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

The differences observed among rat strains in both basal [Na+]i and the several cation transport systems seem to be due to the different genetic background as clearly shown in F2 populations or after bone marrow transplantation in MHS. The same may be true for humans. In spite of all the caution taken in interpreting the data, because of the great possibility of methodological errors, it is likely that the differences observed in many laboratories are due to uneven genetic or ethnic composition of the samples studied, as shown by Dagher and Canessa. One intriguing observation is that most reports of "low Na-K cotransport" values in hypertensive patients are from Mediterranean countries (Italy, France, and Spain), whereas most reports of "high," or "not low Na-K cotransport," or very high values of countertransport came from populations originating from North Europe (Denmark, USA, South African whites). We are not aware of any study on erythrocyte Na-K cotransport performed in Great Britain (the greatest source of American immigrants). Indeed the difference in cotransport values between North and South European hypertensives might be due to different environmental factors, but if this is so, the difference does not depend on the salt consumption or plasma lipids that are similar in our high and low Na-K cotransport hypertensives (Cusi D et al, submitted). The picture seems relatively less confusing for calcium. The most consistent alterations in different models of hypertension is a decreased Ca-pump in SHR, MHS, and DOCA rats, reduced calcium binding in SHR and MHS, and reduced microsomal ATP dependent calcium uptake in SHR and DOCA rats. [Ca++]i, which is increased in established hypertension in man and rats, is normal in young prehypertensive rats and humans, and returns to normal values after pharmacological treatment of hypertension. This pattern of changes suggests that genetic control of these transport systems is weaker, and probably much influenced by different environmental conditions. However, because of the pivotal role of calcium in vascular smooth muscle cell concentration, its intracellular increase may be the common pathway of the different forms of hypertension. What remains unclear is the relation, if any, between calcium and sodium. Blaustein tried to find a link between them, but his hypotheses have yet to be confirmed.
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PMID:Role of cellular sodium and calcium metabolism in the pathogenesis of essential hypertension. 329 35

Although it has been known for many years that prolonged ingestion of ethanol may be associated with numerous side effects, among them cardiovascular alterations, e.g., hypertension, cardiac arrhythmias, strokes, and cardiomyopathy, a direct cause and effect between alcohol and injury to the cardiovascular system has only been accepted recently. However, what mechanism is responsible for these cardiovascular alterations remains to be determined. Since it is well known that chronic alcohol consumption leads to hypophosphatemia and hypomagnesemia, we designed experiments to determine if controlled depletion of either phosphorous or magnesium (Mg2+) lead, in themselves, to cardiovascular disturbances and what effects these mineral depletions exert on myocardial cellular bioenergetics. Biochemical studies were carried out on left ventricular muscle, including mitochondrial and myofibrillar preparations. With respect to phosphate depletion, myocardial creatine phosphate, ATP, and ADP levels were reduced. Phosphate depletion also reduced mitochondrial and myofibrillar creatine phosphokinase activities; significant alterations in mitochondrial oxygen consumption, acid-extractable phospholipid precursors, and mitochondrial oxidation of long chain fatty acids were noted. With respect to magnesium depletion, significant reductions in inorganic oxygen consumption was also reduced. Utilizing these data, we have proposed several schemes for possible alcoholic-induced myocardial and vascular injury.
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PMID:Hypophosphatemia and hypomagnesemia result in cardiovascular dysfunction: theoretical basis for alcohol-induced cellular injury. 329 28

Female spontaneously hypertensive rats (SHR) were injected subcutaneously with mestranol twice a week for 12 weeks. Isolated segments of thoracic aorta were then used to generate relaxation response curves to acetylcholine or ATP after precontraction with phenylephrine. Estrogen treatment attenuated the development of hypertension. Further, augmented endothelium-dependent relaxation to acetylcholine was seen in the estrogen-treated SHR. There was no difference, however, in the relaxation produced by ATP. Since the relaxation of both acetylcholine and ATP is endothelium-dependent, these findings suggest that different mechanisms may be involved in the relaxation produced by acetylcholine and ATP.
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PMID:Endothelium-dependent relaxation in estrogen-treated spontaneously hypertensive rats. 335 42

The intracellular Na+ content of washed erythrocytes from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY) was measured by a high resolution 23Na-nuclear magnetic resonance (NMR) technique using a non-permeant aqueous shift reagent, dysprosium triethylenetetramine hexaacetic acid, Dy(TTHA)3-. The initial intracellular Na+ of freshly isolated and washed erythrocytes was very low (approximately 5 mmol/l) and increased progressively with prolonged incubation in isotonic salt solution at 37 degrees C. There was no significant difference in the erythrocyte Na+ concentration between SHRSP and WKY over the entire period of measurement, nor was any difference detected in their osmotic fragility or total cellular volume, although the osmotic fragility decreased with incubation time. The high energy phosphate metabolites were also studied in the same erythrocytes by 31P-NMR. The level of intracellular ATP decreased with incubation at 37 degrees C but showed no difference between the SHRSP and WKY samples. Inclusion of 1 mmol/l ouabain in the incubation medium substantially retarded the breakdown of intracellular ATP and resulted in a concomitant increase in intracellular Na+. However, neither the ouabain-sensitive nor the ouabain-insensitive component of Na+ influx altered in SHRSP erythrocytes compared with WKY erythrocytes in paired experiments. Our results do not support the hypothesis that altered Na+ transport, resulting in an increase in erythrocyte Na+ concentration, is associated with spontaneous hypertension.
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PMID:High resolution 23Na-nuclear magnetic resonance study of stroke-prone spontaneously hypertensive rat erythrocytes. 361 83

