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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antihypertensive drugs have been of major benefit to people with moderate or severe hypertension and have contributed enormously to fundamental physiological knowledge. Antihypertensive therapy in milder hypertension reduces the incidence of stroke by 40% or more, may reduce myocardial infarction and prevents progression to more severe hypertension or heart failure but is being criticised as not cost-effective. Much of this criticism is based on deductions from inappropriate data. Nevertheless, it is likely that money is in some cases being wasted on the treatment of people who were not truly hypertensive in the first place. It is also likely that drug dosage is often unnecessarily high. Clearly it is vital that treatment is delivered as economically as possible. A reduction in the prevalence of hypertension would be the best way to reduce costs. Obesity and a high alcohol intake are associated with a higher blood pressure at any age. A high salt intake throughout life appears to be associated with a rise in blood pressure in the second half of life and may well be the main factor in hypertension. A radical rethinking of the method of pricing of medical care should be considered, so as to provide incentives to people to adopt life-style measures that lead to avoidance of hypertension (and other cardiovascular risk factors) or, in established hypertension, to a reduction in the need for medication.
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PMID:Managing hypertension: drugs, life-style manipulation or benign neglect? Medical, ethical and economic considerations. 175 Sep 10

We designed this study to establish the structural and functional characteristics of the hypertrophied left ventricle of middle-aged rats during mineralocorticoid-salt hypertension. Treatment was initiated at 12 months of age, and the rats were studied at either 13 or 15 months of age (after 1 or 3 months of treatment). All rats were unilaterally nephrectomized. One group received deoxycorticosterone acetate (DOCA) injections (30 mg/kg s.c.) biweekly and 1% NaCl drinking water (DOCA salt), and the other group was injected with the vehicle (sesame seed oil) and given tap water to drink (sham). During the first 4 weeks of DOCA-salt treatment, arterial pressure reached its peak and left ventricular enlargement was mainly due to increases of 47% in cardiocyte cross-sectional area in the middle layer of the left ventricular wall. The last 2 months were characterized by an accelerated endomyocardial growth. Because absolute left ventricular mass did not increase during the last 2 months of treatment, we conclude that cellular hypertrophy was accompanied by a focal loss of cardiocytes. Myocardial hydroxyproline concentration was initially elevated by 37% but normalized by the third month of treatment. Intracellularly, myofibril volume percent was not changed, but mitochondria volume percent declined (13% in the midmyocardium and 15% in the endomyocardium) and sarcoplasmic volume density increased by 25% and 39%, respectively, in these regions. Left ventricular hypertrophy was associated with enhanced peak cardiac and stroke indexes, measured during increased preload, after both 1 and 3 months of DOCA-salt treatment. Acceleration of flow, however, was depressed in the rats with left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular structure and performance in middle-aged rats with deoxycorticosterone acetate-salt hypertension. 213 30

To investigate the possible involvement of endothelin-1 (ET-1), an endothelium-derived potent vasoconstrictor peptide, in the pathophysiology of hypertension, plasma ET-1 levels in 15-week-old spontaneously hypertensive rats (SHR) and DOCA-salt hypertensive rats were measured with a sandwich-type enzyme immunoassay. The vasocontractile effect of ET-1 in aortic helical preparations was significantly more sensitive in DOCA-salt hypertensive rats than in control sham-operated rats, but plasma levels of ET-1 did not differ between them. Plasma ET-1 levels in genetically hypertensive rats (SHR and stroke-prone SHR) were significantly lower than those in age-matched normotensive Wistar-Kyoto (WKY) rats. The plasma concentrations of big ET-1, a precursor of ET-1, in both SHR and SHR-SP were significantly lower than those of WKY, suggesting that the production of ET-1 is decreased in rats of genetic hypertension. Although the vascular reactivity to ET-1 increased in both DOCA-salt hypertensive and genetically hypertensive rats, present findings of the plasma ET-1 levels suggest that the role of ET-1 in the vascular control system may be different in DOCA-salt hypertensive rats and genetically hypertensive rats.
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PMID:Plasma concentrations of endothelin-1 in spontaneously hypertensive rats and DOCA-salt hypertensive rats. 218 29

