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

Approximately 1% of pregnancies are complicated by essential hypertension. During pregnancy the blood pressure often stabilizes or improves. In patients with sustained hypertension, prospective controlled studies have demonstrated enhanced fetal survival when the blood pressure was controlled with antihypertensive medication. Such medication must be chosen carefully to avoid fetal and mateerial toxicity, and diuretics and salt restriction during pregnancy should be avoided. Among patients with essential hypertension the problem accelerates late in pregnancy in 2% to 11%; the acceleration may be predicted by determination of maternal mean arterial pressures and intravascular volumes early in pregnancy. The treatment of accelerated hypertension is identical to that of severe pre-eclampsia. Fetal loss is considerable but can be lessened by careful fetal and maternal monitoring and early controlled delivery. The risks of pregnancy in most patients with essential hypertension are small, and essential hypertension is not a uniform contraindication to pregnancy.
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PMID:Essential hypertension and pregnancy. 34 89

Evidence is presented demonstrating the role of prostaglandins in salt metabolism and on peripheral vasodilation. A number of animal studies and observations in human hypertensive subjects suggest that the prostaglandin system plays a role in the pathogenesis of hypertension. The most striking and consistent finding over many decades of investigation is the relationship between dietary salt intake and the development of hypertension. Only a small percentage of any population develops hypertension. It is suggested that those people whose kidneys have an abnormal salt-handling capacity develop hypertension when challenged by a chronic high-salt intake. The salutary effects of diuretics or low-salt diet support this concept. Hypertension then is an expression of a renal abnormality. Prostaglandins, one of the renal salt regulating factors of the kidney, amy be involved in this abnormality. Whether there is a defect in the matabolic pathways or an unresponsiveness to normal stimuli of prostaglandins has not been determined. The use of prostaglandins in the treatment of hypertension is being explored. The demonstration that PGA1 can effectively lower blood pressure and reverse hypertensive emergencies indicates that prostaglandins probably have a broader, still unidentified role in the overall management of essential hypertension.
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PMID:Prostaglandins and hypertension. 35 95

Many nonpharmacologic (behavioral) techniques are being proposed for the therapy of essential hypertension. The research in this area is reviewed and divided roughly into two categories: the biofeedback and relaxation methodologies. While feedback can be used to lower pressures during laboratory training sessions, studies designed to alter basal blood pressure levels with biofeedback have not yet been reported. The absence of evidence for such changes through biofeedback limits the usefulness of this technique in hypertension control. The various relaxation methods, such as yoga, transcendental meditation, progressive muscle relaxation, and others have shown more promise. With varying degrees of experimental vigor, many of these techniques have been associated with long-lasting changes in blood pressure. The strengths and weaknesses of the various authors' research designs, data and conclusions are discussed, and suggestions for further experimentation are offered.
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PMID:Nonpharmacologic control of essential hypertension in man: a critical review of the experimental literature. 35 79

The subject of sodium toxicity has been controversial for a long time. There is no question that the element can be noxious when consumed acutely in large quantities and there is little doubt as to cause and effect Conversely the consequences of mederate chronic sodium consumption are much harder to document. The effects are insidious and are subject to modification by a variety of environmental influences such as dietary potassium. In addition most studies of chronic sodium excess have dealt with elusive subject of "essential" hypertension. Interpretations of data have been very difficult, and conflicting reports have occurred. Nevertheless epidemiological, clinical, and animal studies show that chronic excess sodium ingestion acting upon a substrate of genetic susceptibility, is an important etiologic factor in essential hypertension and the expression of its sequelae. Positive correlations have also have been obtained between dietary salt and the incidence of stroke and gastric cancer. Dietary potassium appears to confer some degree of protection from the toxic properties of sodium through some unknown mechanism. Available evidence indicates that a suitable intake of salt for man might be approximately 3.5 g/day and probably less. Salt consumption in most developed countries ranges between 8 to 40 g/day, and modern methods of food processing and preparation deplete the protective potassium. The incidences of hypertension in these countries range between 15 to 40% of their populations, and it exacts a dreadful toll. Recognition of the toxic properties of sodium and knowledge of the mechanisms involved in its toxicity offer great possibilities in the area of preventive medicine It may be possible by the sorting out of hypertension-prone subjects and dietary intervention to prevent or minimize the development of hypertension in susceptible individuals. This says nothing of other aspects of sodium toxicity, of which we are largely ignorant.
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PMID:The toxicity of salt. 35 85

