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

beta-receptor antagonists have for many years been considered appropriate alternatives in the primary management of mild to moderate hypertension. Generally, they have been shown to be safe with a low frequency of serious side-effects. Among the predictable and usually doserelated side-effects are bradycardia, bronchospasm, hypotension, muscle fatigue and cold extremities. Examples of unexpected side-effects are gastrointestinal symptoms such as nausea and disturbed intestinal motility, skin reactions, sexual dysfunction, as well as effects related to the central nervous system (CNS) such as emotional disturbances. The CNS-related side-effects, the mechanisms of which are unclear, consist of subtle effects on general well-being, decreased initiative, a depressed frame of mind and disturbed sleep. Generally, however, beta-blockers in therapeutic dosages do not affect the qualitative functions of the brain. Thus, all beta-blockers on the market seem to have high benefit-risk ratio, but independent of their physiochemical properties and pharmacodynamic profile, they seem to cause side-effects to about the same extent. The results so far available have been obtained by primarily using objective methods. Further comparison has now been initiated using documented subjective methods to investigate whether the objectively documented differences are of any clinical relevance to the patient's quality of life. Although it cannot be claimed with certainty, nonselective beta-blockers seem to cause CNS-related side-effects to a greater extent than beta 1-selective blockers. Differences in the degree of hydrophilicity of the beta-blocker are apparently of no clinical relevance in this respect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quality of life/subjective symptoms during beta-blocker treatment. 198 27

The purpose of this study was to determine if the state of physical training influences sympathetic neural activation during acute stress in humans. We recorded muscle sympathetic nerve activity (microneurography of the peroneal nerve), arterial blood pressure, and heart rate in 12 highly trained, endurance athletes (25 +/- 1 years, mean +/- SEM) and 12 untrained subjects (27 +/- 1 years) before (supine rest control) and during: 1) lower body negative pressure at -5, -10, -15, and -20 mm Hg (orthostatic stress); 2) isometric handgrip at 30% of maximum (exercise stress); and 3) hand immersion in ice water, that is, the cold pressor test (thermal stress). Body weight was not different in the two groups, but the athletes had a lower body fat content (8.9 +/- 1.3% versus 16.1 +/- 2.0%, p less than 0.05). During supine rest, muscle sympathetic nerve burst frequency (24 +/- 3 versus 24 +/- 2 bursts/min, athletes versus untrained subjects) and burst incidence (36 +/- 3 versus 44 +/- 4 bursts/100 heart beats) and arterial blood pressure were not different in the two groups, but heart rate was lower in the athletes (54 +/- 2 versus 67 +/- 3 beats/min, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jan
PMID:Sympathetic neural adjustments to stress in physically trained and untrained humans. 198 81

To assess the possibility that the renin-angiotensin system may play a role in the development of cold-induced hypertension, three groups of rats were used. Two groups were exposed to cold (5 +/- 2 degrees C) while the remaining group was kept at 26 +/- 2 degrees C. One group of cold-treated rats received food into which captopril (0.06% by weight) had been thoroughly mixed. The remaining two groups received the same food but without captopril. Systolic blood pressure of the untreated, cold-exposed group increased significantly above that of the warm-adapted, control group within 4 weeks of exposure to cold. In contrast, chronic treatment with captopril prevented the elevation of blood pressure. Rats were killed after 4 months of exposure to cold. At death, the heart, kidneys, adrenal glands, and interscapular brown fat pad were removed and weighed. Although captopril prevented the elevation of blood pressure in cold-treated rats, it did not prevent hypertrophy of the kidneys, heart, and interstitial brown adipose tissue that characteristically accompanies exposure to cold. Thus, chronic treatment with captopril prevented the elevation of blood pressure when administered at the time exposure to cold was initiated. It also reduced the elevated blood pressure of cold-treated rats when administered after blood pressure became elevated. This suggests that the renin-angiotensin system may play a role in the elevation of blood pressure during exposure to cold.
Hypertension 1991 Jun
PMID:Prevention of cold-induced increase in blood pressure of rats by captopril. 204 37

