Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Male Sprague-Dawley rats, approximately 300 g, were anesthetized. The jugular vein and carotid artery were cannulated and the left femoral vein was exposed. The femoral vein was then ligated, and 2 minutes later albumin, labeled with 125I, was injected. The albumin was allowed to equilibrate in the vascular system for 3 minutes, and then 1 group of animals was euthanized. Further groups of animals were euthanized after 15, 30, and 60 minutes. Tibias were removed from both legs together with samples of muscle and liver. The tibias were separated into diaphyseal cortex, marrow, and proximal and distal ends. All tissue samples and terminal blood samples were counted for radioactivity, and volumes of distribution were calculated. In cortical bone the volume distribution increased from an initial value of 12.9 +/- 1.1 microL/g to 18.6 +/- 2.5 microL/g at 30 minutes in the control leg (mean +/- standard error of the mean, n = 5). In the congested leg, the volume of distribution increased from 10.6 +/- 0.6 to 19.6 +/- 2.1 microL/g during the same time interval. The difference in rate of increase between the congested and control leg was not statistically significant. Albumin seemed to equilibrate within 3 minutes within the marrow. The data are consistent with the hypothesis that macromolecular transport in the interstitial fluid of cortical bone is coupled to convectional flow from endosteal to periosteal surface. This data may help to understand mechanisms by which venous hypertension has been shown to stimulate bone growth and fracture repair, and also the distribution of bone density changes observed after prolonged exposure to microgravity.
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PMID:Clearance of albumin by cortical bone and marrow. 900 92

The integrity of the blood-retinal and blood-glomerular vascular barriers were investigated simultaneously in diabetic individuals to determine whether or not the early forms of diabetic retinopathy and nephropathy are temporally related. The blood-retinal barrier was assessed by the technique of vitreous fluorophotometry. Twenty-four hour urinary excretion of albumin was determined by radioimmunoassay before fluorescein measurement. Posterior vitreous fluorescein leakage was greater in the study cohort than in the control population after diabetes had been present 11-20 years (p < 0.05) and 21 years or more (p < 0.01). Albumin excretion was also increased in the diabetic subjects (p < 0.001) and correlated to duration of diabetes (r = 0.51, p < 0.005). Hypertension raised midvitreous fluorescein levels (p < 0.05), but it had no effect on posterior vitreous values. Hypertension was an independent predictive factor for urinary albumin excretion (p < 0.05). Partial correlation analysis showed that vitreous fluorescence and urinary protein were not significantly correlated when controlled for duration of diabetes and for age. Early proteinuria did not predict retinal vascular leakage, nor did increased fluorescein leakage predict renal decompensation in the diabetic subjects. The data suggest that during the early stages of retinal and renal abnormalities associated with insulin-dependent diabetes, the eye and kidney follow different temporal courses to abnormal function.
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PMID:Early retinal and renal abnormalities in diabetes. 920 98

Proteinuria and nephropathy have been found to cluster in families of non-insulin-dependent diabetic (NIDDM) Pima Indian, and in Caucasian insulin-dependent diabetic (IDDM) patients. No information is at present available for Caucasian NIDDM patients. The aim of the present study was to determine whether micro-macroalbuminuria (AER+) is associated with albumin excretion rate abnormalities in diabetic and non-diabetic siblings of probands with NIDDM and AER+. We identified 169 Caucasian families with one NIDDM proband (the patient with longest known NIDDM duration) (101 families with only NIDDM siblings, 33 families with both NIDDM and non-NIDDM siblings and 35 families with only non-NIDDM siblings). Of the probands 56 had AER+ [Prob-NIDDM-(AER+)], 78 had AER-[Prob-NIDDM-(AER-)], 74 siblings of Prob-NIDDM-(AER+), and 113 siblings of Prob-NIDDM-(AER-) also had NIDDM. Data on albuminuria and retinopathy from multiple sibling pairs when the size of the sibship was more than two was adjusted according to a weighting factor. The odds ratio for AER+, in siblings of Prob-NIDDM-(AER+) adjusted for age, hypertension, glycated haemoglobin A1c and other confounding variables was 3.94 (95% confidence intervals: 1.93-9.01) as compared to siblings of Prob-NIDDM-(AER-). The 74 siblings of Prob-NIDDM-(AER+) had higher prevalence of proliferative retinopathy than siblings of Prob-NIDDM-(AER-) (14 vs 2%; p < 0.01). We also identified 66 non-diabetic siblings of 41 NIDDM probands with AER+ and 36 non-diabetic siblings of 27 NIDDM probands with AER-. Albumin excretion was two times higher, although still within the normal range, in the non-diabetic siblings of Prob-NIDDM-(AER+) than in siblings of Prob-NIDDM-(AER-) [median = 13.5 (range 0.5-148) vs 6.6 (range 1-17) micrograms/min (p < 0.05)]. In conclusion higher rates of albumin excretion aggregate in Caucasian families with NIDDM. Proliferative retinopathy is more frequently observed in families showing a clustering of AER+ and NIDDM. These findings suggest that familial factors play a role in the pathogenesis of renal and retinal complications in NIDDM.
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PMID:Clustering of albumin excretion rate abnormalities in Caucasian patients with NIDDM. The Italian NIDDM Nephropathy Study Group. 924 3

