Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urodilatin (ANF(95-126)), an analogue of the atrial natriuretic factor (ANF(99-126)), has recently been isolated from human urine. To study haemodynamic and renal effects of synthetic urodilatin, 18 healthy male volunteers (age 26.1 +/- 0.8 years; X +/- SEM) received i.v. bolus injections of urodilatin at doses of 1, 2 or 4 micrograms kg-1 body weight (bw) (n = 6 per dosage group). Urodilatin dose-dependently increased heart rate and cardiac index. A dose-dependent increase in plasma cyclic GMP levels was also observed. Urinary cyclic GMP excretion, urine flow and natriuresis increased 7-fold, 5-fold and 4-fold, respectively. Renal effects were not different between dosage groups. Compared with ANF(99-126), after urodilatin the reduction in mean pulmonary arterial pressure (PAP) was more pronounced (2 micrograms kg-1, n = 6; ANF -1.8 +/- 0.5, URO: -5.5 +/- 1.1 mmHg, P less than 0.05). Furthermore, after urodilatin the reduction of PAP lasted continuously from 2 up to 90 min after injection, while ANF(99-126) produced only a transient decrease of PAP. Similarly the reduction of pulmonary capillary wedge pressure (PCWP) by urodilatin from 9.3 +/- 1.2 to 3.8 +/- 0.9 mmHg (P less than 0.05) was also sustained up to 90 min post administration. These data in healthy volunteers suggest that, due to prolonged reduction of PAP and PCWP with increases of cardiac index and reduction of systemic vascular resistance, urodilatin might exhibit beneficial effects in cardiovascular disease.
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PMID:Haemodynamic and renal effects of urodilatin in healthy volunteers. 131 96

Hyperlipidemia is one of many atherogenic risk factors encountered by patients undergoing chronic hemodialysis (HD). We have studied lipid profiles in these patients and have found less hypertriglyceridemia in those undergoing high-flux HD than those receiving traditional HD. Mean +/- SEM triglyceride level was 1.62 +/- 0.15 mmol/L (143.3 +/- 13.6 mg/dL) in high-flux dialysis patients, 2.39 +/- 0.27 mmol/L (211.6 +/- 24.1 mg/dL) in conventional dialysis patients, and 1.55 +/- 0.13 mmol/L (137.1 +/- 11.5 mg/dL) in normal age- and sex-matched controls. In addition, we found that in patients undergoing high-flux HD, females had higher high-density lipoprotein2 (HDL2) levels (0.62 +/- 0.03 mmol/L [23.8 +/- 1.3 mg/dL]) than males (0.33 +/- 0.04 mmol/L [12.9 +/- 1.7 mg/dL]) (P < 0.01). The mechanism(s) responsible for divergent lipid profiles in subsets of HD patients deserves further investigation. Whether reductions of hypertriglyceridemia and/or increases of HDL2 will diminish the incidence of cardiovascular disease in dialysis patients is unknown.
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PMID:Improved lipid profiles in patients undergoing high-flux hemodialysis. 141 4

In 29 lean, premenopausal, never-treated hypertensive women (142 +/- 2/93 +/- 1 mmHg, mean +/- SEM) plasminogen activator inhibitor (PAI-1) was elevated (11.0 +/- 1.5 U/ml vs 6.3 +/- 1.0 U/ml, p less than 0.05) compared to healthy, normotensive women (113 +/- 2/71 +/- 2 mmHg). Euglobulin clot lysis time tended to be longer in the hypertensive than in the normotensive women (p = 0.06). PAI-1 was positively correlated to triglycerides (r = 0.60, p less than 0.001), haematocrit (r = 0.45, p less than 0.05), insulin (r = 0.38, p less than 0.05) and body mass index (r = 0.38, p less than 0.05), and inversely correlated to HDL cholesterol (r = -0.43, p less than 0.05) in the hypertensive women. Fibrinogen was not significantly different in the hypertensive and normotensive women, while the hypertensive smokers had higher fibrinogen than the hypertensive non-smokers (3.01 +/- 0.17 g/l vs 2.54 +/- 0.10 g/l, p less than 0.05). All participants were investigated in the same phase of the menstrual cycle. Despite that, oestradiol was significantly lower in the hypertensive than in the normotensive women (0.57 +/- 0.06 vs 0.81 +/- 0.09 nmol l-1, p less than 0.05), while progesterone was similar in the two groups. These results suggest that premenopausal, never-treated hypertensive women are characterized by low oestradiol levels as well as decreased fibrinolytic activity. PAI-1 seems to be associated with other risk factors for cardiovascular disease in hypertensive women.
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PMID:Evidence of decreased fibrinolytic activity in hypertensive premenopausal women. 143 14

