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

The failure of clinical trials in the treatment of hypertension to show protection against mortality from coronary heart disease has prompted a major reconsideration of the indications and modes of therapy. One area of concern is the lipid disturbances seen with diuretics and non-ISA (intrinsic sympathomimetic activity) beta blockers; another is the negative inotropic effect of beta blockers. The more widespread use of vasodilators--either alpha-blockers, angiotensin-converting enzyme (ACE) inhibitors, or calcium channel blockers--therefore seems appropriate. Among the calcium channel blockers, nicardipine appears to be a particularly attractive choice, in part because of its lack of negative inotropism.
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PMID:Effects of antihypertensive therapy on cardiac function. 296 86

Nuclear medical techniques (such as isotope nephrograms, renal scintigrams) which are suitable as screening methods, have been unable to improve the diagnosis of reno-vascular hypertension. Amongst conventional procedures, the excretion urogram following a bolus injection was the most informative, particularly if performed together with nephro-tomography. Although ultrasound is of some use in evaluating the kidneys, the excretion urogram remains essential for the diagnosis of reno-vascular hypertension. Additional exposures and modifications (e.g. early phase urogram only add unnecessary radiation and cost without providing additional information. On the other hand, it would be useful to obtain digital subtraction angiograms of the renal arteries during the contrast injection. In this way, reliable information can be obtained on the cause of reno-vascular hypertension in more than 90% of patients. Similar results can be obtained by photographic subtraction (ISA). This should be used where DSA apparatus is not available. Angio-CT and sequential CT is not reliable for the diagnosis of renal artery stenosis. On the other hand, these methods provide density measurements or time-density curves of selected areas in the cortex or medulla of the kidney, which indicated abnormalities of the circulation and provide a comparison of the two sides.
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PMID:[Digital subtraction angiography and other non-invasive procedures for evaluating renal circulation and hypertension]. 301 72

1. Elucidation of some of the mechanisms responsible for blood pressure elevation in pregnancy has permitted therapy to be based on more rational principles. The decreased arterial reactivity encountered in normotensive pregnancy is most likely mediated by prostaglandins; preventive therapy using low dose aspirin is an option to prevent development of proteinuria in pre-existing hypertension and provide prophylaxis against pregnancy-induced hypertension. 2. Antihypertensive therapy utilizing sympathetic inhibition with either methyldopa or alpha- and beta-adrenoceptor blockade yields the most promising results. Vasodilation with hydralazine, calcium entry blockers (nifedipine), intravenous labetalol or diazoxide is primarily used in severely hypertensive patients. The use of orally administered nifedipine in severely hypertensive women is associated with encouraging results. 3. It is clear that women with blood pressure levels greater than 170/110 mm Hg need antihypertensive therapy for maternal safety; it remains to be proven to what extent foetal growth and welfare can be improved in women with diastolic pressure levels 85-110 mm Hg when adrenoceptor blocking agents are used for blood pressure control. Initial studies are suggestive of improved foetal growth, prevention of proteinuria and the respiratory distress syndrome but more long-term controlled studies are required. 4. In a recent study, at our institution, of foetal growth during long term antihypertensive therapy, treatment with pindolol yielded better foetal growth than therapy with atenolol. It is as yet unclear whether the ISA or beta 2-mediated vasodilation associated with pindolol was responsible for the improved foetal growth. Further controlled studies are indicated in hypertension in pregnancy to confirm the suggested benefits of beta-adrenoceptor blocker therapy.
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PMID:Hypertension in pregnancy: whom and how to treat. 332 31

The effects of acebutolol (with intrinsic sympathomimetic activity (ISA] and metoprolol (without ISA) on arm blood pressure, ankle systolic blood pressure, claudication distances (CD) and maximal walking distances (MWD) were compared in patients with essential hypertension and intermittent claudication. Fourteen patients participated in a long-term, open, randomized cross-over study. After randomization the patients received either acebutolol, 200 mg b.i.d., or metoprolol, 100 mg b.i.d. After eight weeks the drugs were shifted and after another eight weeks they were withdrawn. Arm and ankle blood pressure, CD and MWD were determined before randomization and after 4, 8, 12 and 16 weeks, and again 4-6 weeks after withdrawal of the drugs. The arm blood pressure was reduced by 20/13 mmHg after acebutolol and by 22/21 mmHg after metoprolol. In spite of a significant decrease in arm blood pressure there were no significant changes in ankle blood pressure, CD or MWD after the two drugs. After withdrawal of the drugs and after the arm blood pressure had returned to the control value no significant changes were seen in CD, MWD or ankle blood pressure. It is concluded that beta-blockers have no deleterious effect on CD, MWD or ankle blood pressure in patients with hypertension and intermittent claudication. No effect of ISA was demonstrated.
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PMID:The effects of acebutolol and metoprolol on walking distances and distal blood pressure in hypertensive patients with intermittent claudication. 351 64

