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)

We have studied serum glycyl-prolyl-p-nitroanilidase (GPNAase) activity and its distribution in various parts of the body in patients with acute myocardial infarction, chronic ischemic heart disease, valvular heart disease with or without congestive heart failure and essential hypertension. Serum GPNAase activity in patients with acute myocardial infarction was significantly lower as long as 12 days after the onset as compared with normal controls. The serum enzyme activity in patients with congestive heart failure was also significantly lower than that of controls and there was a tendency of its gradual decrease with the progress of the disease. There was no significant difference between the activity in control group and that in age-matched patients with essential hypertension. There was no significant change of the activity in patients with chronic ischemic heart disease. The GPNAase activities in sera obtained from various parts of the body by cardiac catheterization were essentially similar.
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PMID:Glycyl-prolyl-p-nitroanilidase (GPNAase) activity in cardiovascular diseases. 47 Jan 43

The various aspects of the sexual life of 100 female patients aged 40-60 with acute myocardial infarction were compared with those of a control group of 100 female patients of the same age, hospitalized for other diseases. Sexual frigidity and dissatisfaction were found among 65% of the coronary patients as compared with 24% of the controls. The commonest cause for sexual dissatisfaction was premature ejaculation or impotence in the husband. The incidence of premarital sexual relations was greater among the frigid patients when compared with those who achieved orgasm. The coronary patients had an earlier menopausal age than the controls. The number of coronary patients who underwent artificial abortions in the past was lower than in the control group. All these findings were statistically significant at a level of P less than 0.05. No connection was found between extramarital relations and sexual frigidity. There was no relation found between sexual frigidity and diabetes, essential hypertension, marital status, pathological gynecological findings, or localization of the infarction. Until now, sexual frigidity and dissatisfaction appear to have been a neglected aspect in the female coronary patient.
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PMID:Sexual life and sexual frigidity among women developing acute myocardial infarction. 100 33

The effect of some clinical peculiarities of the disease upon the restoration of the patient's capacity for work was studied along with the factors increasing the risk of repeated disablement after resuming the professional functions. The discussion is based on the results obtained in an out-patient study of 285 males who have been employed before their myocardial infarction in administrative-managerial jobs. Three groups of factors characterizing the functional state of the cardiovascular-system in the pre-infraction, acute and post-infarction periods are distinguished. It was demonstrated that the functional state of the heart when the patients resumed their work was characterized by the degree of chronic coronary and cardiac insufficiency, the scope of every-day physical activity, and was one of the essential criteria for the evaluation of the degree of rehabilitation. The first group of factors (essential hypertension, chronic coronary insufficiency preceeding the development of myocardial infarction) and the second group (clinical and anatomical peculiarities of acute myocardial infarction) are of secondary importance in determining the degree of rehabilitation. At the same time, the functional background of the cardiovascular system teinted prior to the infarction and the depth of the infarction, as well as the reduced level of the heart's functional capacity before resuming the professional functions, belong to the factors that increase the risk of secondary disablement in persons who have resumed working after a sustained myocardial infarction.
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PMID:[Factors affecting restoration of work capacity after myocardial infarct]. 123 May 26

1. Endothelin, a novel vasoconstrictor 21-residue peptide isolated from the supernatant of cultured porcine endothelial cells, has been shown to be increased in plasma in a variety of cardiovascular disease states, including acute myocardial infarction, acute renal failure and essential hypertension. We determined the time course of plasma and pulmonary lymph endothelin-like immunoreactivity in relation to the progressive deterioration of cardiopulmonary function in an ovine septic shock model leading to multi-organ failure syndrome and death within 42 h of a continuous intravenous infusion of Escherichia coli endotoxin (40 ng min-1kg-1). 2. Plasma and pulmonary lymph endothelin-like immunoreactivity were measured by r.i.a. using a specific antiserum raised in rabbits against porcine endothelin-1. Endothelin-like immunoreactivity was further determined in lung tissue and the thoracic duct lymph of endotoxin-treated sheep by reversed-phase h.p.l.c. In control instrumented conscious sheep not infused with endotoxin, there were no significant changes in any of the measured cardiopulmonary and biochemical variables, with plasma and pulmonary lymph endothelin-like immunoreactivity remaining below the detection limit (less than 1 pg/tube) throughout the 72 h study period. 3. Conscious sheep receiving endotoxin showed a major hypotensive septic syndrome, including persistently decreased systemic blood pressure, systemic vascular resistance, stroke volume, left ventricular stroke work, associated with sustained pulmonary vasoconstriction and protein-rich pulmonary oedema (greater than five-fold increase in pulmonary lymph flow and protein clearance), and marked lactic acidosis, leading to the death of animals within 14-42 h despite institution of mechanical ventilation and adequate intravascular volume replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Time course of plasma and pulmonary lymph endothelin-like immunoreactivity during sustained endotoxaemia in chronically instrumented sheep. 165 37