1. Cigarette smoking is known to increase the risk of cardiovascular disease in both men and women. Experimental and epidemiological studies have demonstrated that cigarette smoking is associated with several indices of increased platelet activation and platelet/vessel wall interaction in men. The aim of the present study was to test the hypothesis that cigarette smoking is linked to an increased platelet activity in women also. 2. In 26 healthy smoking and non-smoking women (age 21-49 years) the urinary excretion of the thromboxane A2 metabolite 2,3-dinor-thromboxane B2 (an index of platelet activation) and of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1 alpha (an index of platelet/vessel wall interaction) were analysed by g.c.-m.s. in samples collected on days 3, 10 and 20 of their respective menstrual cycles. 3. The urinary excretion of 2,3-dinor-thromboxane B2 did not vary significantly during the menstrual cycle, either in the smokers or in the non-smokers. It was consistently higher (P less than 0.004) in the group of smokers (average of day 3, 10 and 20, 395 +/- 61 pg/mg of creatinine; mean +/- SEM) than in the group of non-smokers (average 188 +/- 22 pg/mg of creatinine). 4. The urinary excretion of 2,3-dinor-6-keto-prostaglandin F1 alpha did not differ between the groups on any of the days studied (average on days 3, 10 and 20 in the smokers and non-smokers was 281 +/- 50 and 227 +/- 30 pg/mg of creatinine, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cigarette smoking and urinary excretion of markers for platelet/vessel wall interaction in healthy women. 164 17

We report the effects of monitored smoking cessation on adrenergic regulation in chronic smokers. The beta 2 adrenoceptor density of mononuclear leukocytes (MNLs) and plasma catecholamines was analyzed before cessation and 2, 3, and 8 weeks after cessation. We found a progressive increase in beta-adrenoceptor density after smoking cessation. During smoking the beta-adrenoceptor density was 1.456 +/- 83 (mean +/- SEM) binding sites per cell (n = 10), whereas 3 weeks after cessation the density was 1,774 +/- 157 sites per cell (n = 10; p less than 0.05), and at 8 weeks, 1,900 +/- 227 sites per cell (n = 8; p less than 0.05), representing an overall increase of 23%. Smoking cessation had no effect on binding affinity nor on lymphocyte subgroup distribution. The density of MNL cell beta-adrenoceptors in age-matched nonsmoking men was higher, at 1,896 +/- 271 sites per cell, than that of the chronic smokers before cessation, 1,419 +/- 117 sites per cell (n = 14; p less than 0.01). Plasma epinephrine decreased as a result of cessation from 0.36 pmol/ml (0.26-0.44, 95% confidence interval; baseline) to 0.26 pmol/ml (0.20-0.32) at 8 weeks (p less than 0.05), and norepinephrine decreased from 2.09 pmol/ml (1.38-2.80) to 1.69 pmol/ml (1.14-2.24; p = 0.06). We conclude that stopping smoking progressively increases beta 2-adrenoceptor density on MNL cells. Eight weeks after cessation the adrenoceptor density reaches the corresponding level of nonsmokers. These reversible changes in adrenergic regulation after smoking cessation may be associated with the relatively rapid reduction in cardiovascular disease risk among ex-smokers.
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PMID:Cigarette smoking alters sympathoadrenal regulation by decreasing the density of beta 2-adrenoceptors. A study of monitored smoking cessation. 171 16