The antihypertensive effect of atenolol, a new beta 1 receptor blocking agent, was studied in a double blind non cross-over trial in 40 patients (pts) affected by mild to moderately severe essential hypertension with normal plasma renin activity. After a run-in period (15 days) of placebo treatment pts were assigned to two groups. The first (group A) continued placebo treatment for 30 days, the second (Group B) were given atenolol (ICI 66082) 100 mg daily for 30 days also. Atenolol significantly reduced systolic and diastolic blood pressure in recumbent and standing position and heart rate at rest. No significantly changes of the same parameters were observed in group A. Body weight and plasma renin activity was unchanged in both groups. Atenolol treatment never was discharged in order to side effects. These results seem to suggest that atenolol can be an useful drug in the treatment of systemic blood hypertension.
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PMID:[Efficacy and tolerability of a cardioselective beta-blocking drug (atenolol) in the treatment of essential hypertension. A double blind study (author's transl)]. 35 98

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

With advancing age blood pressure rises in most populations with the exception of some isolated tribes. In western countries 30 to 40% of the people above the age of 60 years have casual blood pressure levels greater than or equal to 160/95 mm Hg. Advancing age per se produces a number of physiological changes related to blood pressure, such as a decrease in cardiac output, an increase in peripheral vascular resistance and a decrease in plasma renin-angiotensin-aldosterone levels. The mechanism causing the elevation in pressure with age are unknown though increased rigidity of the great vessels contributes to the rise in systolic pressure. There is a decline in the sensitivity of the baroreceptor reflex, but the contribution of this to the elevation of pressure has not be elucidated. Elderly patients with uncomplicated essential hypertension have a low cardiac output and high peripheral vascular resistance. The rise in blood pressure is associated with an increased cardiovascular morbidity and mortality even in the elderly hypertensives. The available data on the efficacy of hypotensive treatment in the elderly is scanty. There are no data proving that hypotensive therapy prolongs life. Controlled studies on the prevention of organ damage especially cerebrovascular accidents are inconclusive, showing either a significant decrease or no effect. Isolated reports illustrate, however, that drastic blood pressure reduction can provoke serious side effects, thus decreasing the quality of life. Hypotensive treatment is indicated in elderly hypertensive patients with hypertensive retinopathy grade III or IV, congestive heart failure or cerebral haemorrhage, in elderly patients with a markedly elevated diastolic blood pressure (greater than or equal to 120 mm Hg) and a trial of hypotensive therapy should be offered in milder forms of hypertension when it is accompanied by certain specific symptoms such as angina, headache and dyspnoe. The management of elderly hypertensive patients is more difficult than in the young. General measures are often not well accepted. The dose adjustment of the hypotensive agent is more critical and volume depletion or orthostatic hypotension are more likely to occur.
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PMID:Aging and the cardiovascular system. 37 49

Of the various hypertensive disorders in which mineralocorticoid hormones are involved mainly those are reviewed in which, apart from aldosterone, hyporeactivity of the adrenergic nervous system may play a permissive role. The simultaneous occurrence and extent of participation of these two factors in essential hypertension are being appreciated increasingly. Their share in the mosaic of hypertension may add to the accumulating knowledge of this disease entity. In exploring the underlying mechanisms of hypertension common regulatory pathways involving aldosterone and the adrenergic nervous system may lead to new aethiopathogenetic insights.
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PMID:An apraisal of the role of aldosterone and the sympathetic nervous system in essential hypertension. 38 Nov 38

The purpose of this double-blind study was to compare the effects on blood pressure of tienilic acid and hydrochlorothiazide in patients with essential hypertension. The biochemical effects of tienilic acid in relation to those of hydrochlorothiazide were also determined over a long-term period of therapy. Sixty-six outpatients with mild to moderate essential hypertension were treated for seven months with either 250 mg of tienilic acid or 50 mg of hydrochlorothiazide after a 3 week placebo period. When warranted, dosage was increased to a maximum of 500 mg of tienilic acid and 100 mg of hydrochlorothiazide daily. Results indicate that tienilic acid reduced blood pressure significantly and to the same extent as hydrochlorothiazide. No significant side effects were observed. The effects on potassium, blood urea nitrogen and creatinine were comparable in both groups. However, serum uric acid rose with hydrochlorothiazide but fell with tienilic acid. In view of this effect, tienilic acid may have certain advantages over thiazide therapy in the treatment of hypertension.
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PMID:Long-term usage of tienilic acid in essential hypertension. 38 97


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