Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:N-domain angiotensin I-converting enzyme with 80 kDa as a possible genetic marker of hypertension. 1290 Apr 33

The izumi shrimp (Plesionika izumiae Omori, 1971) is an unused resource which can be caught off the southern coast of Tokushima Prefecture. We have previously found that an izumi shrimp hydrolysate significantly inhibited the age-associated spontaneous increase in blood pressure in stroke-prone spontaneously hypertensive rats. In this present study, two angiotensin I-converting enzyme inhibitory peptides were isolated from an izumi shrimp hydrolysate by using high-performance liquid chromatography, and their amino acid sequences were determined to be Val-Trp-Tyr-His-Thr and Val-Trp. A single oral administration of synthetic Val-Trp-Tyr-His-Thr or Val-Trp significantly decreased the blood pressure in stroke-prone spontaneously hypertensive rats. The antigenicity and allergenicity of the izumi shrimp hydrolysate against BALB/c mice were very low. These results demonstrate that the angiotensin I-converting enzyme inhibitory peptides isolated from the izumi shrimp hydrolysate had an anti-hypertensive effect on rats.
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PMID:Determination of antihypertensive peptides from an izumi shrimp hydrolysate. 1832 50

The aim of the present study was to determine the impact of increased consumption of phytosterols or phytostanols on blood pressure and renal blood pressure regulatory gene expression in stroke-prone spontaneously hypertensive (SHRSP) and normotensive Wistar-Kyoto (WKY) inbred rats. SHRSP and WKY inbred rats (10/group) were fed a control diet or a diet supplemented with phytosterols or phytostanols (2.0 g/kg diet). After 5 weeks, SHRSP rats demonstrated higher systolic and diastolic blood pressures than WKY inbred rats. SHRSP rats that consumed the phytosterol or phytostanol supplemental diets displayed a 2- or 3-fold respective increase in the diastolic blood pressure than those that consumed the control diet. Angiotensinogen (Agt), angiotensin I-converting enzyme 1 (Ace1), nitric oxide synthase (Nos) 1, Nos3, cyclooxygenase 2 (Cox2) and THUMP domain containing 1 were expressed at higher levels in SHRSP compared with WKY inbred rats. Renin and angiotensin II receptor type 1a were expressed at lower levels in SHRSP than WKY inbred rats. Phytostanol supplementation up-regulated the expression of Ace1 and Nos3 in SHRSP rats. Phytosterol supplementation increased the mRNA levels of Nos1 and spondin 1 (Spon1) in SHRSP and WKY inbred rats. Cox2 mRNA levels were elevated in both phytosterol- and phytostanol-supplemented SHRSP and WKY inbred rats. Therefore, the increased blood pressure in SHRSP rats may be partly due to altered renal expression of blood pressure regulatory genes. Specifically, up-regulation of Ace1, Nos1, Nos3, Cox2 and Spon1 were associated with the increased diastolic blood pressure observed in phytosterol- or phytostanol-supplemented SHRSP rats.
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PMID:Influence of dietary phytosterols and phytostanols on diastolic blood pressure and the expression of blood pressure regulatory genes in SHRSP and WKY inbred rats. 1902 22

An enzymatic hydrolysate of sardine protein (sardine peptide, SP) derived from sardine muscle possesses angiotensin I-converting enzyme (ACE) inhibitory activity. In the present study, we investigated the effect of SP on the blood glucose levels in stroke-prone spontaneously hypertensive rats (SHRSPs). Ten-week-old SHRSPs were assigned to three groups. The control group was given tap water for 4 weeks, while the experimental groups were given water containing SP (1 g/kg/d) or an ACE inhibitor, captopril (8 mg/kg/d). Treatment with SP and captopril decreased ACE activity in the kidney, aorta, and mesentery. There were no differences in fasting blood glucose levels among the three groups, whereas SP and captopril administration significantly suppressed the increase in blood glucose after glucose loading in the control SHRSPs. No difference was observed in plasma insulin levels among the three groups. Thus treatment with captopril and ACE-inhibitory sardine peptides ameliorated the glucose tolerance of this rat strain.
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PMID:Sardine peptide with angiotensin I-converting enzyme inhibitory activity improves glucose tolerance in stroke-prone spontaneously hypertensive rats. 1980 78

