Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Polyarteritis was diagnosed in three girls, 9 to 10 years old, by kidney and skin biopsies. They were treated with a combination of prednisone (1.5 to 2 mg/kg) and cyclophosphamide (2 mg/kg) for up to 12 months. The illness was severe in all three, complicated by hypertension, seizures, pulmonary infiltrates, renal failure, or hallucinations. All three patients are alive and well with no or minimal residual symptoms two to three years after therapy was discontinued. The treatment with corticosteroids or with a combination of steroids and immunosuppressive drugs seems to improve the prognosis of polyarteritis considerably.
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PMID:Polyarteritis in children. 0 83

The effect of timolol versus propranolol on hypertension, hemodynamics, and plasms renin activity was evaluated in 20 men. After two weeks of placebo, 11 men received timolol 30 to 60 mg daily, and nine men received propranolol, 240 to 480 mg daily, for five weeks in a double-blind randomized study. The 20 men then received placebo again for two weeks. Right heart catheterization was performed in all 20 patients after two weeks of the first placebo and after five weeks of timolol or propranolol. Equipotent doses of timolol and propranolol were equally effective in significantly lowering supine and upright systolic and diastolic blood pressure and heart rate recorded on an outpatient basis. Equipotent doses of timolol and propranolol caused similar hemodynamic effects including similar significant depression of cardiac index. Equipotent doses of timolol and propranolol caused similar marked depression of plasma renin activity. The hypotensive action of timolol and of propranolol was unrelated to their effect on plasma renin activity.
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PMID:Effect of timolol versus propranolol on hypertension and hemodynamics. 0 61

The haemodynamic effect pattern of beta-blockers in hypertension is discussed. The time curve of the antihypertensive effect differs from that of cardiac beta-blockade. The antihypertensive effect is characterized by a slower onset at the start of treatment and a more gradual disappearance when therapy is withdrawn. It appears that the crucial effect of beta-blockers in hypertension is a gradually developing reduction in total peripheral vascular resistance. The mechanism of this apparent vasodilator action is unknown. Various possible factors involved are mentioned. One is a reduced efficiency of transmitter release from the peripheral adrenergic neuron. Such an action may contribute to the antihypertensive effect, as judged by results of animal experiments described.
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PMID:Haemodynamic effects of beta-adrenorecptor blockers in hypertension. 0 45

At the Dunedin Hypertension Clinic beta-blockers are the drugs of choice for most hypertensive patients, usually in combination with diuretics (especially in older subjects) and often with other drugs in the more severe cases. All beta-blockers have an antihypertensive effect, regardless of other characteristics (e.g. cardio-selectivity, instrinsic sympathomimetic effect, or membrane activity). d-Propranolol has no significant effect on blood pressure. Beta-blockers do not prevent stress-induced (mental arithmetic) rises in blood pressure in hypertensive subjects through the level of blood pressure reached during stress tends to be lower because the base line is lower. Twice-daily dosage of beta-blockers is usually satisfactory.
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PMID:Experience with beta-adrenoreceptor blockers in hypertension. 0 49

Renal disease and hypertension is a continuing challenge to the nephrologist. At present there are few effective methods of dealing with the common renal diseases such as glomerulonephritis, but fortunately there is now a wide selection of potent antihypertensive agents. Drug resistant hypertension should be a rarity in clinical practice. Malignant hypertension remains a therapeutic emergency. If a patient with hypertension has renal functional impairment it is essential to lower the blood pressure to normal. In the presence of renal failure this should be done with caution so as to avoid a further deterioration in the glomerular filtration rate. However, if the blood pressure is controlled and especially if the renal failure is a result of hypertension alone, renal function may stabilise or even improve, often dramatically.
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PMID:The kidney and antihypertensive therapy. 0 53

Resistant hypertension can be defined in terms of lack of blood pressure response to hypotensive agents, but there may be a big difference between standing and lying blood pressure levels. In general target organ damage and papilloedema improve if the standing blood pressure is controlled; however, progression can occasionally be documented when only the supine blood pressure remains uncontrolled. Resistant hypertension was a frequent phenomenon when ganglion blocking agents and hydrallazine were the only effective hypotensive agents. With the advent of the thiazides, effective control of the blood pressure became the exception rather than the rule; however, it was not until the advent of adrenergic blocking agents that reduction of supine blood pressures was regularly achieved. The addition of hydrallazine or prazosin to a combination of a thiazide and beta-adrenoreceptor blocking agent produces a further significant fall in the blood pressure lying and standing. This combination will control the blood pressure in most patients, but a few remain refractory to maximum doses and will require treatment with oral diazoxide or minoxidil. Both these powerful vasodilators are very effective in resistant hypertension. Oral diazoxide permits excellent control and allows a 10-fold reduction in the doses of other agents. Minoxidil usually needs to be combined with moderate doses of beta-blocking agents to reduce the marked reflex tachycardia. Only a 50% reduction in other hypotensive agents was achieved in patients treated with minoxidil and two patients proved resistant to minoxidil, but subsequently responded to oral diazoxide.
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PMID:The treatment of resistant hypertension. 0 54