Experimental prevention of hypertension and related cardiovascular diseases has been studied in rat models for hypertension and stroke and not only salt reduction but also increased intakes of potassium, calcium, magnesium, protein, some amino acids and fatty acids and dietary fibers have been proven to be effective and indicated the importance of nonpharmacological dietary prevention of cardiovascular diseases. These experimental findings contribute to dietary risk factor analyses and the prevention of hypertension and its complications in man, as demonstrated by a cross-sectional epidemiological study on cardiovascular diseases and alimentary comparison (WHO-CARDIAC Study).
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PMID:Experimental intervention of hypertension and cardiovascular diseases. 220 60

Racial differences in the prevalence, course, and pathophysiologic characteristics of hypertension in black and white populations are reviewed. Accumulated epidemiologic data indicate that the prevalence of hypertension among blacks is greater than that among whites in almost all age- and sex-matched groups. Hypertensive blacks have a higher incidence of left ventricular dysfunction, stroke, and renal damage, but a lower incidence of ischemic heart disease, than do hypertensive whites. A significant pathophysiologic difference between blacks and whites is salt sensitivity; normotensive, as well as hypertensive, blacks tend to be salt sensitive. Blacks also tend to have lower renin levels than do whites, while dopamine response to a salt load is diminished among blacks as compared with whites. These differences and others lead to the recommendation that hypertension among blacks should be managed initially with salt restriction; if dietary control is insufficient, administration of an antihypertensive agent with 24-hour efficacy, which lowers vascular peripheral resistance, promotes sodium excretion, and potentially improves renal hemodynamics, is recommended. A calcium channel blocker may satisfy these requirements.
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PMID:Hypertension: racial differences. 222 Jul 99

The influence of the prenatal and postnatal maternal environment on stroke susceptibility was evaluated by reciprocally crossing the spontaneously hypertensive (SHR) and the Dahl salt-sensitive (SS/Jr) inbred rat strains to produce reciprocal F1 hybrids that were nurtured, respectively, during prenatal and postnatal life by SHR or SS/Jr mothers. Following placement on a high-salt diet containing 8% NaCl at 35 days of age, F1 rats reared by SHR mothers had shorter survival times and were more likely to die with cerebral hemorrhage than F1s reared by SS/Jrs. Across reciprocal F1 female groups, enhanced susceptibility to stroke was associated with greater elevations of systolic blood pressure, but this association was not seen across reciprocal F1 male groups. There was also an association between blood pressure and stroke within each F1/gender subgroup: Rats eventually suffering strokes developed higher blood pressure after placement on the high-salt diet than rats that did not suffer stroke. Lower day 35 body weights (before exposure to the high-salt diet) were associated with greater likelihood of stroke both across the reciprocal F1 groups, and within three of the four F1/gender subgroups. The differences in stroke susceptibility between the reciprocal F1 groupings may be due to systematic differences in the prenatal and/or postnatal environments of SHR and SS/Jr mothers and may be mediated by variations in the nutritive capacity of the two inbred mothers.
Stroke 1990 Nov
PMID:Modification of stroke susceptibility by genotype-dependent maternal influences. 223 71

The ability of the Na-Ca exchanger to modify vascular relaxation was studied in rings isolated from tail arteries of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The arteries were contracted with norepinephrine (NE) 1 microM and after stabilization they were transferred to a Ca-free physiological salt solution still in presence of NE. The time to 50% relaxation (T-50) in these conditions was significantly greater in SHRSP (78 +/- 7 s) than in WKY (50 +/- 7 s). When the calcium pump was stopped with vanadate (VAN), the Ca uptake by the sarcoplasmic reticulum with ryanodine (RY) and the Na-Ca exchanger with a Na-free PSS, the relaxation was slowed (T-50 increased to 198 +/- 16 s in SHRSP and to 162 +/- 14 s in WKY). Releasing the Na-Ca exchanger only (i.e. still with VAN and RY but with normal Na in the bath) the T-50 for relaxation in Ca-free PSS was, in WKY, nearly as fast as in control conditions (54 +/- 8 s). However, the Na-Ca exchanger in SHRSP was not so effective, and the T-50 for relaxation was slower than in control conditions (122 +/- 10 s). We conclude that the activity of the Na-Ca exchanger is depressed in tail arteries of SHRSP. This abnormality in resistance vessels, would contribute to the enhanced vascular tone present in hypertension.
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PMID:Decreased activity of the sodium-calcium exchanger in tail artery of stroke-prone spontaneously hypertensive rats. 224 41

