Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to examine the effects of wave propagation properties (global reflection coefficient gamma IG; pulse wave velocity, c(ph); and characteristic impedance zeta(o) on the mechanical performance of the coupled left ventricle-arterial system. Specifically, we sought to quantify effects on aortic pressure (P(ao)) and flow Q(ao) while keeping constant other determinants of P(ao) and Q(ao) (left ventricular end-diastolic volume, V(ed), and contractility, heart rate, and peripheral resistance, R(s)). Isolated rabbit hearts were subjected to real-time, computer-controlled physiological loading. The arterial circulation was modeled with a lossless tube terminating in a complex load. The loading system allowed for precise and independent control of all arterial properties as evidenced by accurate reproduction of desired input impedances and computed left ventricular volume changes. While propagation phenomena affected P(ao) and Q(ao) morphologies as expected, their effects on absolute P(ao) values were often contrary to the current understanding. Diastolic (Pd) and mean (Pm) P(ao) and stroke volume decrease monotonically with increases in gamma G, c(ph), or zeta(o) over wide ranges. In contrast, these increase had variable effects on peak systolic P(ao) (Ps): decreasing with gamma G, biphasic with c(ph), and increasing with zeta(o). There was an interaction between gamma G and c(ph) such that gamma G effects on P(m) and P(d) were augmented a higher C(ph) and vice versa. Despite large changes in system parameters, effects on Pm and Ps were modest ( < 10% and < 5%, respectively); effects on Pd were always two to four times greater. Similar results were obtained when the single-tube model of the arterial system was replaced by an asymmetrical T-tube configuration. Our data do not support the prevailing hypothesis that P(s) (and therefore ventricular load) can be selectively and significantly altered by manipulating gamma G, c(ph), and/or zeta o.
Hypertension 1996 May
PMID:Wave propagation in coupled left ventricle-arterial system. Implications for aortic pressure. 862 Dec

To examine the cardiovascular effects on the fetus of an elevated umbilical vascular resistance resulting in fetal hypoxemia, we embolized the fetal side of the placenta in pregnant sheep and measured cardiovascular and hormonal changes and cellular growth in fetal heart. Chronically catheterized fetal sheep were embolized (n = 6) for 21 days between 0.74 and 0.88 of gestation into the descending aorta until arterial oxygen content was decreased by 40-50% of the preembolization value. Control animals (n = 6) received saline only. During embolization, fetuses became chronically hypoxemic (P < 0.001) and hypertensive (P < 0.001), with a progressive increase in umbilical artery resistance index (P < 0.001). There was also an increase in fetal plasma norepinephrine throughout the study period (P < 0.05). On day 21 of embolization, fetuses showed asymmetrical growth restriction, increased heart weight (P < 0.01), and increase in right and left ventricular wall thickness (P < 0.05) compared with control animals. The protein-to-DNA ratio, an index of cell size, increased in the right ventricular myocardium in the embolized group (P < 0.001), suggesting myocardial cell hypertrophy. We conclude that, during chronic placental damage leading to fetal hypoxemia with an increase in umbilical artery resistance index, fetuses developed arterial hypertension and asymmetrical growth restriction and that increases in afterload to the heart and plasma norepinephrine likely caused fetal myocardial hypertrophy.
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PMID:Chronic fetal placental embolization and hypoxemia cause hypertension and myocardial hypertrophy in fetal sheep. 903 10

While hypertension is known to cause left ventricular and vascular hypertrophy, the relationship between alterations of vascular and cardiac structures in patients with hypertrophic cardiomyopathy has not been fully clarified. We measured intima-media thickness of carotid arteries by ultrasonography in patients with hypertrophic cardiomyopathy (n = 16), normotensive subjects (n = 358), and hypertensive subjects (n = 386) in a cohort of 7940 male employees of a bus company. Our object was to determine whether vascular alteration occurs in hypertrophic cardiomyopathy similarly as in hypertension. Hypertrophic cardiomyopathy (wall thickness > or = 15 mm; asymmetrical hypertrophy without hypertension) was screened with family history and electrocardiography followed by echocardiography. The intima-media thickness in patients with hypertrophic cardiomyopathy (mean, 0.61 mm) did not differ from that of normotensive subjects (0.60 mm) but was significantly less than that of hypertensive subjects with left ventricular hypertrophy (wall thickness > or = 14 mm; n = 22; 0.73 mm). In a scatterplot of intima-media thickness versus interventricular septal thickness, these two parameters were significantly correlated in normotensives and hypertensives. The patients with hypertrophic cardiomyopathy distributed outside the 95% confidence range of the normotensive and hypertensive subjects. In summary, the increase in intima-media thickness of the carotid artery paralleled left ventricular hypertrophy in normotensive and hypertensive subjects. Patients with hypertrophic cardiomyopathy had a normal intima-media thickness regardless of the hypertrophied left ventricle. Thus, information on intima-media thickness may be useful in differentiating hypertensive left ventricular hypertrophy from hypertrophic cardiomyopathy.
Hypertension 1997 Jan
PMID:Intima-media thickness of the carotid artery in hypertensive subjects and hypertrophic cardiomyopathy patients. 903 28