The pathogenetic process of diabetic retinopathy and the role of different systemic risk factors in IDDM and NIDDM is not completely understood. The aim of the present cross-sectional clinical study was (1) to compare the prevalence of systemic risk factors for diabetic retinopathy in IDDM and NIDDM patients, (2) to determine relations between these risk factors and the degree of retinopathy and (3) to evaluate the relationship between retinopathy and neuropathy. The study included 1,218 IDDM and 784 NIDDM patients attending our hospital during 1994. The mean diabetes duration was 15.4 and 13.2 years, respectively. IDDM patients with proliferative retinopathy were characterized by higher mean age of 46.4 +/- 1.08 vs. 21.8 +/- 0.42 years and longer diabetes duration of 30.0 +/- 0.79 vs. 7.7 +/- 0.26 years. Among the NIDDM patients, those ones with proliferative retinopathy had the lowest mean age of 40.5 +/- 1.42 vs. 49.7 +/- 0.61 years (p < 0.01) at diabetes manifestation. There was no statistical difference between mean HbA1c concentrations in relation to retinopathy stages. Albumin excretion was increased in both IDDM and NIDDM patients with proliferative retinopathy (p < 0.01) along with increased BMI of IDDM and increased insulin requirement of NIDDM patients (p < 0.01). Multiple regression analysis showed that proliferative retinopathy with the inclusion of non-proliferative retinopathy of IDDM and NIDDM patients was significantly correlated with diabetes duration, albumin excretion, somatic and autonomic neuropathy (p < 0.01). In NIDDM patients proliferative retinopathy with the inclusion of non-proliferative retinopathy was correlated with the age at diabetes manifestation and with cholesterol levels (p < 0.05). In IDDM and NIDDM patients proliferative retinopathy was found to be correlated with somatic and autonomic neuropathy, albumin excretion (p < 0.01) and hypertension (p < 0.05). The importance of the significant correlation of autonomic neuropathy both with background and proliferative retinopathy in IDDM and NIDDM patients needs to be prospectively investigated.
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PMID:Relations between diabetic retinopathy and cardiovascular neuropathy--a cross-sectional study in IDDM and NIDDM patients. 943 26

Microalbuminuria has been associated with a cluster of metabolic and nonmetabolic risk factors, suggesting that it might indicate the presence of generalized microvascular damage in patients with essential hypertension. To explore whether microalbuminuria is associated with early target organ damage, two groups of essential hypertensive patients, with (n = 17) (HtAlb+) and without (n = 16) (HtAlb-) microalbuminuria, and a control group (C) of healthy normotensive subjects (n = 20) were studied. The study groups, selected among participants of a large epidemiologic trial, were carefully matched for several potentially confounding variables such as gender, age, duration of hypertension, and body mass index. Albumin excretion rate was evaluated by radioimmunoassay in three nonconsecutive timed overnight collections after 3 weeks of pharmacologic wash-out. Left ventricular mass was assessed by M-B-mode echocardiography, carotid wall thickness by a high resolution ultrasound scan, and renal vascular impedance by Doppler scan. Office as well as 24-h ambulatory pressure monitoring (Takeda TM-2420) were also evaluated. There was no difference between the two hypertensive groups for office and 24-h blood pressure levels except for a lower daytime/nighttime systolic blood pressure ratio in the group with microalbuminuria. Microalbuminuric patients showed signs of early organ damage as compared to normoalbuminuric patients and normal subjects, namely greater left ventricular mass indices (LVMI 167+/-7 g/m2 in HtAlb+; 139+/-9 g/m2 in HtAlb-; 118+/-5 g/m2 in C, P < .001) and increased wall thickness of common carotid arteries (intima plus media thickness 12.5+/-0.2 mm in HtAlb+; 11.7+/-0.3 mm in HtAlb-; 11.2+/-0.2 mm in C, P < .001) as well as higher intrarenal vascular resistance (mean resistive index 0.62+/-0.01 in HtAlb+; 0.59+/-0.01 in HtAlb-; 0.59+/-0.01 in C, P < .05). In conclusion, microalbuminuria is an early marker of diffuse target organ damage in essential hypertension and therefore can be useful to identify patients for whom more aggressive preventive strategies or additional treatment measures are advisable.
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PMID:Microalbuminuria is an early marker of target organ damage in essential hypertension. 960 81