Adverse drug reactions (ADRs) can be broadly classified as either "a nuisance" or "life-threatening". Voluntary reporting systems gradually accumulate a quite impressive list of suspected ADRs with antihypertensive drugs as their use becomes widespread. Such data gives no clue to true or relative incidence. The absolute and comparative incidence of ADRs can only be determined fairly by a system of unbiased general data collection of ADRs from which the data for antihypertensive drugs is then selected. The Boston Collaborative Drug Surveillance Program provides such a source of information. Data from the Boston Program reveals that most of the listed ADRs with antihypertensive drugs occur very infrequently, that "nuisance" ADRs occur in 10 to 29% of patients in whom they are used, and that "life-threatening" ADRs occur in less than 1%. ADRs tend to discourage patient compliance with medication aims. In selecting specific antihypertensive therapy the clinician should be mindful not only of the severity of the hypertension to be treated, but also of the nature, type, and severity of potential ADRs, the personality and likely complicance of the patient, and the need for patient education regarding drug effects, possible unwanted effects, and what measures should be taken when ADRs occur.
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PMID:Adverse drug reactions during treatment of hypertension. 0 55

Mortality and cerebral glycolytic metabolism were studied after bilateral ligation of the common carotid artery in normotensive Wistar rats (NTR), and spontaneously hypertensive rats (SHR) derived from Wistar strain. In the first 24 hours after occlusion of carotid arteries, 72 per cent of 108 SHR died, whereas it was fatal in only 16 per cent of 43 NTR. In SHR, cerebral lactate and cerebral lactate/pyruvate ratio (L/P ratio) increased by 12.4 and 12.1 times the control, respectively at five to six hours after ligation, and remained raised even in rats surviving for two to three days thereafter. Changes in cerebral lactate and L/P ratio were minimal in NTR. Cerebral ATP decreased markedly at five to six hours after ligation in SHR studied. These results indicate that bilateral carotid artery ligation causes severe brain damage in SHR but not in NTR, suggesting hypertension per se to be operative for the development of cerebral ischaemia.
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PMID:Mortality and cerebral metabolism after bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats. 0 30

Plasma renin activity (PRA) was measured in 38 cases of aortitis syndrome. The values of resting peripheral vein blood PRA were 32.2 +/- 4.2 (SE) mmug/ml. These values were 3 times higher than those of normal subjects. Hypertension due to renal arterial stenosis was observed in 18 cases. Their resting PRA values were 41.2 +/- 6.0 mmug/ml, while in the remaining 20 patients without renovascular hypertension those values were 24.2 +/- 5.4 mmug/ml. The patients belonging to aortic arch type or extensive type had 2 times higher PRA values than those of abdominal type. The patients with stenosis or obstruction of common carotid arteries had significantly higher PRA values than the patients without these lesions. Hyperresponse of renin secretion to upright posture was also observed in the same patients with carotid artery stenosis. Abnormal renin release in Takayasu's arteritis disappeared after denervation of the carotid sinus nerve. The present study suggests that the unstable state of carotid sinus reflex is the main cause for the hypersecretion of renin.
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PMID:Elevated plasma renin activity in aortitis syndrome. 0 6

Cardiac output was measured by a pulse contour method in reno-vascular hypertensive rats, deoxycorticosterone (DOC) hypertensive rats and normotensive control Wistar rats in the conscious state. All rats were male in sex and 12-13 weeks of age (2-3 weeks after operation in the hypertensive rats). Cardiac output per body weight was not significantly different among the groups. Therefore, the hypertension in the experimentally hypertensive rats in the conscious state was ascribable to an increased total peripheral resistance. After anesthesia with pentobarbital and thoracotomy, the DOC rats were no longer hypertensive. However, in the renovascular hypertensive rats, the hypertensive state due to an increase in vascular resistance persisted after anesthesia, thoracotomy, and even ganglion blockade with hexamethonium bromide, indicating the importance of non-neural factors in the renovascular hypertension. Aortic compliance measured in vivo under anesthesia was smaller in either the renovascular or DOC hypertensive rats than in the control rats before and after ganglion blockade, which suggests a non-neural hardening of elastic vessels in the experimental hypertensions.
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PMID:Hemodynamics of experimentally hypertensive rats in conscious and anesthetized states. 0 8


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