Criteria for the diagnosis of exercise hypertension have not yet been established. Published values for blood pressure increase during dynamic exercise in normotensive healthy persons differ greatly dependent on age, sex, heart frequency and load of dynamic exercise. Upper normal systolic values during exercise reach levels between 200 and 230 mm Hg. The incidence of exercise hypertension is therefore reported to range from 1 to 10% of the total population. Follow-up studies show that 10 to 60% of persons with isolated exercise hypertension proceed to chronic arterial hypertension. No results are available on exercise hypertension as a risk factor in contrast to the well-known link between increased systolic and diastolic casual blood pressure and cardiovascular diseases. The development of left-ventricular hypertrophy depends mainly on the average systolic blood pressure during a 24-hour period. Peak values of systolic blood pressure during the day or blood pressure variability are less important. Drug treatment of isolated exercise hypertension is not generally accepted. Non-drug treatment is to be preferred, e.g. weight reduction in overweight, dietary sodium restriction and endurance training. Drug treatment must be considered, if non-drug treatment is unsuccessful and/or risk factors, for example hypercholesterolemia, diabetes, cigarette smoking, or complications of target organs, i.e. coronary heart disease or cerebral infarction, do exist. In antihypertensive treatment of increased exercise blood pressure, the influence of the drugs on the hemodynamic and metabolic parameters must be observed, especially in patients with concomitant coronary heart disease. Increases in blood pressure due to dynamic exercise are better attenuated by antihypertensive drugs than those caused by isometric exercise. The drugs of choice are beta-blockers, preferably beta 1-blockers without ISA. Alternatively, calcium antagonists of the verapamil-type or ACE-inhibitors may be used. In contrast to other antihypertensive drugs, labetalol, calcium antagonists and ACE-inhibitors have no influence on the exercise-induced increase of cardiac index and therefore little effect on the work capacity of the circulatory system.
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PMID:[Differential therapy of exercise hypertension]. 358 8

Beta-adrenoceptor blockade is responsible for the therapeutic action of beta-adrenoceptor-blocking drugs in the treatment of hypertension and angina pectoris. Many aspects of their effects can therefore be studied in relatively simple clinical pharmacologic experiments. Cardiac beta-adrenoceptor blockade can be measured in terms of the reduction of isoprenaline-induced and exercise-induced tachycardia. Based on these experimental procedures pindolol is, on a weight-for-weight basis, about 20 times more potent than propranolol. The duration of action of pindolol, measured by the reduction in exercise-induced tachycardia, is longer than that of many other beta-adrenoceptor-blocking drugs such as propranolol, alprenolol, and slow-release oxprenolol tested at equipotent beta-adrenoceptor-blocking doses. Pindolol is a beta-adrenoceptor-blocking drug with partial agonist activity (intrinsic sympathomimetic activity [ISA]). Drugs of this type are as effective in inhibiting beta-adrenoceptor stimulation as drugs devoid of this property, but unlike the latter they produce some stimulation of beta adrenoceptors. The ISA of pindolol is sufficient to counterbalance the diminution in resting sympathetic tone that results from beta-adrenoceptor blockade. In hemodynamic studies pindolol does not alter or only slightly reduces normal cardiac output. This is in contrast to drugs lacking ISA, which consistently depress cardiac output. In addition, propranolol has been shown to markedly reduce blood flow in the calf, whereas pindolol and placebo do not differ from one another in their effect on this parameter. A linear correlation exists between the logarithm of plasma concentrations of pindolol and cardiac beta-adrenoceptor blockade expressed as a reduction of exercise-induced tachycardia. The high systemic availability of pindolol after oral administration, due to good oral absorption and low first-pass effect, is revealed not only in pharmacokinetic studies but also in pharmacodynamic experiments; beta-adrenoceptor blockade 75 minutes after intravenous administration was equivalent to that observed 2 hours after the same doses given orally.
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PMID:Clinical pharmacology of pindolol. 612 94