Although Type 2 (non-insulin-dependent) diabetes mellitus (Type 2 DM) is more common in South Asians than in Europeans in the UK, very little is known about complications and their risk factors in South Asians. We sought microalbuminuria in a cross-sectional study of 583 European and 889 South Asian Type 2 DM clinic attenders to Ealing Hospital, London, over 1 year. Albumin/creatinine ratios were measured in early morning urines. Prevalence of microalbuminuria was greater in South Asians compared to Europeans (40% versus 33% in men, p = 0.003, and 33% versus 19% in women, p < 0.0001). Glycaemic control was worse and prevalence of hypertension, retinopathy and heart disease was higher in South Asians. Key risk factors for microalbuminuria in both ethnic groups were glycaemic control, diabetes duration, blood pressure, triglyceride and retinopathy, but none accounted for the higher microalbuminuria prevalence in South Asians. Age and sex adjusted odds ratio for microalbuminuria was 1.78 (95% CI 1.02, 2.82, p = 0.02) in South Asians versus Europeans. After adjustment for confounders, this became 2.07, 95% CI 1.13, 3.79, p = 0.02. We conclude that microalbuminuria is more common in South Asians with Type 2 DM than in Europeans and, although risk factor relationships appeared similar in both groups, and some risk factors were more prominent in South Asians, this cannot account for the high prevalence of microalbuminuria observed in South Asians.
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PMID:Comparison of prevalence and risk factors for microalbuminuria in South Asians and Europeans with type 2 diabetes mellitus. 970 71

To investigate associations between early atherosclerosis and possible risk factors for it in young patients with established Type 1 diabetes mellitus (DM), we measured the combined intima-media thickness (IMT) of the common carotid arteries with high resolution ultrasound in 310 young patients (age < or = 40 years, mean 27.9 +/- 6.5) with a diabetes duration > or = 2 years, and in two control groups of similar age (control 1:40 healthy subjects, control 2: 40 Type 1 DM recently diagnosed patients). Albumin excretion rate and lipids (total cholesterol and triglycerides) were measured and retinopathy and hypertension (systolic blood pressure > 140 or diastolic blood pressure > 90 mmHg) sought in the patients. Mean maximum IMT was 0.52 +/- 0.06 mm in control group 1 and 0.50 +/- 0.05 mm in control group 2 with a mean difference of 0.02 mm (95% CI: -0.01, 0.04). The more established Type 1 DM patients had a significantly greater IMT (0.57 +/- 0.13 mm, p < 0.001) than both control groups. In a subgroup analysis, patients with microvascular diabetic complications (n = 99) had a significantly greater IMT (0.63 +/- 0.17 vs 0.55 +/- 0.10 mm, p < 0.001) than those without (n = 211). In a multiple linear regression analysis with a significance level of < or = 0.10, the carotid artery IMT of our established diabetic patients was related to age, male gender, triglycerides and nephropathy, suggesting the latter as the main diabetes-specific risk for intima-media thickening in young Type 1 DM patients.
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PMID:Determinants of carotid artery wall thickening in young patients with Type 1 diabetes mellitus. 979 86

