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

The influence of the parathyroid glands (PTG) on the development of high blood pressure (BP) in stroke prone spontaneously hypertensive (SHR/SP) and Wistar Kyoto (WKY) rats has been studied. After ablation of their own PTG's SHR/SP received PTG's from WKY rats and vice versa. After transplantation (TRPL) a normal calcium and parathyroid hormone (PTH) status was preserved during the whole observation period. One group of animals received a high salt diet (8% NaCl) for 4 weeks after transplantation, the other group received a normal rat chow for 3 months. In SHR/SP, which had PTG-transplants from WKY rats, the development of BP was clearly attenuated compared to sham operated rats in both experimental groups. WKY rats with PTG's from SHR/SP became hypertensive after two weeks during salt loading and after six weeks under normal diet. Sham operated WKY rats remained normotensive. The results demonstrate that the parathyroid gland is involved in the pathogenesis of hypertension, but the only known secretory product of PTG's parathyroid hormone, seems not to be responsible for these effects.
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PMID:Influence of transplantation of parathyroid glands on blood pressure development in stroke prone spontaneously hypertensive rats and in normotensive Wistar Kyoto rats. 189 8

The prevalence of hypertension increases with age. The majority of the hypertensive population is over age 55. Although the treatment of systolic hypertension remains incompletely understood, the reduction of diastolic hypertension with pharmacotherapy has been shown to reduce complications from hypertension in persons over age 55. The older hypertensive patient is at risk for the same complications as the younger patient: angina, myocardial infarction, arteriosclerosis obliterans, stroke, myocardial hypertrophy, congestive heart failure, and renal failure; the risk of sudden death and multi-infarct dementia in the older patient may be somewhat higher. The older hypertensive individual may have reduced plasma volume and defective salt and water conservation, reduced renal function, impairment of baroreceptor reflexes and sympathetic reactivity, and altered drug pharmacokinetics, or may have arteriosclerosis leading to pseudohypertension. Many circumstances interfere with adequate compliance with therapeutic regimens among the elderly. Concomitant medical conditions increase the possibility of drug interactions and require that the practitioner be able to adjust the antihypertensive program to the patient.
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PMID:Treatment considerations for the hypertensive patient over age 55. 189 46

Mortality, cardiovascular risk factors, and diet were compared in Tianjin province, People's Republic of China; in North Karelia Province, Finland; and in the United States as a whole. People in Tianjin received 7 percent of their energy intake from saturated fats, whereas people in the United States received 13 percent and those in North Karelia received 20. The mean blood cholesterol levels for men were 158 milligrams per deciliter (mg per dl) for Tianjin, 216 mg per dl for the United States, and 241 mg per dl for North Karelia. The smoking prevalence among men was highest in Tianjin (66 percent), followed by the United States (42 percent) and Finland (36 percent). The differences among mortality rates for the three locales were less pronounced among women than among men. Age-standardized total mortality for women was highest for Tianjin and lowest in North Karelia. The reverse was true for men. Age-standardized total mortality for men was lowest in Tianjin and highest in North Karelia. Age-standardized ischemic heart disease mortality for men was lowest in Tianjin (99 per 100,000) and highest in North Karelia (730 per 100,000). For women, the corresponding figures were 83 per 100,000 in Tianjin and 164 per 100,000 in North Karelia. Although salt intake was higher in Tianjin than in North Karelia, the blood pressure was on average lower in persons from Tianjin than in those from North Karelia. The stroke mortality rate in Tianjin, however, was much higher than in either Finland or the United States. The strong discrepancy in stroke mortality relative to prevalence of hypertension and salt intake raises the issue of the etiology of stroke in Tianjin. Recently it has been reported that hemorrhagic stroke may be more common among people whose blood cholesterol level is very low and blood pressure level high. This joint condition may be relatively common in Tianjin and calls for longitudinal and case-control studies to clarify the relationships among these factors in Tianjin.
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PMID:Mortality, cardiovascular risk factors, and diet in China, Finland, and the United States. 189 38

Arterial hypertension is sustained by either of two long-term mechanisms of arteriolar vasoconstriction or by an inappropriate reaction between them. One mechanism is renin-mediated, the other is related to antecedent renal sodium retention. The plasma renin value directly reflects the presence and degree of renin-mediated vasoconstriction, and, inversely, defines the predominance of sodium-related vasoconstriction. A hypotensive response, or lack of it, to angiotensin-converting enzyme inhibitor is similarly informative. Because the normal kidney exposed to high arterial pressure and normal salt intake will reduce its renin secretion to near zero, any renin secretion in a hypertensive setting can be considered abnormal. Typically, high-renin hypertensive patients are more vasoconstricted than low-renin patients with similar blood pressures. The intense vasoconstriction leads to relative hypovolemia, hemoconcentration, hyperviscosity, postural hypotension, and in severe forms even to acrocyanosis, all of which are dramatically reversed with anti-renin therapy. Conversely, low-renin equally hypertensive patients have relatively more sodium volume and are less vasoconstricted; they are generally responsive to natriuretic drugs (e.g., diuretics or calcium antagonists) and appear relatively protected from vascular sequelae such as stroke and heart attack. These observations provide a new means for evaluating prognosis and a basis for mechanistically differentiating and treating hypertensive patients, allowing increasingly simpler and more-specific long-term therapies.
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PMID:Abnormal sodium metabolism and plasma renin activity (renal renin secretion) and the vasoconstriction volume hypothesis: implications for pathogenesis and treatment of hypertension and its vascular consequences (heart attack, stroke). 191 96