To ascertain an involvement of vascular endothelial cells in cardiovascular disease, we have determined plasma levels of two endothelium-derived substances, endothelin (ET) and thrombomodulin (TM), in essential hypertension (EH) and ischemic heart disease. Plasma ET was determined by radioimmunoassay (RIA) after extraction. Plasma TM levels were determined by enzymunoimmunoassay. Plasma ET levels were significantly elevated in patients with EH involving target organ damage, vasospastic angina pectoris (VSA), and acute myocardial infarction (AMI), especially in those associated with cardiogenic shock. There was a weak but significant correlation between plasma ET levels and serum creatinine concentration in patients with EH. Plasma ET levels were elevated even before the coronary spasm in patients with VSA, whereas they did not show any further increase during the spasm. In contrast, plasma TM levels in patients with EH and VSA did not show a significant difference from that in normal subjects. These results suggest that ET plays an important role in the pathophysiology of EH and ischemic heart disease, and also that increases in plasma ET cannot be simply attributed to a leakage of the peptide from the injured endothelial cells.
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PMID:Plasma immunoreactive endothelin, but not thrombomodulin, is increased in patients with essential hypertension and ischemic heart disease. 172 16

To elucidate the pathophysiologic significance of the family of endothelin (ET) peptides, we have investigated plasma and urinary immunoreactive (ir-) ET levels and its molecular forms in normal and pathological conditions. Plasma and urine ET were extracted with an Amprep C2 column. The molecular form of ET was determined by a combination of radioimmunoassay and reverse-phase high-performance liquid chromatography. Although plasma ir-ET was composed mainly of big ET and endothelin-1 (ET-1) in normal subjects, that in acute myocardial infarction, chronic renal failure (CRF), essential hypertension, and vasospastic angina pectoris was characterized by an increase of high molecular ir-ET in addition to increases in big ET and ET-1. Urinary ir-ET in both normal subjects and patients with CRF was composed mainly of a high molecular form in addition to big ET and ET-1. These results suggest that the biosynthetic and/or degradation process of ET under pathological conditions appears to be different from that under normal conditions.
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PMID:Molecular form of immunoreactive endothelin in plasma and urine of normal subjects and patients with various disease states. 172 26

Careful consideration of all relevant scientific evidence and a critical assessment of data quality show that thiazide diuretics are not cardiotoxic. Of 12 reported trials only two recorded more coronary heart disease events in thiazide-treated patients than in controls. One of these two was a subgroup of a larger study (Heart Attack Prevention in Primary Hypertension, HAPPHY) which found no difference between thiazide-treated and beta-blocker-treated patients. The other, the Oslo study, was too small to allow valid conclusions. Results from a subgroup in the Multiple Risk Factor Intervention Trial (MRFIT) that appeared to supply evidence for thiazide-related cardiotoxicity are suspect when examined critically. Further evidence from 24- to 28-h ECG monitoring does not support the hypothesis that thiazide diuretics, either in the presence or absence of hypokalemia, increase the frequency or severity of ventricular arrhythmias. Reports of a thiazide-induced intracellular magnesium deficiency as a cause of ventricular arrhythmias have also not been confirmed; the development of arrhythmias in acute myocardial infarction appears to be due to an increase in catecholamine levels rather than hypokalemia. There appears to be little evidence to support the assumption that long-term use of thiazide diuretics aggravates or accelerates atherosclerosis of the coronary arteries; any fall in serum cholesterol appears to be transient. For the great majority of patients with uncomplicated hypertension, without a previous myocardial infarction, congestive heart failure, diabetes mellitus or gout, thiazide diuretics appear to be both safe and effective antihypertensive agents.
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PMID:The cardiotoxicity of thiazide diuretics: review of the evidence. 221 84