The morbidity and mortality associated with diabetes mellitus are essentially related to the vascular lesions that develop over time in this condition. Both the macrocirculation and microcirculation are involved, and as a consequence, vital organs such as the brain, retina, heart, and kidney and the limbs become damaged. Because microalbuminuria represents the earliest and probably most sensitive indication of endothelial dysfunction in diabetes mellitus, the results of pharmacologic intervention with angiotensin-converting enzyme inhibitors, which treat glomerular hypertension were the first indication of potential beneficial effects in reducing diabetic nephroplasty. The nature of endothelial dysfunction related to diabetes is probably not homogeneous, since microcirculation networks are affected at different periods and with variable intensity. This appears to be the case for the aorta, the heart, segments of the digestive tract, the skin, and the skeletal muscle, the largest consumer of insulin. Although the aorta and large arteries contain a small portion of the total blood volume, their distribution of blood flow (pulse pressure) to peripheral organs may affect endothelial function in the microcirculation. Changes in the structure of conduit arteries, partly responsible for the alteration in compliance characteristics, could well be related to the way these arteries are fed by the vasa vasorum system. This report describes a new in vitro approach to examine capillary permeability in normal and alloxan-induced diabetic rabbits. Preliminary results indicate that the size of terminal arterioles of the vasa vasorum (increased diameter) and the capillary permeability to albumin (markedly enhanced) in this specialized network are profoundly affected in the thoracic aorta obtained from diabetic animals. Albumin extravasation into the interstitial fluid compartment of the aorta is likely to lead to structural and physicochemical changes: in fact, removal of interstitial macromolecules via lymphatic drainage is poor in the blood vessel wall of large arteries. This experimental approach is likely to be useful in the exploration of medications affecting the structure and function of conduit vessels.
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PMID:The blood vessel, linchpin of diabetic lesions. 1009 22

The objective of the present study was to determine whether long-term arterial hypertension renders the microvasculature more vulnerable to the deleterious inflammatory responses elicited by ischemia and reperfusion (I/R). Intravital fluorescence microscopy was used to monitor leukocyte adherence and emigration, platelet-leukocyte aggregation, and albumin extravasation in mesenteric postcapillary venules of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) after 10 minutes of ischemia and subsequent reperfusion. Significant and comparable increases in leukocyte adherence/emigration and the formation of platelet aggregates were elicited by I/R in both WKY and SHR. Albumin extravasation was enhanced after I/R in SHR, but not in WKY. Monoclonal antibodies directed against the adhesion glycoproteins CD18, P-selectin, or ICAM-1 showed similar patterns of protection against the I/R-induced inflammatory responses in WKY and SHR. The enhanced albumin extravasation noted in postischemic venules of SHR was prevented by immunoneutralization of either CD18 on leukocytes or ICAM-1 on endothelial cells. These results suggest that, whereas long-term arterial hypertension does not significantly modify the leukocyte and platelet recruitment normally elicited in venules by I/R, it does result in an exaggerated albumin leakage response, which is mediated by an interaction between beta(2) (CD18) integrins on leukocytes and ICAM-1 on endothelial cells.
Hypertension 1999 Aug
PMID:Microvascular responses to ischemia/reperfusion in normotensive and hypertensive rats. 1045 43

Albumin excretion in urine is positively correlated with the presence of ischemic heart disease and atherosclerotic risk factors. We studied prospectively whether a slight increase of urinary albumin excretion, ie, microalbuminuria, adds to the increased risk of ischemic heart disease among hypertensive subjects. In 1983 and 1984, blood pressure, urinary albumin/creatinine concentration ratio, plasma total and HDL cholesterol levels, body mass index, and smoking status were obtained in a population-based sample of 2085 subjects, aged 30 to 60 years, who were free from ischemic heart disease, diabetes mellitus, and renal or urinary tract disease. Untreated arterial hypertension or borderline hypertension was present in 204 subjects, who were followed until 1993 by the National Hospital and Death Certificate Registers with respect to development of ischemic heart disease. During 1978 person-years, 18 (9%) of the hypertensive subjects developed ischemic heart disease. Microalbuminuria, defined as a urinary albumin/creatinine ratio above the upper decile (1.07 mg/mmol), was the strongest predictor of ischemic heart disease, with an unadjusted relative risk of 4.2 (95% CI 1.5 to 11.9, P=0.006) and a relative risk of 3.5 (95% CI 1.0 to 12.1, P=0.05) when adjusted for all other atherosclerotic risk factors, including age and gender. In conclusion, microalbuminuria confers a 4-fold increased risk of ischemic heart disease among hypertensive or borderline hypertensive subjects. Urinary albumin excretion should be measured regularly in a hypertension clinic, and a rigorous control of blood pressure and of other atherosclerotic risk factors is recommended in hypertensive patients with microalbuminuria.
Hypertension 2000 Apr
PMID:Arterial hypertension, microalbuminuria, and risk of ischemic heart disease. 1077 58


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