In the light of the proposal that dietary salt intake should be reduced as a community health care measure designed to lower blood pressure and consequently mortality and morbidity from stroke and heart disease, the evidence that there is a link between salt intake and blood pressure is reviewed. In addition the effects of salt restriction on mild hypertension are surveyed as is the feasibility of sustaining a community-based campaign to reduce salt intake. It is concluded that whilst it would be possible to mount a concerted health care programme directed towards lowering the salt intake of the general population the benefits in terms of blood pressure would be extremely small. The impact on stroke and heart disease is unknown and possible adverse effects have not been examined.
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PMID:Salt restriction, a sceptic's viewpoint. 192 Dec 47

In the present study we examined whether the angiotensin I converting enzyme inhibitor, captopril, would protect stroke-prone spontaneously hypertensive rats (SHRSP) from stroke and renal pathology over a 26-week period. In the control group of six untreated SHRSP fed Stroke-Prone Rodent Diet and 1% NaCl drinking solution, all animals developed severe hypertension and stroke by 16.1 weeks of age. In eight salt-loaded SHRSP treated with oral captopril (50 mg/kg/day) beginning at 8.4 weeks of age, systolic blood pressure was slightly but temporarily suppressed and then continued to rise; by 12 weeks of age systolic blood pressure reached levels of severe hypertension, 240 +/- 8 mm Hg, and did not differ from that of untreated SHRSP. No deaths or brain lesions were noted in captopril-treated SHRSP despite severe hypertension maintained through 26 weeks of age when the study ended. Captopril treatment prevented increases in urinary protein excretion (14 +/- 2 v 63 +/- 16 mg/day at 11.7 weeks of age, P less than .01) and the severe brain, renal, and cardiac vascular lesions observed in untreated SHRSP. When maintained on Stroke-Prone Rodent Diet and saline, plasma renin activity of untreated SHRSP surviving until 14.5 weeks of age was markedly increased (29.1 +/- 9.4 ng Ang I/mL/h) compared with either untreated SHRSP (9.2 +/- 2.5 ng Ang I/mL/h, P less than .01) or Wistar-Kyoto rats (3.5 +/- 1.0 ng Ang I/mL/h, P less than .01) maintained on standard diet and water.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic benefit of captopril in salt-loaded stroke-prone spontaneously hypertensive rats is independent of hypotensive effect. 193 Aug 50

Primary hypertension is considered a polygenic, inherited disorder; to date, the nature of the genes involved remains unknown. In this study we present evidence for a structural difference in the gene coding for renin between the stroke-prone, spontaneously hypertensive rat (SHRSP) and its normotensive control, the Wistar-Kyoto rat (WKY). Restriction fragment analysis using hybridization against probes complementary to defined regions of the renin gene identified a deletion, approximately 700 base pair in size, within the first intron in SHRSP compared with WKY. This restriction fragment length polymorphism (RFLP) affects a part of the gene that is characterized by the presence of a multimeric tandem repeat element, where the occurrence of insertional/deletional events might be expected and have recently been shown in other rat strains. In order to test for a possible phenotypical representation of this RFLP, we studied a population (n = 115) of F2 hybrid rats derived from cross-breeding SHRSP with WKY. Using direct blood pressure measurements in conscious animals, we ruled out a cosegregation of systolic or diastolic blood pressure with renin genotype. Several other phenotypical parameters examined (heart rate, absolute and relative magnitude of changes in blood pressure induced by stress or dietary sodium loading, plasma renin activity, ventricular hypertrophy and tissue water content) also showed no cosegregation with genotype. Our findings are in contrast to a recently published study examining an RFLP of the renin gene distinguishing salt-sensitive and salt-resistant Dahl rats. Thus, cosegregation of genotype and phenotype are not consistent, although in both cases, structural differences in the same region of the renin gene separate the hypertensive strain from its normotensive controls. These data may suggest differential roles of the renin-angiotensin system in these two models of genetically predetermined hypertension.
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PMID:Structural alterations of the renin gene in stroke-prone spontaneously hypertensive rats: examination of genotype-phenotype correlations. 197 91

