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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical approach to prevention, cogently documented in the Task Force guidelines, implies the medicalization of prevention. The concentration of resources on those most in need is efficient, the widening of physicians' responsibility is welcome, and the influence on the recipients diffuses into the community. The Task Force report, however, fails to stress the problems and the limitations of this approach. The adverse effects of "labeling" can be serious. They need to be measured and taken into account, and there should be no screening without counseling and long-term care; the latter cannot be guaranteed unless there is a comprehensive general practitioner system. Screening readily generates overmedication, particularly since many physicians lack the skills, the inclination, or the staff to provide expert and continuing health advice. Concern for high-risk individuals should be only one part of a much wider preventive strategy. This is illustrated by the close correlations between the prevalence of high-risk status and the population mean value (0.85 for hypertension vs. mean blood pressure, 0.97 for excess use of alcohol vs. population mean intake). The medical approach, important though it is, must not distract attention from the more fundamental population strategy of prevention.
J Gen Intern Med
PMID:British perspective on the U.S. Preventive Services Task Force guidelines. 223 Oct 54

The U.S. Preventive Services Task Force recommendations for screening for hypertension and high blood cholesterol are generally consistent with preexisting national guidelines promulgated by the Joint National Committee for Detection, Evaluation, and Treatment of High Blood Pressure and the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Cholesterol in Adults. While a welcome addition to the armamentarium of the clinician, the Task Force recommendations represent only a partial solution to our current epidemic of blood-pressure- and cholesterol-related cardiovascular disease. A meaningful reduction in society's burden of cardiovascular disease can be achieved only by complementing the Task Force recommendations with community-based mass treatment strategies aimed at shifting the distribution of blood pressure and cholesterol toward a biologically more normal pattern.
J Gen Intern Med
PMID:Reflections on the U.S. Preventive Services Task Force recommendations for screening for hypertension and hypercholesterolemia. 223 Oct 58

1. Endothelial cells of blood vessels generate factors which can modulate underlying smooth muscle tone, inducing vasorelaxation, (endothelium-derived relaxing factor, EDRF, and endothelium-derived hyperpolarizing factor) and/or vasoconstriction (endothelium-derived contracting factors, EDCFs, including the peptide endothelin). 2. EDRF is nitric oxide (NO) or a RNO compound from which this oxide is released. Its half-life is very short (6-50 sec), and it produces rapid vasodilations and inhibits platelet aggregation. 3. NO is formed from the terminal guanidino of L-arginine, but not of D-arginine. NO effects and NO formation are inhibited by NG-monomethyl-L-arginine (L-NMMA), but not by D-NMMA. These inhibitory effects are blocked by L-arginine. 4. Removal of endothelium or pathological situations that can induce endothelial dysfunction (atherosclerosis, diabetes, hypertension or subarachnoid hemorrhage) cause increases on the vascular contractility elicited by agonists (noradrenaline, serotonin, EDCFs, etc.). These findings suggest that EDRF produces a physiological inhibitory modulation of vascular smooth muscle tone and its alteration produces or facilitates the development of diseases such as hypertension or coronary and cerebral vasospasm.
Gen Pharmacol 1990
PMID:Role of endothelium-formed nitric oxide on vascular responses. 227 79

1. Vascular endothelium releases different substances (endothelium-derived contractile factors, EDCFs), which mediate vasoconstrictor responses induced by several agents. 2. Clear differences have been reported in endothelium-dependent contractions, which suggest at least three distinct EDCFs, named EDCF1, EDCF2 and EDCF3, respectively. 3. EDCF1 is a cyclooxygenase metabolite(s) of arachidonic acid. EDCF2 is a polypeptide released from cultured endothelial cells. It has been isolated and identified as a 21-amino acid peptide called endothelin, which is described as the most potent vasoconstrictor agent known to date. EDCF3 is an unidentified contractile factor(s), which is neither EDCF1 nor EDCF2. 4. The physiological role of these endothelial contractile factors is not yet clear. However, they have been implicated in the local mechanisms involved in blood flow regulation, as well as in some pathological conditions, such as hypertension or cerebral vasospasm.
Gen Pharmacol 1990
PMID:Endothelium-derived contractile factors. 227 80

Young (7 weeks) spontaneously hypertensive rats (SHR) were kept on food-restriction (33%) during 4 weeks with (0.3% saline as drinking water) or without sodium supplementation. Body weight and indirect systolic blood pressure (tail plethysmography) were followed each weak. During the last week of the intervention period 24 hour excretions of sodium, dopamine and noradrenaline were measured. Vascular pressor responses to noradrenaline were evaluated in pithed rats and the sympathetic nerve activity was assessed from the disappearance of endogenous noradrenaline in the heart after synthesis inhibition. Despite a clear retardation of the growth rate in food-restricted rats the development of hypertension was not influenced. Food-restriction was associated with a moderate suppression of sympathetic activity. Furthermore, the vascular pressor responses to noradrenaline were decreased but this was reversed following sodium supplementation. It is concluded that despite evidence of sympathetic suppression weight reduction does not reduce the blood pressure in SHR once the blood pressure has started to rise.
J Neural Transm Gen Sect 1990
PMID:Blood pressure and sympathetic activity in spontaneously hypertensive rats during food restriction. 229 2

