Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a radioimmunoassay for atrial natriuretic peptide (ANP) we studied plasma concentrations of immunoreactive ANP in order to investigate the pathophysiological role of ANP in patients with various diseases. Plasma ANP levels were elevated in patients with congestive heart failure (394 +/- 260 pg/ml, n = 8) and chronic renal failure (219 +/- 86 pg/ml, n = 11). In patients undergoing hemodialysis plasma ANP levels were markedly high and decreased after hemodialysis from 433 +/- 166 pg/ml to 204 +/- 92 pg/ml (n = 11). ANP was removed from blood to dialysate (21 +/- 13 pg/ml of dialysate, n = 6, dialysate flow: 500 ml/min). Plasma ANP level was conversely correlated with creatinine clearance (r = -0.812, p less than 0.001) in patients with renal diseases (n = 29). In patients with atrial fibrillation, pace maker implantation, lung disease, chronic glomerulonephritis, nephrotic syndrome, essential hypertension, liver disease and cerebrovascular disease, plasma ANP levels were not significantly different from those in normal subjects (70 +/- 32 pg/ml, n = 28). These results suggest that ANP may be a circulating hormone playing pathophysiological roles in congestive heart failure and chronic renal failure.
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PMID:Plasma concentrations of atrial natriuretic peptide in various diseases. 294 55

The effects of oxprenolol on blood pressure levels, pulmonary ventilatory function, myocardial contractility and myocardial oxygen consumption are described in 66 patients with essential hypertension and no clinical evidence of obstructive lung disease of heart failure. Two groups of patients were treated with medication for a total of 16 weeks. Group 1 received oxprenolol and diuretics for the first eight weeks and a placebo plus diuretics for the second eight weeks. Group 2 received the same drugs in reverse order. The results of the study indicate that oxprenolol is an effective antihypertensive drug that does not hamper lung volume capacity or myocardial contractility and markedly reduces myocardial oxygen consumption, although it may cause a mild increase in airway resistance.
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PMID:Effect of oxprenolol on blood pressure, pulmonary ventilatory function and myocardial contractility in hypertensive patients. 739 73

We hypothesized that ozone (O3) exposure acutely affects cardiovascular hemodynamics in humans and, in particular, in subjects with essential hypertension. We studied 10 nonmedicated hypertensive and six healthy male adults. Each subject, after catheterization of the right heart and a radial artery, was exposed in an environmentally controlled chamber to filtered air (FA) on one day and to 0.3 ppm O3 on the following day for 3 h with intermittent exercise. Relative to FA exposure, O3 exposure induced no statistically significant changes in cardiac index, ventricular performance, pulmonary artery pressure, pulmonary and systemic vascular resistances, ECG, serum cardiac enzymes, plasma catecholamines and atrial natriuretic factor, and SaO2. The overall results did not indicate major acute cardiovascular effects of O3 in either the hypertensive or the control subjects. However, mean preexposure to postexposure changes were significantly (p < 0.02) larger with O3 than with FA for rate-pressure product (1,353 beats/min/mm Hg) and for heart rate (8 beats/min); these responses were not significantly different between the hypertensive and the control subjects. Significant O3 effects were also observed for mean FEV1 (-6%), and AaPO2 (> 10 mm Hg increase), which were not significantly different between the two groups. These results suggest that O3 exposure can increase myocardial work and impair pulmonary gas exchange to a degree that might be clinically important in persons with significant preexisting cardiovascular impairment, with or without concomitant lung disease.
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PMID:Cardiovascular effects of ozone exposure in human volunteers. 970 Jan 33

Incidence, determinants, and outcome of atrial fibrillation in hypertensive subjects are incompletely known. We followed for up to 16 years 2482 initially untreated subjects with essential hypertension. At entry, all subjects were in sinus rhythm. Subjects with valvular heart disease, coronary artery disease, preexcitation syndrome, thyroid disorders, or lung disease were excluded. During follow-up, a first episode of atrial fibrillation occurred in 61 subjects at a rate of 0.46 per 100 person-years. At entry, subjects with future atrial fibrillation differed (all P<0.05) from those without by age (59 versus 51 years), office, and 24-hour systolic blood pressure (165 and 144 versus 157 and 137 mm Hg, respectively), left ventricular mass (58 versus 49 g/height[m](2.7)), and left atrial diameter (3.89 versus 3.56 cm). Age and left ventricular mass (both P<0.001) were the sole independent predictors of atrial fibrillation. For every 1 standard deviation increase in left ventricular mass, the risk of atrial fibrillation was increased 1.20 times (95% CI, 1.07 to 1.34). Atrial fibrillation became chronic in 33% of subjects. Age, left ventricular mass, and left atrial diameter (all P<0.01) were independent predictors of chronic atrial fibrillation. Ischemic stroke occurred at a rate of 2.7% and 4.6% per year, respectively, among subjects with paroxysmal and chronic atrial fibrillation. These data indicate that in hypertensive subjects with sinus rhythm and no other major predisposing conditions, risk of atrial fibrillation increases with age and left ventricular mass. Increased left atrial size predisposes to chronicization of atrial fibrillation.
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PMID:Atrial fibrillation in hypertension: predictors and outcome. 1257 85

We report the case of a 56 year-old Gabonese man under treatment by candesartan-hydrochlorothiazide for essential hypertension. After 2 months of treatment, he presented with pneumonia and severe respiratory failure. The chest radiography showed centrilobular nodules resembling tumor metastases, but no evidence of a primary tumor. Laboratory and imaging found no evidence of infectious or autoimmune disease. The computed tomography findings led to a diagnosis of diffuse alveolitis. The candesartan treatment was stopped and oral corticosteroid therapy (50 mg/day) initiated. The rapid favorable outcome supports the diagnosis of a drug-induced infiltrative lung disease.
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PMID:[Centrilobular nodules with ground-glass opacities in the lungs]. 2289 Jan 34