Genetic low density lipoprotein (LDL) deficiency and high density lipoprotein (HDL) excess have been associated with enhanced longevity. This investigation assessed the prevalence of lipoprotein abnormalities in octogenarians free of clinical evidence of cardiovascular disease (CVD) in the Framingham Heart Study. Plasma lipid and lipoprotein cholesterol determinations were carried out by standard techniques between 1971 and 1974. Participants who were free of clinical evidence of CVD in an examination approximately 10 years later (1981 to 1982) had their lipoprotein values tabulated based on the earlier examination. There were 106 women and 57 men who met these criteria, with mean ages of 83.3 and 82.9 years, respectively, at examination 16 (called cases). Mean levels (+/- SEM) of LDL cholesterol in cases were 152 +/- 3 mg/dL for women, and 147 +/- 5 mg/dL for men. For HDL cholesterol, these values were 57 +/- mg/dL for women and 46 +/- 2 mg/dL for men. These values were not statistically different from those of other study subjects (who did not meet the CVD criteria or were decreased) or middle-aged controls. In contrast, HDL cholesterol levels below the tenth percentile of normal were not observed in any male cases and in only 1.0% of female cases (P less than .05) as compared with observations in control subjects. The data are consistent with the concept that there is not an overrepresentation of either decreased LDL cholesterol or elevated HDL cholesterol values in subjects who subsequently become healthy octogenarians, but that these subjects are exceedingly unlikely to have reduced HDL cholesterol levels.
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PMID:Plasma lipoproteins in healthy octogenarians: lack of reduced high density lipoprotein cholesterol levels: results from the Framingham Heart Study. 272 73

In type 2 diabetes with "secondary failure of sulfonylurea therapy" good metabolic control can seldom be achieved by insulin therapy even with high insulin doses. Hyperinsulinemia however is a possible risk factor of cardiovascular disease in type 2 diabetes. Maintaining the effects of sulfonylurea action insulin should be added in as small amounts as possible to avoid hyperinsulinemia and to ameliorate hyperglycemia. 16 type 2 diabetics with "secondary failure" were treated either with insulin alone (group A; n = 8) or with 3.5 mg b.i.d. glibenclamide plus small amounts of intermediate insulin (group B; n = 8) in a randomised order. After the inpatient period outpatient control was performed monthly up to six months, later on four times a year up to two years. Both groups were comparable with regard to age, duration of diabetes, body weight and metabolic control. The daily insulin dose was 14 +/- 2 IU (means +/- SEM) after one month and 19 +/- 2 IU after two years in group B. In contrast 30 +/- 3 IU and 43 +/- 5 IU respectively were needed in group A (p less than 0.001). All patients B were treated with one daily injection, all patients A needed two injections. Resulting in nearly identical metabolic control in group A basal insulin levels exceeded those in group B after two years significantly (28.6 +/- 3.7 vs. 18.6 +/- 1.6 mcU/ml; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Combination therapy with insulin/sulfonylurea in the long-term therapy of type II diabetes following "secondary failure"]. 314 87

The nutritional status of 267 male US Navy Sea, Air, and Land (SEAL) trainees was assessed to determine dietary patterns. Diet records, blood samples, 24-h urine collections, and physical characteristics were analyzed. Energy intake was 3886 +/- 73 kcal/d (SEM) with 15.7 +/- 0.2, 42.9 +/- 0.6, and 41.2 +/- 0.5% of the energy derived from protein, carbohydrate (CHO), and fat, respectively. Mean cholesterol intake (1008 +/- 35.7 mg/d [SEM]) exceeded the US Dietary Goal (less than or equal to 300 mg/d) and serum cholesterol concentration was 5.25 +/- 0.41 mmol/L (SEM). Over 38% of the trainees had cholesterol concentrations greater than 5.3 mmol/L, an indicator of high risk for cardiovascular disease. Mean sodium intake was 250 +/- 22 mmol/d. Over 86% of the trainees consumed greater than 144 mmol/d. Urinary Na excretion was high (146.7 +/- 6.7 mmol/d [SEM]) and correlated with Na intake (r = 0.365; p = 0.001). Potassium and selected vitamin intakes approximated the Military Recommended Dietary Allowances. Fat, cholesterol, and Na intakes were high relative to the dietary goals. Whether more dietary CHO would improve performance in endurance training remains to be determined.
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PMID:Nutritional survey of the US Navy SEAL trainees. 318 22