Paraplegia is a fearful and not uncommon complication of aortic clamping in surgical procedures involving thoracic and abdominal aorta. We report a case of transient spinal cord ischemia during the early postoperative period of aortobifemoral bypass in a 69-year-old male with arteriosclerosis obliterans, hypertension, type II diabetes mellitus and COLD. The anesthetic procedure was combined (peridural + intubation and mechanical ventilation + isofluorane). Two hypotensive episodes of about 80 mmHg developed, one after induction and another in the Reanimation area. The first one had a short duration, whereas the second one required the administration of colloids, crystalloids and blood. The infrarenal aortic clamping time was 35 minutes. In the early postoperative period the patient had clinical features consistent with spinal ischemia, which progressively recovered. To prevent spinal ischemia during surgery a shorter duration than 30 minutes of aortic clamping, a higher distal perfusion pressures higher than 60 mmHg during clamping, and the attempt to exclude the least possible number of intercostal and/or lumbar vessels are recommended. Drugs (corticosteroids, naloxone) and hypothermia can be useful.
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PMID:[Spinal cord ischemia in the postoperative period of aortic surgery]. 207 98

The present study was aimed at examining the effects of awareness of hypertension on blood pressure and sympathetic responses to the cold pressor test. Nineteen-year-old men with similarly elevated mean blood pressure at a medical screening, but without knowledge of this, were randomized into two groups. The first group (n = 16) was sent a letter saying that their pressure was too high, and the second (n = 13) was sent a neutral letter. Information increased mean blood pressure both after 15 min sitting, by an average of 11.5 mm Hg (P less than .01), and after 30 min supine rest, by an average of 4.5 mm Hg (P less than .05). Changes in heart rate (8.4 +/- 2.4 v 1.9 +/- 1.7 beats/min) and plasma epinephrine (0.11 +/- 0.04 v 0.01 +/- 0.03 nmol/L) during execution of a cold pressor test were significantly greater in the informed group (P less than .05). Plasma dopamine was lower in the informed group (P less than .05). Thus, psychological stress caused by the awareness of hypertension may increase blood pressure and sympathetic responses to a provocative maneuver. Ideally, studies on sympathetic function in essential hypertension should be undertaken on subjects unaware of their blood pressure status.
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PMID:Awareness of hypertension increases blood pressure and sympathetic responses to cold pressor test. 208 Oct 12

An ultrastructural study of adult mongrel dogs and cats was made to evaluate the changes in the microcirculation during cerebral oedema formation. Two to five cold injuries were made in one hemisphere in dogs and one lesion was made in cats. In several dogs arterial hypertension was induced with a balloon in the aorta. Intracranial pressure (ICP) and water content were measured. The specimens from the oedematous region were studied with transmission electron microscopy (TEM) and electron probe x-ray micro-analysis (EPMA). The TEM data showed swelling of the endothelium and astrocytic foot processes, enlarged perivascular spaces and increased number of endothelial vesicles. The EPMA findings indicated increases in Fe and Ca content in the perivascular spaces. In some cases, the amount of chloride in red cells was increased. The altered distributions of these metals suggested tissue injury and impairment of red cell and vessel wall functions.
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PMID:An electron microscopic and electron probe study of the microcirculation in cold-induced oedema. 208 61