The authors examined 112 subjects free from cardiac disease, with essential hypertension and myocardial infarction. In all subjects a 12-lead ECG at rest was made as well as a polycardiographic and echocardiographic examination. The authors found that in the group of healthy subjects there is a direct significant linear correlation between the size of the systole of the left atrium and age. The size of the left atrium and the atrial filling fraction were significantly smaller in healthy subjects than in subjects with hypertension and myocardial infarction. The authors draw attention to the necessity to re-evaluate the accepted norm of left atrial size in patients with hypertension and myocardial infarction. The authors found that between the magnitude of the systole of the left atrium and the ejection fraction of the left ventricle a significant relationship of parabolic shape exists. The mentioned correlations suggest that with deterioration of left ventricular function the ratio of the left atrial systole increases up to a certain extent (40% of the ejection fraction); after this borderline is exceeded, the haemodynamic contribution of the left atrium declines again till it is insignificant. PTF-V1 on the ECG which is generally considered a sign of an enlarged atrium reflects in the group of patients with acute myocardial infarction above all the degree of reduction of systolic and diastolic left ventricular function and not changes in the size and function of the left atrium.
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PMID:[Noninvasive monitoring of the hemodynamic importance of the left atrium]. 232 79

The effects of serotonin and its pharmacological antagonists on the physical flow properties of the blood have been studied far less than their effects on blood vessels, although they may be equally important. Indirect evidence suggests that in pathological circumstances serotonin may locally increase whole blood viscosity, particularly at low shear rates, decrease red cell deformability and increase the adhesiveness of white cells. Although the viscosity of the plasma alone is not affected, the rheological effects of serotonin on blood cells is probably dependent on the presence of platelets. These mechanisms may have a systemic effect in some forms of hypertension as well as in situations of local ischaemia such as Raynaud's phenomenon, atherosclerotic pregangrene of the leg or acute myocardial infarction. Specific serotonergic-antagonists, administered either orally or intravenously, normalize the increased whole blood viscosity and decreased blood filterability found in essential hypertension, following myocardial infarction and in severe leg ischaemia. The effect on red cell deformability is usually greatest when the cells are resuspended in platelet rich plasma. Ketanserin given intravenously for seven days to patients with very severe leg ischaemia, significantly improves whole blood viscosity, increases red cell transit time and most dramatically decreases pore clogging. This last effect was at least partly due to a change in the physical properties, but not the number of the white cells. The reported beneficial clinical effects of such an antagonist in various forms of peripheral ischaemia and essential hypertension may well be due, at least partly, to the normalization of the rheological properties of the blood.
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PMID:Serotonin and the flow properties of blood. 241 54

The pharmacologic therapy of mild primary hypertension (diastolic blood pressure less than 105 mm Hg) has effectively reduced hypertensive arteriolar end organ disease such as cerebrovascular accidents, congestive heart failure, and nephropathy, but there has been no convincing evidence that coronary heart disease (CHD) or its complications, acute myocardial infarction or angina, have been reduced. The risks of therapy with certain antihypertensive drugs may outweigh their treatment benefits as it relates to CHD. The optimal treatment strategy should be to reduce all CHD risk factors, reverse the hemodynamic abnormalities present by lowering the systemic vascular resistance (SVR), preserving cardiac output (CO) and perfusion, and to select the best antihypertensive drug for concomitant medical diseases or problems while maintaining a good quality of life. Antihypertensive drugs that have favorable or neutral effects on CHD risk factors include alpha blockers, calcium channel blockers, central alpha agonists, and angiotensin-converting enzyme inhibitors. On the other hand, diuretics and beta blockers without intrinsic sympathomimetic activity have unfavorable effects on many CHD risk factors. Baseline and serial evaluation of the effects of these drugs on serum lipids, lipid subfractions, glucose, uric acid, electrolytes, exercise tolerance, left ventricular hypertrophy, blood pressure, SVR, CO, perfusion, concomitant diseases, and side effects is necessary to evaluate overall cardiovascular risk.
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PMID:New insights and new approaches for the treatment of essential hypertension: selection of therapy based on coronary heart disease risk factor analysis, hemodynamic profiles, quality of life, and subsets of hypertension. 238 95


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