1 The effect of a beta-adrenoceptor blocker without intrinsic sympathomimetic activity (propranolol) and a beta-adrenoceptor blocker with ISA (pindolol) on circadian heart rate was studied in 10 patients (3 women and 7 men) with an average age of 55 years and the following diagnoses: coronary heart disease (n = 7) and hypertension (n = 3). The therapy was carried out in a randomized, cross-over study, with 3 x 40 mg propranolol and 3 x 5 mg pindolol. 2 Propranolol lowered the averaged circadian heart rate significantly (P less than 0.001) from 78 to 68 beats/min. The rate decreased both during the day and at night and the reduction was greater the higher the control value. The minimal hourly heart rate also decreased significantly (P less than 0.005) from 65 to 69 beats/min. 3 After pindolol the averaged circadian heart rate was not markedly changed. It reached a stable rate of around 70 beats/min. At a heart rate of below 70 beats/min an increase in rate was observed, whereas above 70 beats/min a reduction was found. The mean heart rate during the day remained unchanged. There was a significant relationship between the level of the control heart rate and the decrease in rate (r = 0.85, P less than 0.005). 4 In a bicycle exercise test of 1 Watt/kg body weight over a period of 6 min, both beta-adrenoceptor blockers lowered blood pressure and heart rate to the same extent.
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PMID:The effect of intrinsic sympathomimetic activity of beta-adrenoceptor blockers on circadian heart rate. 612 72

The hypothesis of insulin resistance in the pathogenesis of arterial hypertension as part of the hormonal metabolic X syndrome and our 5H syndrome resp. (association of hyperinzulinism with hyperglycaemia-NIDDM-hyperlipoproteinaemia, hypertension and a hyperandrogenic state in women) is based on sympathomimetic, sodium retention and trophic effects of insulin. In the submitted paper the authors review opinions supporting and refuting the validity of this hypothesis. Based on the results of different studies in recent years another genetic predisposition comes also to the foreground, i.e. reduced vascularization of the skeletal muscles which on the background of insulin resistance leads to enhanced development of hypertension with subsequent hypertrophy of the vascular wall and left ventricle and to the development of arteriosclerosis. From the clinical aspect this stimulating pathogenetic concept within the framework of the hormonal and metabolic X syndrome and 5H syndrome makes it possible to use a more adequate approach to prevention and treatment not only of arterial hypertension but also of associated phenomena which enhance the risk of cardiovascular morbidity and mortality in the population. The authors summarize factors which during non-pharmacological treatment promote insulin resistance and those which improve it. When drugs are selected for pharmacological treatment, priority is given to those which improve the insulin sensitivity index (ACE-inhibitors, alpha blockers) or are at least neutral in this respect (Ca antagonists, beta blockers with ISA and cardioselective). The drugs must not enhance associated hyperlipoproteinaemia, hypercoagulability, hyperviscosity, hyperuricaemia) and they should exert a positive effect on the regression of hypertrophic vascular walls and the left ventricle.
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PMID:[Insulin resistance and arterial hypertension]. 772 34

This review addresses the vascular effects of beta-blockers in patients with normal peripheral circulation, with hypertension or with peripheral arterial disease. Despite conflicting data from many uncontrolled and relatively small studies some general conclusions can be drawn. In the absence of peripheral vascular disease there is no good evidence of any adverse effects of beta-blocker treatment on peripheral circulation. Nevertheless, it may be useful to change from non-selective to beta-1 selective beta-blockers or to beta-blockers with ISA when patients complain of cold extremities. In hypertensive patients, beta-blocker therapy may similarly cause cold extremities, especially with non-selective beta-blockade. Successful long-term antihypertensive treatment, as with beta-blockers, may restore normal vascular architecture. In patients suffering from peripheral arterial disease, beta-blockers are not generally contraindicated although they should be administered with extreme caution when disease is severe. In less severe forms of occlusive disease, beta-blockers have little effect on peripheral circulation and may even improve flow to the diseased area by an inverse steal effect.
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PMID:Peripheral vascular effects of beta-blockers. 799 66

beta-Blockers are known to protect a vulnerable aorta from acute dissection, as well as reducing the risk of recurrent dissection. This case presentation reports the history of a 60-year-old male suffering from acute aortic dissection following discontinuation of beta-blocker therapy. The patient has shown arterial hypertension for about 20 years treated solely by beta-blockers. Two days after stopping the use of metoprolol, a nonselective beta 1-blocker without ISA, the patient developed severe chest pain during exercise. Diagnosis of type I-aortic dissection according to DeBakey was achieved by transthoracal echocardiography and computed tomography. Successful surgery by replacement of the ascending aorta was performed about 1 h following admission to the intensive care unit. During the procedure, tamponade of the left ventricle occurred followed by cardiogenic shock. Postoperative management was complicated by prolonged respiratory therapy and acute gastrointestinal bleeding; 1-year follow-up showed no evidence of disease. Thus, in this case acute dissection may be the consequence of discontinuing the use of metoprolol, possibly due to uncontrolled hypertension or specific response to the beta-blocker.
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PMID:Aortic dissection due to discontinuation of beta-blocker therapy. 826 79


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