The aim of this study was to verify the possible role of serotonin on vascular basal tone and over-reactivity in systemic and pulmonary circuits in hypertensive patients. We studied 15 hypertensive (G1) and 10 normotensive (G2) subjects. Right-side pressure and intravascular-arterial pressure measurements were obtained in baseline conditions and during alpha-adrenergic activation by cold-pressor-test (CPT), before and after intravenous injection of ketanserin 10 mg (K), an S2-receptor antagonist. Systemic and pulmonary pressures and resistances were higher in G1 than in G2 in the steady state. K induced a significant reduction of both pressures and resistances in G1, no change in systemic response to CPT in the 2 groups and a significant reduction in the pulmonary vascular reactivity to adrenergic stimulus only in G1. These data confirm the vasodilator action of serotonin-blockade. The observation of vasodilatation in pulmonary circulation is not in favor of its dependence on vascular endothelium damage. In fact the arterial endothelium lesions due to hypertension are present only in the systemic circuit. Concerning result of CPT: 1) serotonin doesn't seem responsible for vascular over-reactivity in hypertension, unchanged by K; 2) the particular pattern of pulmonary vascular contractility in G1 may be interpreted as resulting from an elective depressive action of S2-blockade, depending on a different distribution of S1 and S2 receptors in the two circuits.
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PMID:[Effects of serotoninergic block on reactivity of systemic and pulmonary circulation in hypertensive patients]. 210 31

CBF and ICP were measured in cats following cerebral cold injury and mannitol infusion. Mannitol was found to reduce the intracranial hypertension caused by the injury. The restoration of CBF and ICP was of short duration and was followed by a reduction of CBF and elevation of ICP. A repeated restoration of CBF by a second dose of mannitol was followed by a more severe impairment of CBF. The prolonged beneficial effect of mannitol on CBF after brain injury has to be reassessed.
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PMID:Transient effect on mannitol on cerebral blood flow following brain injury. 212 73

In feral populations of African green monkeys or vervets (Cercopithecus aethiops), between 5 and 15% of adults have spontaneously elevated blood pressure (BP). We report here the initial biological and pharmacological characterization of this potential animal model of hypertension. Captive male monkeys with elevated systolic pressures show a modest pressure increase in response to stressors such as capture, phlebotomy and cold challenge. Acute captopril administration lowers BP in monkeys with high blood pressure (HBP), but has no effect on BP in control animals. Furosemide does not acutely reduce BP. Animals with elevated BPs have lower levels of angiotensin II than do age- and weight-matched controls. An acute infusion of atrial natriuretic factor (ANF) diminishes BP and stimulates urinary output in control and HBP vervets. However, both effects are more pronounced in animals with HBP. Heart rate is not affected by any of the experimental manipulations. Taken together, these data suggest that African green monkeys with spontaneously elevated BP may be a useful experimental model for particular types of human hypertension. Additional studies are required to complete the endocrine and pharmacological characterization of individual animals with HBP.
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PMID:Characterization of a primate model of hypertension. The response of hypertensive and normotensive male vervets (Cercopithecus aethiops) to cold pressor stress, captopril administration, and acute bolus of atrial natriuretic factor. 213 42

The present study aimed at testing the hypothesis of a link between mental stress and blood platelet function. Twenty-nine 19-year-old men were recruited from the 98th percentile of mean blood pressure (116 mmHg) at a routine medical screening. They were not informed about their elevated blood pressures at the time of the screening. One year later they were randomized into two groups. Group 1 (n = 16) was exposed to mental stress by a letter informing them about their high blood pressure, while group 2 (n = 13) was sent a neutral letter. At an examination 2 weeks later, heart rate (p less than 0.05) and plasma adrenaline (p less than 0.05) responses to a cold pressor test were exaggerated in the informed group. The plasma beta-thromboglobulin (beta TG) concentration was elevated in the informed group (p less than 0.05) as was mean blood pressure (p less than 0.05). beta TG correlated positively with hematocrit (r = 0.59, p less than 0.005) and mean blood pressure (r = 0.43, p less than 0.05), and negatively with plasma HDL (r = -0.61, p = 0.001). The study shows that awareness of hypertension induces a hyperadrenergic state which is associated with the platelet release reaction. Under these circumstances platelet release seems to be correlated to established coronary heart disease risk factors.
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PMID:Awareness of high blood pressure stimulates platelet release reaction. 214 19


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