Disturbances in peripheral norepinephrine release or removal by neuronal and extraneuronal uptake may have pathogenetic significance in cardiovascular disease states. We investigated the mechanisms of removal of norepinephrine in the forearm of healthy subjects under basal conditions, using measurements of arterial and venous plasma norepinephrine concentrations, blood pressure, heart rate, and forearm blood flow. The specific inhibitor of neuronal uptake, desipramine, was infused intra-arterially into the brachial artery of five subjects. Net norepinephrine overflow from the forearm increased markedly, revealing considerable local release of norepinephrine. Six other subjects received four intra-arterial infusions of norepinephrine, 1.18 pmol/kg/min, with various doses of desipramine and the extraneuronal uptake-inhibiting drug hydrocortisone. The forearm extraction rate for circulating norepinephrine decreased with increasing doses of desipramine (from 69.4 +/- 3.0 [SEM] to 35.3 +/- 8.4%; p less than 0.001). Increasing doses of hydrocortisone during continued inhibition of neuronal uptake resulted in decreased forearm extraction of norepinephrine (from 63.3 +/- 4.9 to 40.6 +/- 4.4%; p less than 0.01). In six other subjects who received the highest dose of hydrocortisone without concomitant inhibition of neuronal uptake, forearm extraction of norepinephrine decreased from 57.1 +/- 4.9 to 51.5 +/- 4.7% (p less than 0.05). These results suggest that neuronal uptake contributes markedly to the removal of circulating and endogenously released norepinephrine in the forearm. For circulating norepinephrine, a corticosteroid-sensitive mechanism of extraneuronal uptake was also demonstrated. These results indicate that neuronal and extraneuronal uptake can be estimated separately in this vascular bed. Similar organ-specific studies in patients may reveal disturbances in mechanisms of norepinephrine removal.
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PMID:Demonstration of neuronal and extraneuronal uptake of circulating norepinephrine in the forearm. 358 5

To clarify the independent relationships of obesity and overweight to cardiovascular disease risk factors and sex steroid levels, three age-matched groups of men were studied: (i) 8 normal weight men, less than 15% body fat, by hydrostatic weighing; (ii) 16 overweight, obese men, greater than 25% body fat and 135-160% of ideal body weight (IBW); and (iii) 8 overweight, lean men, 135-160% IBW, but less than 15% fat. Diastolic blood pressure was significantly greater for the obese (mean +/- SEM, 82 +/- 2 mmHg) than the normal (71 +/- 2) and overweight lean (72 +/- 2) groups, as were low density lipoprotein levels (131 +/- 9 vs. 98 + 11 and 98 + 14 mg/dl), the ratio of high density lipoprotein to total cholesterol (0.207 +/- 0.01 vs. 0.308 +/- 0.03 and 0.302 +/- 0.03), fasting plasma insulin (22 +/- 3 vs. 12 +/- 1 and 13 +/- 2 microU/ml), and the estradiol/testosterone ratio (0.076 +/- 0.01 vs. 0.042 +/- 0.02 and 0.052 +/- 0.02); P less than 0.05. Estradiol was 25% greater for the overweight lean group (40 +/- 5 pg/ml) than the obese (30 +/- 3 pg/ml) and normal groups (29 +/- 2 pg/ml), P = 0.08, whereas total testosterone was significantly lower in the obese (499 +/- 33 ng/dl) compared with the normal and overweight, lean groups (759 +/- 98 and 797 +/- 82 ng/dl). Estradiol was uncorrelated with risk factors and the estradiol/testosterone ratio appeared to be a function of the reduced testosterone levels in obesity, not independently correlated with lipid levels after adjustment for body fat content. Furthermore, no risk factors were significantly different between the normal and overweight lean groups. We conclude that (a) body composition, rather than body weight per se, is associated with increased cardiovascular disease risk factors; and (b) sex steroid alterations are related to body composition and are not an independent cardiovascular disease risk factor.
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PMID:Body composition, not body weight, is related to cardiovascular disease risk factors and sex hormone levels in men. 365 69


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