Nitric oxide (NO) is involved in blood pressure regulation, and its synthesis is inhibited by methylarginines. It has been hypothesized that one of these, asymmetrical dimethylarginine (ADMA), may contribute to dialysis-associated hypertension because it accumulates in the plasma of hemodialysis (HD) patients in a concentration high enough (4 mumol/L) to inhibit NO synthesis in experimental model systems. A precolumn HPLC technique was used to quantify methylarginines (ADMA and symmetrical dimethylarginine [SDMA]) in plasma from HD patients before and after dialysis, from continuous ambulatory peritoneal dialysis (CAPD) patients, and from healthy subjects. Plasma ADMA concentrations were 0.59 +/- 0.22 (SD) mumol/L in HD patients predialysis (n = 19) and 0.70 +/- 0.27 mumol/L in CAPD patients (n = 11), versus about half of the concentration in control subjects (0.36 +/- 0.08 mumol/L, n = 7). The concentrations of SDMA (not an inhibitor of NO formation) were approximately four to five times the ADMA concentrations in both HD and CAPD patients, in contrast to a ratio of 1:1 in the control subjects. Methylarginine concentrations were reduced by 23% and 40% postdialysis, as calculated from ADMA and SDMA values, respectively. No significant correlations were observed between ADMA concentrations, on the one had, and blood pressure, creatinine and dialysis dose (Kt/V urea), on the other hand. It is concluded that plasma levels of ADMA are considerably lower than those reported earlier in patients treated with HD and also below the levels that hitherto have been thought to have clinical relevance. The role of ADMA in inhibiting NO in dialysis-associated hypertension is questioned.
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PMID:Serum levels of NG, NG-dimethyl-L-arginine, a potential endogenous nitric oxide inhibitor in dialysis patients. 929 36

M-mode, two-dimensional, and Doppler echocardiography were performed in 38 chronic renal failure (CRD) patients on conservative management, 35 patients on hemodialysis, and 36 matched controls. The controls were matched for age, sex, and comorbidities. The incidence of hypertension, left ventricular (LV) end diastolic volume, LV end systolic volume, and LV mass index were significantly higher in patients on hemodialysis compared to the controls. The LV parameters in the predialysis patients were not significantly different from the controls, except the LV end systolic internal dimensions were significantly higher in the CRF patients. Multiple regression analysis underscored the strong association between increase in LV mass index (LVMI) and hypertension. The diabetic patients with renal failure had large LV internal diameter and end diastolic volume compared to non-diabetics. Systolic function was well preserved even in hypertensive and diabetic patients with uremia. The incidence of diastolic dysfunction and asymmetrical septal hypertrophy were not significantly different in the three groups of patients.
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PMID:Left ventricular morphology in chronic renal failure by echocardiography. 941 37

The asymmetrical breakdown of the blood-brain barrier to Evans-blue was studied in male and female rats during epileptiform seizures and in acute hypertension. The animals were divided into six groups. Group I: control female; Group II: control male; Group III: female + acute hypertension; Group IV: male + acute hypertension; Group V: female + seizure; Group VI: male + seizure. Asymmetric breakdown of the blood-brain barrier had been seen in female rats treated with pentylenetetrazol. Pentylenetetrazol-induced seizure produces less disruption of the blood-brain barrier in right cerebral hemisphere than in left cerebral hemisphere in female rats. There were no asymmetrical changes of blood-brain barrier permeability between the left and right hemispheres in acute hypertension in both sexes, and male rats treated with pentylenetetrazol.
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PMID:Asymmetrical changes in blood-brain barrier permeability during pentylenetetrazol-induced seizures and in acute hypertension. 975 55