Subcellular membrane fractions were isolated from mesenteric arteries and vas deferens of salt-resistant and salt-sensitive Dahl rats on low-salt (0.4% NaCl) high-salt (8.0% NaCl) diets. Only the salt-sensitive Dahl rats on the high-salt diet developed sustained high blood pressure (BP) after 5 weeks of the high-salt diet. Protein contents, membrane associated enzyme activities, calcium ion (Ca2+) binding and ATP-dependent CA2+ transport were compared in fractions isolated from all four groups. No obvious changes were observed, except for minor enhancement in magnesium ion (Mg2+)- and CA2+ ATPase activities of mesenteric arterial membranes isolated from salt-sensitive Dahl rats on high-salt diet compared to those from other groups of rats. The membrane fractions from vas deferens of salt-sensitive Dahl rats on the high-salt diet, on the other hand, showed decreased ATP-dependent Ca2+ transport compared to those from salt-sensitive Dahl rats on the low-salt diet. No difference was observed in membrane fractions isolated from salt-resistant Dahl rats on high-salt diet compared to those on low-salt diet. The significance of these observations are discussed in relation to the findings previously obtained from corresponding smooth muscle tissues of spontaneous hypertensive rats (SHR).
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PMID:Subcellular membrane properties in vascular and non-vascular smooth muscles of Dahl hypertensive rats. 395 84

To elucidate possible role of alterations in levels of glycosylated hemoglobin and ATP of blood in pathogenesis of diabetic impairments, 29 children with insulin-dependent diabetes mellitus were studied. In these children the blood content of the glycosylated hemoglobin was distinctly increased simultaneously with a decrease in ATP level. The alterations were especially distinct in the children the parents of which suffered from ischemic heart disease, myocardial infarction, insult, hypertension, diabetes mellitus. Development of diabetes mellitus in these children was characterized by the most severe manifestations (especially frequent and severe diabetic lesions, distinct decreases in secretion of insulin and in efficiency of the hormone). A hypothesis is discussed on possible importance of accelerated glycosylation of proteins and of a decrease in ATP synthesis for development of diabetic lesions.
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PMID:[Blood levels of glycosylated hemoglobin and ATP in diabetes mellitus in children]. 402 34

The effects of prolonged bicuculline-induced seizures on cerebral blood flow and metabolism were determined in paralyzed, mechanically ventilated neonatal dogs. Transient changes occurring early in the course of status epilepticus included significant arterial hypertension, hypocarbia, elevation of plasma norepinephrine levels, and decline in brain glucose concentration. Cerebral blood flow remained elevated throughout the 45 minutes of seizure. Determination of cerebral metabolite values by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy and by in vitro enzymatic analysis of frozen brain samples showed significant decreases in the level of phosphocreatine and relatively less change in ATP values. Progressive intracellular acidosis occurred, coincident with elevation of brain lactate concentrations. We conclude that the physiological and metabolic alterations that occur during prolonged seizures are not uniform, but change with time. Any hypothesis advanced to explain the mechanism of neuronal injury during prolonged seizures must take into account these temporally related changes.
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PMID:31P NMR study of cerebral metabolism during prolonged seizures in the neonatal dog. 403 47

Stroke-prone spontaneously hypertensive rats with arterial blood pressure above 210 mmHg were taken for the present study after appearance of neurological symptoms. Regional cerebral blood flow, glucose metabolism, and protein synthesis rate were evaluated on the same brain section by means of triple-labelled autoradiographic techniques. Consecutive sections were used in the pictorial presentation of glucose, ATP, and serum protein extravasation. In addition, NADH-fluorescence was recorded. Two different patterns of hypertension-induced brain lesions could be distinguished: in two animals sharply demarcated cysts were visible in the cortical grey matter. In these animals no regional inhomogeneities of flow and metabolism were present remote from the infarct. In contrast, in three animals cysts were located in the white matter, leading to pronounced hemodynamic and metabolic disturbances throughout the brain. It is concluded that edema-induced brain swelling was the main cause for reduction in blood flow and metabolism.
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PMID:Regional cerebral blood flow, glucose metabolism, protein synthesis, serum protein extravasation, and content of biochemical substrates in stroke-prone spontaneously hypertensive rats. 404 48

This presentation has reviewed evidence from our laboratory that both structural and functional changes participate in the initiation and maintenance of hypertension in spontaneously hypertensive rats (SHR). Structural changes are present in the muscular arteries of the mesenteric and renal vasculature at 3- to 5-week-old SHR as compared with WKY. The major structural change in SHR arteries was increased cross-section area with increased thickness of the media owing to hyperplasia of smooth muscle; lumen sizes were interchanged. Later, at 10-12, 21, and 28 weeks of age, there was further increase in medial thickness owing to hyperplasia, and some hypertrophy and changes in elastic arteries also became evident. Increases in medial thickness of elastic arteries included hypertrophy as well as hyperplasia. Changes in lumen diameter were never observed in arteries fixed in a relaxed state at physiological flow rates. In addition, a deficit in Ca handling (decreased ATP-dependent Ca2+ accumulation) was observed in plasma-membrane vesicles from mesenteric arteries of SHR prior to and after the development of hypertension. It persisted when hypertension was reversed by hydralazine in SHR. It was present in various forms of experimental hypertension. It was present whenever hypertension was present and disappeared with normalization of blood pressure by withdrawal of the stimulus. The Ca-handling deficit was found in several nonarterial tissues and may be a generalized genetic defect in SHR. It was always accompanied by increased alkaline phosphatase activity of plasma membranes, and this was suggested to reflect the smooth-muscle hyperplasia occurring simultaneously. A model of the initiation and maintenance of hypertension based on medial thickening and deficient Ca handling as primary, interacting causes of genetic hypertension is proposed.
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PMID:Early structural changes in precapillary vessels in hypertension and their relationship to functional changes. 608 10

Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia]. 609 92


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