme inhibitors (ACEI) can regulate neuronal B(1) and B(2) receptors. SHR received, from the age of 4 wk, one of the two ACEI (lisinopril or zofenopril, 10 mg x kg(-1) x day(-1)) or for comparison, the selective AT(1) antagonist (losartan, 20 mg x kg(-1) x day(-1)) in their drinking water for a period of 4, 12, and 20 wk. Age-matched untreated SHR and Wistar-Kyoto rats (WKY) were used as controls. B(2) receptor binding sites in most laminae were higher in SHR than in WKY from the age of 8 to 24 wk. Whereas B(1) receptor binding sites were significantly present in young SHR and WKY, they were barely detectable in adult rats. ACEI (16 and 24 wk) and AT(1) antagonist (24 wk) enhanced the number of B(2) without changing B(1) receptor binding sites. However, at 8 wk the three treatments significantly increased B(1) and decreased B(2) receptors in lamina I. It is concluded that 1) the higher density of B(2) receptors in the spinal cord of SHR is not due to hypertension, 2) kinin receptors are regulated differently by ACEI in neuronal and vascular tissues, and 3) aging may have a profound impact on levels of B(1) and B(2) receptors in the rat spinal cord.
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PMID:Chronic effects of angiotensin-converting enzyme inhibition on kinin receptor binding sites in the rat spinal cord. 1258 40

Polymorphism of the promoter region of the angiotensinogen gene (ATG) and an angiotensin I-converting enzyme gene (ACE) insertion/deletion (I/D) polymorphism were studied in three different groups of Kazakhs (control group, patients with cardiovascular disease (CAD) and patients with arterial hypertension (AH)) using three methods. A comparative analysis of the distribution of genotype and allele frequencies was conducted.
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PMID:[Polymorphism of the promotor region of the angiotensinogen gene and the gene for angiotensin I-converting enzyme in arterial hypertension and myocardial ischemia of the Kazakh ethnic groups]. 1266 27

This paper reviews bioactive peptides, biogenic peptides, opioid peptides, immunostimulating peptides, mineral soluble peptides, antihypertensive peptides and antimicrobial peptides originating from food materials and enzymatic hydrolysis of proteins. Antihypertensive peptides are extensively reviewed and have been divided into angiotensin I-converting enzyme inhibitory peptides and others. These peptides are produced in the enzymatic hydrolysate of treated food materials such as milk, animal and fish meat, maize, wheat, soybeans and egg, and also from microbe-fermented products. Peptides with strong antihypertensive effects on spontaneously hypertensive rats are discussed and are divided into high and low angiotensin I-converting enzyme inhibitory activities. In addition, new topics from our studies on antihypertensive peptides are introduced. Efficacies of these peptides in clinical studies and differences with medicinal substances are summarized. Recent studies in this area shown the possibility of using biogenic peptides for improvements in treatment or prevention of hypertension.
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PMID:Biogenic peptides and their potential use. 1276 42

We have previously described angiotensin I-converting enzyme (ACE) forms in urine of normotensive (190 and 65 kDa) and hypertensive patients (90 and 65 kDa, N-domain ACEs). Based on the results described above, experimental and genetic models of hypertension were investigated to distinguish hemodynamic and genetic influence on the generation of ACE profile in urine: Wistar-Kyoto and Brown Norway rats (WKY and BN), spontaneously and stroke-prone spontaneously hypertensive rats (SHR and SHR-SP), one kidney/one clip rats (1K1C), deoxycorticosterone acetate (DOCA) salt-treated and untreated rats, and enalapril-treated SHR (SHRen). Two peaks with ACE activity were separated from the urine of WKY and BN rats submitted to an AcA-44 column, WK-1/BN-1 (190 kDa), and WK-2/BN-2 (65 kDa), as described for urine of normotensive subjects. The same results were obtained for urine of 1K1C and DOCA salt-treated and untreated rats, analyzed to evaluate the influence of hemodynamic factors in the ACE profile in urine. The urine from SHR, SHR-SP, and SHRen presented 80 (S-1, SP-1, Sen-1) and 65 (S-2, SP-2, Sen-2) kDa ACE forms, differing from the urine profile of normotensive rats, but similar to that described for hypertensive patients. The presence of 80 kDa ACE in urine of SHR, SHR-SP, and SHRen and its absence in urine of experimental hypertensive rats (1K1C and DOCA salt) support the hypothesis that this enzyme could be a possible genetic marker of hypertension. Taken together, our results provide evidence that ACE forms with 90/80 kDa isolated from the urine of hypertensive subjects and genetic hypertensive animals behaves as a possible genetic marker of hypertension and not as a marker of high blood pressure.
Hypertension 2003 Oct
PMID:N-domain angiotensin I-converting enzyme with 80 kDa as a possible genetic marker of hypertension. 1290 Apr 33

Gene encoding components of the renin angiotensin system (RAS) have been implicated with the increased risk of cardiovascular disease (CVD). Two variants of the angiotensinogen (AGT) gene, M235T and T174M, have been shown to be associated with increased risk of hypertension. In the present study, we examined the association of these two polymorphisms and their synergistic interaction with the angiotensin I-converting enzyme (ACE) deletion homozygote genotype (D/D) on subjects with coronary heart disease (CHD) and hypertension. We studied 131 healthy individuals, 141 angiographically verified CHD patients, and 159 hypertensive subjects. The identification of the ACE and AGT gene polymorphisms was carried out using a PCR-based restriction endonuclease digestion method. There was no significant difference in the distribution of the M235T and T174M variants between the two test groups and the control group. Association was also not seen when analysis was carried out in patients when subgrouped according to the extent of the severity of the disease. In addition, the risk was not restricted to subjects carrying the D allele of the ACE gene and T235T of AGT. M235T and T174M variants do not contribute to the increased risk of CHD or hypertension in the Indian population.
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PMID:Coronary heart disease, hypertension, and angiotensinogen gene variants in Indian population. 1293 41

The genes in the renin-angiotensin system are important physiologic candidates in studies of the genetic susceptibility to hypertension. Limited information has been available in most studies on the extent of variation in the candidate loci or the modifying effects of different environmental settings. We consequently genotyped 13 polymorphisms at the angiotensin I-converting enzyme (ACE) locus at an average distance of 2 kb in 2776 family members from Nigeria, Jamaica and an African-American community in the US. Allele and haplotype frequencies were similar in the three populations, with modest evidence of European admixture in the US. Two markers were consistently associated with ACE level in the three samples and the proportion of variance accounted for by ACE8 was similar in the three groups. No evidence of consistent association of single markers was noted with blood pressure across the three population samples, however. Likewise, in a haplotype-based analysis, despite significant associations within each population, the findings were not replicated consistently across all three samples. We did observe, however, that the overtransmitted haplotypes among hypertensives were drawn from a single clade, suggesting that susceptibility may cluster in patterns not captured directly by our markers.
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PMID:Angiotensin I-converting enzyme polymorphisms, ACE level and blood pressure among Nigerians, Jamaicans and African-Americans. 1497 Aug 46


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