1. The present experiments were designed to investigate the role of asymmetrical NG,NG-dimethyl-L-arginine (ADMA) in causing hypertension associated with the focal and segmental glomerulosclerosis (FSGS) produced by a single bolus of puromycin aminonucleoside (PAN) and successive injection of protamine for 7 days in rats which had undergone unilateral nephrectomy. 2. After the unilateral nephrectomy, and administering PAN and protamine, histological examinations of the kidney revealed a typical FSGS, that is, evident abnormalities including segmental mesangial proliferation, obliteration of glomerular capillary lumens and adhesions between the glomerulus and Bowman's capsule could be observed. Changes in the glomerular epithelial cells consisted of the swelling with bleb formation. 3. In the FSGS rats, urine volume and urinary protein were significantly (P<0.05 and P<0.005) increased throughout 4-week experimental period, while the creatinine clearance was significantly (P<0.005) and transiently decreased, and recovered 4 weeks later. These changes were associated with the sustained elevation of the systolic blood pressure. 4. ADMA levels in aortic endothelial cells, plasma and urine were significantly (P<0.05 and P<0.005) increased in the FSGS rats, but the level in the kidney remained unchanged. 5. The basal level and net production of cyclic GMP in the aortic vessel wall with endothelium when stimulated by norepinephrine and acetylcholine were significantly (P<0.05 and P<0.01) attenuated in the FSGS rats. 6. There were significant and positive correlations between systolic blood pressure (y) and ADMA levels (x) in endothelial cells (y=4.43x+122.2, r=0.979, P<0.0001), plasma (y=0.10x+71.9, r=0.921, P<0.001) and urine (y=0.48x+126.9, r =0.699, P<0.005), but not significant in the kidney (y=0.06x+102.7, r=0.252, NS). 7. These findings suggest that ADMA as an endogenous inhibitor of NO synthesis may play an important role for the pathogenesis in the hypertension associated with the experimental FSGS in the rat.
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PMID:Endogenous asymmetrical dimethylarginine and hypertension associated with puromycin nephrosis in the rat. 980 29

Reports of Ask-Upmark kidney, initially described as a congenital defect in renal development, are uncommon. We report a case with the features of bilateral asymmetrical segmental atrophy in a patient with childhood-onset hypertension. As an adult, she developed cerebral, celiac, and renal artery aneurysms. She underwent successful clipping of the cerebral aneurysm and renal artery repair with preservation of renal function. Novel radiologic techniques make possible the noninvasive diagnosis of segmental atrophy and its complications.
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PMID:Ask-Upmark kidney associated with renal and extrarenal arterial aneurysms. 1019 35

The present study investigated gender differences among adult patients with obstructive hypertrophic cardiomyopathy (OHCM) and resting gradient. Using outflow gradients >10 mmHg and the presence of asymmetrical septal hypertrophy of the left ventricle as inclusion criteria, 122 patients were identified among patients referred for echocardiographic examinations between May 1990 and October 1996. Clinical, echocardiographical and follow-up data were compared between male and female patients. The female patients were significantly older than male patients (mean age +/-SD 66.7+/-10.5 vs 54.8+/-12.5 years). The female patients had a smaller interventricular septal wall thickness, less frequent systolic anterior movement of the mitral valve, more frequent association with hypertension, and less frequent association with ischemic heart disease (IHD) and giant T wave inversion. In this study population, adult female patients presented with OHCM 12 years later than males. Whether this represents female patients' reluctance to seek medical attention early, a different disease process that affects predominantly elderly females, or a gender-specific end organ response to aging, hypertension, IHD and other processes, or the protective effects of estrogen remains to be determined.
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PMID:Gender differences in the presentation of adult obstructive hypertrophic cardiomyopathy with resting gradient: a study of 122 patients. 1059 91

Although echocardiography is a useful diagnostic tool in hypertrophic cardiomyopathy (HCM), it is sometimes difficult to differentiate it from hypertensive heart disease (HHD): some patients with HCM show symmetrical hypertrophy, whereas patients with HHD sometimes show asymmetrical septal hypertrophy. We used a radioiodinated long-chain fatty acid tracer to visualize the altered myocardial fatty acid metabolism of HCM and HHD. Carnitine is the essential substance for the beta-oxidation of long-chain fatty acids. We recently reported that serum free carnitine levels in HCM were elevated and that they were significantly correlated with the severity of myocardial fatty acid metabolic disorder. Therefore, we investigated serum carnitine levels in patients with HCM and HHD, which can contribute to the differentiation of each other. We studied 56 patients with HCM and 20 patients with essential hypertension. Serum free carnitine levels were significantly higher in patients with HCM than those with HHD (HCM 52.5+/-9.5 nmol/mL, HHD 46.6+/-6.4 nmol/mL, P<0.01), but they showed no statistical difference between patients with HHD and normal subjects. Serum acylcarnitine levels were significantly lower in patients with HCM than those with HHD (HCM 10.1+/-4.0 nmol/mL, HHD 14.5+/-4.9 nmol/mL, P<0.0005), although they did not differ between patients with HHD and normal subjects. Scintigraphic analyses with a long-chain fatty acid analog revealed that myocardial tracer uptake was much reduced in patients with HCM compared with that in patients with HHD (quantitative analysis: HCM 2.11+/-0.12, HHD 2.22+/-0.17, P<0.05; semiquantitative analysis: HCM 13.6+/-6.3, HHD 2.0+/-1.5, P<0.0001). In conclusion, the differences in serum carnitine levels between HCM and HHD reflect altered myocardial fatty acid metabolic impairment, and the levels can help to distinguish these 2 diseases.
Hypertension 2000 Aug
PMID:Can serum carnitine levels distinguish hypertrophic cardiomyopathy from hypertensive hearts? 1094 80


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