Beam-walking in the rat is a useful model for studying the effects of drugs on motor recovery following brain injury. In the present experiment, the effect of clonidine HCl on beam-walking recovery was investigated. Groups of rats were first trained to traverse a narrow elevated beam and then subjected to a right sensorimotor cortex suction-ablation injury. After 24 h, each rat received a single dose of clonidine HCl (20, 60, or 200 micrograms/kg, i.p., salt weight) or saline. Recovery of beam-walking ability was scored over the next 12 days. Treatment with clonidine significantly slowed the rate of recovery (Kruskal-Wallis H = 8.755, df = 3; 0.02 less than P less than 0.05). Furthermore, the impairment persisted for at least 5 days after the rats were treated (Kruskal-Wallis H = 8.47, df = 3; 0.02 less than P less than 0.05). These data are consistent with the hypothesis that norepinephrine, working through central alpha 2-adrenergic receptors, influences motor recovery after a unilateral sensorimotor cortex lesion in the rat. Since many stroke patients are treated with centrally acting antihypertensive drugs, the potential effects of specific classes of these drugs during the recovery period, should be carefully considered.
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PMID:Clonidine impairs recovery of beam-walking after a sensorimotor cortex lesion in the rat. 230 22

A case-control study on stroke was carried out in 1985 in conjunction with a prevalence survey on neurologic disorders in 22 rural communities of the People's Republic of China. 585 cases of stroke, detected from the survey, together with an equal number of matched controls were investigated. The statistically significant factors associated with stroke in this study were: hypertension (history, findings at examination); high salt intake; family member(s) with cerebrovascular disease and/or hypertension; heart disease (history, abnormal findings at examination); history of transient ischemic attacks, and arteriosclerotic funduscopic findings. These factors were analyzed separately for hemorrhagic and ischemic strokes.
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PMID:Risk factors for stroke in rural areas of the People's Republic of China: results of a case-control study. 233 24

To gain insight into the membrane alteration that could account for the hyperresponsiveness of platelets in hypertension, we have investigated whether, in resting platelets of hypertensive rats, the metabolism of phospholipids was modified. Because preliminary results indicated a specific acceleration of phosphatidylcholine turnover in spontaneously hypertensive rats, the possible relation between such an abnormality and hypertension was investigated by studying phosphorus-32 labeling of phosphatidylcholine (taken as an index of its turnover) in various experimental models of hypertension. The data showed that phosphatidylcholine turnover 1) was considerably increased in platelets from spontaneously hypertensive (even at the prehypertensive stage) and stroke-prone rats compared with Wistar or Wistar-Kyoto control rats, 2) did not differ between deoxycorticosterone-salt-treated hypertensive and control rats, and 3) was increased in Dahl salt-sensitive rats fed a high NaCl diet (hence hypertensive rats), compared with either the rats fed a low NaCl diet or the salt-resistant rats. These results indicate that an increase in phosphatidylcholine turnover is a consequence of neither hypertension nor high salt intake and appears likely to be of genetic origin. These data allow us to suggest the existence, in platelets, of a relation between phosphatidylcholine turnover, free cytoplasmic Ca2+, and responsiveness to stimuli. Because phosphatidylcholine is assumed to participate in signal transduction, an increase in its turnover in platelets might be considered as a primary membrane abnormality that, in primary hypertension, results in platelet hyperresponsiveness.
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PMID:Platelet phosphatidylcholine turnover in experimental hypertension. 237 51


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