Epidemiologic research indicates that glucose intolerance and hypertension are interrelated phenomena, each powerfully predisposing to atherosclerotic cardiovascular disease. Both diabetic and hypertensive patients have greater amounts of atherogenic risk factors, including dyslipidemia, hyperuricemia, elevated fibrinogen, and left ventricular hypertrophy. Diabetic persons have an increased prevalence of hypertension (50%), and glucose intolerance is more common in hypertension (15% to 18%). Both share a strong relationship to excess weight, but the excess of hypertension in diabetic persons occurs in both lean and obese subjects. Diabetes doubles the risk of hypertension associated with overweight. The risk of coronary disease, stroke, and peripheral arterial disease increases with increasing blood pressure to the same degree in diabetic persons as in nondiabetic persons, but at any level of blood pressure, diabetic persons have a doubled risk of these outcomes. Both diabetic and hypertensive patients are particularly prone to silent or unrecognized myocardial infarctions. Greater efforts at primary prevention of both hypertension and diabetes are clearly needed, including efforts at weight control, exercise, limitation of salt intake, and control of blood lipid levels. In either diabetic or hypertensive candidates for cardiovascular disease, optimization of the chances of avoiding sequelae requires a comprehensive multifactorial approach. Prevention requires more than normalization of either the blood sugar or blood pressure. Rational preventive measures must also include weight reduction, a fat-modified diet, cessation of smoking cigarettes, raising high-density lipoprotein, lowering low-density lipoprotein, and reduction of fibrinogen. Hypertension, obesity, insulin resistance, hyperinsulinemia, hypertriglyceridemia, and low high-density lipoprotein cholesterol tend to coexist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The epidemiology of impaired glucose tolerance and hypertension. 200 55

Echocardiographic measurement of left ventricular mass has provided a way of evaluating the undesirable effects of high blood pressure on the heart in the same way as for obesity, excess salt intake and blood hyperviscosity. Recently, the left ventricular mass was shown to correlate (r = 0.81) with the hemodynamic stimuli of blood pressure, stroke volume and left ventricular contractility. Prospective trials at Cornell and Framingham indicate that left ventricular mass is a powerful predictive factor of the risk of complications in hypertension. In the first of these trials, we demonstrated in a 5 year follow-up study of 140 men with uncomplicated hypertension that the incidence of death, myocardial infarction or angina requiring myocardial revascularisation, was four times greater in patients with increased left ventricular mass and that this association was independent of the blood pressure levels. Then, in a 10 year follow-up study of hypertensive patients of both sexes, we established that the left ventricular mass was the most powerful predictive factor of mortality and morbidity and that this was so marked (15% death rate in subjects with LVH vs 1% in subjects with normal left ventricular mass--p less than 0.00001--, cardiovascular accidents in 26% of subjects with LVH compared with 12% in subjects with normal left ventricular mass--p less than 0.0001) that only left ventricular mass and age were independant predictive factors of morbid events in multiple variable analysis. In the Framingham study, the frequency of coronary events in a 4 year follow-up period of healthy subjects from the original cohort (average age 69 years) was significantly related to the left ventricular mass and independent of other risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relationship between left ventricular mass and prognosis of arterial hypertension]. 208 Aug 92

Endothelial cells modulate vascular tone by releasing endothelium-derived relaxing (EDRF) and contracting factors. An imbalance of these factors in hypertension could contribute to increased peripheral vascular resistance. Mesenteric resistance arteries of Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were suspended in a myograph filled with physiological salt solution (37 degrees C; 95% O2-5% CO2). In WKY rings contracted with norepinephrine, acetylcholine (10(-9)-10(-4) M) evoked endothelium-dependent relaxations (88 +/- 2%, IC50 7.3 +/- 0.1; n = 31). Hemoglobin (10(-5) M) but not meclofenamate (10(-5) M) reversed the relaxations delineating EDRF as the mediator. Nitric oxide (3 X 10(-9)-10(-5) M) induced comparable relaxations as acetylcholine. In SHRSP, relaxations to acetylcholine but not those to nitric oxide were impaired (61 +/- 5%, IC50 greater than 6.6 +/- 0.4; n = 24; P less than 0.005). In SHRSP, meclofenamate but not the thromboxane synthetase inhibitor CGS 13080 normalized endothelium-dependent relaxations. Relaxations to sodium nitroprusside were enhanced in SHRSP both in rings with and without endothelium. Thus our results are compatible with the concept that endothelium-dependent relaxations in resistance arteries are mediated by nitric oxide. In SHRSP, endothelium-dependent relaxations are impaired because of a cyclooxygenase-dependent substance interfering with the release and/or action of EDRF.
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PMID:Impaired endothelium-dependent relaxations in hypertensive resistance arteries involve cyclooxygenase pathway. 210 97


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