Prevention and management of hypertension are the major public health challenges worldwide. Uncontrolled high blood pressure may lead to a shortened life expectancy and a higher morbidity due to a high risk of cardiovascular complications such as coronary heart disease (which leads to heart attack) and stroke, congestive heart failure, heart rhythm irregularities, and kidney failure etc. In recent years, it has been recognized that many dietary constituents may contribute to human cardiovascular health. There has been an increased focus on identifying these natural components of foods, describing their physiological activities and mechanisms of actions. Grain, vegetables, fruits, milk, cheese, meat, chicken, egg, fish, soybean, tea, wine, mushrooms, and lactic acid bacteria are various food sources with potential antihypertensive effects. Their main bioactive constituents include angiotensin I-converting enzyme (ACE) inhibitory peptides, vitamins C and E, flavonoids, flavanols, cathecins, anthocyanins, phenolic acids, polyphenols, tannins, resveratrol, polysaccharides, fiber, saponin, sterols, as well as K, Ca, and P. They may reduce blood pressure by different mechanisms, such as ACE inhibition effect, antioxidant, vasodilatory, opiate-like, Ca(2+) channel blocking, and chymase inhibitory activities. These functional foods may provide new therapeutic applications for hypertension prevention and treatment, and contribute to a healthy cardiovascular population. The present review summarizes the antihypertensive food sources and their bioactive constituents, as well as physiological mechanisms of dietary products, especially focusing on ACE inhibitory activity.
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PMID:Bioactive natural constituents from food sources-potential use in hypertension prevention and treatment. 2362 3

Increasing fruit and vegetable consumption is a key lifestyle modification in the prevention and treatment of hypertension. Kiwifruit has previously been shown to have favorable effects on blood pressure (BP), likely through inhibiting angiotensin I-converting enzyme activity. We hypothesized that the replacement of 2 fruit servings in a healthy diet with 2 green kiwifruit a day would significantly improve BP and other markers of cardiovascular function, including heart rate, stroke volume, cardiac output, and total peripheral resistance, in a group of hypercholesterolemic men. Using a controlled cross-over study design, 85 subjects completed a 4-week healthy diet run-in period before randomization to one of two 4-week intervention sequences in which they either consumed 2 green kiwifruit a day plus a healthy diet (intervention) or consumed a healthy diet alone (control). Blood pressure and other measures of cardiovascular function (using a Finometer MIDI [Finapres Medical Systems B.V, Amsterdam, The Netherlands] and standard oscillometric device) and anthropometric measurements were taken before and at the end of the treatment periods. A physical activity questionnaire was completed during the last visit. Subjects were found to be predominantly normotensive (43.5%) or prehypertensive (50.6%) and quite physically active (>30 minutes of moderate to vigorous physical activity/day in >80% subjects). No significant differences were seen for BP or any of the other markers, including heart rate, stroke volume, cardiac output, and total peripheral resistance. In conclusion, in this hypercholesterolemic, nonhypertensive group, no beneficial effects on BP or other markers of cardiovascular function were seen when consuming 2 kiwifruit a day against the background of a healthy diet.
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PMID:Daily kiwifruit consumption did not improve blood pressure and markers of cardiovascular function in men with hypercholesterolemia. 2465 90

Combinations of multiple predisposing polymorphisms and their interactions with modifiable factors may result in synergistic effects on early ischemic stroke risk. We evaluated the potential interaction of apolipoprotein (apo) E and angiotensin I-converting enzyme (ACE) gene polymorphisms and hypertension on early ischemic stroke risk in Serbian population. We analyzed 65 stroke patients (mean age 35 yrs) and age- and body mass index matched 330 controls. ACE genotypes were determined by polymerase chain method (PCR) and apoE genotypes by PCR appended by HhaI restriction fragment-length polymorphism/MADGE analysis. Odds ratios (ORs) for stroke were 1.35 (95% confidence interval (CI) 0.50-3.62) in subjects with one studied polymorphism and 3.78 (95% CI, 1.28-11.18) in those with two. Compared with nonhypertensive subjects bearing no polymorphisms, ORs were 2.73 (95% CI 0.32-17.55) and 4.80 (95% CI 0.50-28.12) for nonhypertensive subjects with one and two polymorphisms, 8.53 (95% CI 1.04-62.47) and 30.00 (95% CI 3.21-186.45) for hypertensive. These data suggest a gene-dose effect of the examined gene variants and a synergistic effect of these polymorphisms and hypertension in the pathogenesis of early ischemic stroke.
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PMID:The Interaction of Apolipoprotein E and Angiotensin I-Converting Enzyme Dna Polymorphisms with Hypertension on Early Ischemic Stroke Risk. 2768 51


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