1. Effects of treatment with piretanide (10 and 30 mg/kg per day p.o.) for 9 weeks on blood pressure, urinary excretion of electrolytes, and vascular reactivities to pressor substances were investigated in 10-week-old spontaneously hypertensive (SHR) rats. 2. Piretanide (30 mg/kg) prevented development of hypertension and produced a significant reduction in blood pressure from the 2nd week of the treatment. A slight decrease in blood pressure was observed in rats treated with the lower dose of piretanide. 3. Piretanide produced significant and dose-dependent diuresis throughout the experiment. Although significant natriuresis was observed in the 1st and 4th week of the treatment, natriuresis disappeared in the 8th week. Urinary excretion of potassium was decreased significantly by piretanide throughout the experiment. 4. Attenuation of pressor responses to phenylephrine and angiotensin II was observed after chronic administration of piretanide (30 mg/kg). 5. These data demonstrate the contribution of attenuated vascular reactivities to pressor substances as well as a diuretic action to the antihypertensive effect of piretanide during its long-term administration in SHR rats.
Gen Pharmacol 1989
PMID:Reduction in blood pressure and vascular reactivities to pressor substances by chronic treatment with piretanide in spontaneously hypertensive rats. 265 50

To determine the importance of individual factors to thromboembolic stroke (TES) risk, the authors performed a hospital-based case-control study. Ninety cases (56 men and 34 women, ages 15 to 65) discharged from the hospital between January 1981 and December 1984 with a diagnosis of TES supported by computed tomography were matched to 174 control patients (106 men and 68 women). Data on potential risk factors were obtained from the medical record and telephone interview. Using multivariate analysis, three variables were significantly associated with TES risk: hypertension (odds ratio [OR] = 3.4; 95% confidence interval [CI] 1.9-6.0), diabetes (OR = 4.0; 95% CI 2.0-8.3), and smoking (OR = 2.0; 95% CI 1.2-3.6). The data were also analyzed using a direct risk assessment method. This analysis describes the risk in patients with any one factor compared with patients without any of the factors. The direct estimates of risk increased by 71% for hypertension (OR = 5.8), 28% for diabetes (OR = 5.1), and 90% for smoking (OR = 3.8). The authors conclude that hypertension, diabetes, and smoking are the major risk factors for TES in patients 65 years old or younger.
J Gen Intern Med
PMID:The contributions of individual factors to thromboembolic stroke. 272 32

This study was designed to determine the clinical characteristics of hypertensive patients whose blood pressures are substantially higher in the medical office than in their natural environments. Thirty-nine percent of patients enrolled in a nonpharmacologic hypertension treatment program had systolic or diastolic office blood pressures (OBPs) that were at least 10 mm Hg higher than their ambulatory blood pressures (ABPs). Although these white-coat responders (WCRs) had higher systolic OBPs than did non-white-coat responders (NRs), both their systolic (p less than 0.02) and their diastolic (p less than 0.0001) ABPs were significantly lower than those of NRs. Furthermore, patients with white-coat hypertension did not have greater blood pressure reactivity in their natural environments, suggesting that their blood pressure elevations may be specific to the medical setting. White-coat hypertensives were older (p less than 0.005), had less angry dispositions (p less than 0.01), and reported less overt anger expression (p less than 0.005). They were also taking more antihypertensive medications than were the other patients in the study (p less than 0.001).
J Gen Intern Med
PMID:The white-coat hypertension response: prevalence and predictors. 278 60

The authors estimated the sex- and age-adjusted prevalence of affective, substance use, and anxiety disorders in persons in a general population sample who identified themselves as having arthritis, diabetes, heart disease, high blood pressure, chronic lung disease, or no chronic medical conditions. Persons who reported ever having arthritis, heart disease, chronic lung disease, or high blood pressure had a significantly increased adjusted prevalence of each of the three groups of lifetime psychiatric disorders, relative to a no-chronic conditions comparison group (each p less than 0.05). Persons who ever had diabetes had an increased adjusted prevalence of lifetime affective and anxiety but not substance use disorder. Persons with current (i.e., active) arthritis, heart disease, or high blood pressure had a significantly increased adjusted prevalence of recent (6-month) anxiety disorder, whereas those with current chronic lung disease had an increased adjusted prevalence of recent affective and substance use but not anxiety disorder.
Gen Hosp Psychiatry 1989 Sep
PMID:Affective, substance use, and anxiety disorders in persons with arthritis, diabetes, heart disease, high blood pressure, or chronic lung conditions. 279 44

1. Dopamine (DA) binding sites in the left and right ventricle of hypertensive rats were assessed after two weeks of induction of hypertension by left renal artery occlusion. 2. The ratio of left ventricular (LV) weight to total body weight was significantly increased in hypertensive rats from 2.046 +/- 0.120 mg g-1 to 3.125 +/- 0.090 mg g-1 (P less than 0.01) while no significant difference was noted in the right ventricle (RV). 3. The hypertrophied LV was associated with a 78% increase in its protein content, however, the ratio of protein content to ventricular wet weight was not significantly different from controls. No change in RV protein content and concentration was observed. 4. Dopamine affinity of sarcolemmal protein was not significantly different in control and experimental LV and RV and the ratio of DA affinity in LV:RV was 10:1. 5. Saturation of LV with DA was reached at around 7 min whereas RV was saturated at approximately 15 min.
Gen Pharmacol 1987
PMID:Dopamine receptors in the hypertrophied rat heart. 295 87


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