Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Erythrocytes from 15 uremic children aged from 7 months to 16 years were analyzed for adenosine triphosphatase (total ATPase and ouabain sensitive ATPase i.e. Na+, K+-ATPase), sodium and potassium ions and ATP concentration, in some cases before and after therapeutic measures had been undertaken. No correlation was found between the levels of Na+, K+-ATPase and serum creatinine and all uremic children had Na+, K+-ATPase levels within the range for normal children. The children with rapidly progressive uremia had higher activities of Na+, K+-ATPase at the corresponding serum creatinine concentration than those with slowly progressive uremia. Longitudinally the Na+, K+-ATPase activities fell and the erythrocyte Na+-K+ ratio increased in slowly progressive uremia. Introduction of a low-protein, high-energy diet giving accelerated growth did not change the Na+, K+-ATPase activities, the concentrations of erythrocyte sodium and potassium ions or ATP. Hemodialysis gave a slight increase of Na+, K+-ATPase and of the erythrocyte Na+-K+ ratio, whereas renal transplantation resulted in a remarkable increase of Na+, K+-ATPase activity and decrease of Na+-K+ ratio. A distinct feature of uremic children with hypertension was a low erythrocyte Na+-K+ ratio and a high Na+, K+-ATPase level.
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PMID:Characteristics of active sodium and potassium transport in erythrocytes in children with different stages of symptomatic uremia. 645 27

Cardiac hypertrophy develops during the course of blood pressure elevation in spontaneously hypertensive rats (SHRs) and is associated with defective calcium transport by cardiac sarcoplasmic reticulum (SR). AT 20 weeks of age, calcium uptake is reduced in SHRs (42 +/- 1.3 vs 64 +/- 1.6 nmol X mg-1 X min-1 in age-matched normotensive Wistar-Kyoto rats, P less than 0.01), while Ca2+ ATPase activity is enhanced (44 +/- 1.1 vs 35 +/- 0.7 nmol X mg-1 X min-1 in WKYs, P = 0.02); this results in low stoichiometry between calcium uptake and ATP hydrolysis in SHRs. The steady-state levels of the phosphoprotein intermediate [EP] of the transport ATPase are higher in normotensive rats (0.97 +/- 0.1 vs 0.67 +/- 0.08 nmol X mg-1 in SHRs, P less than 0.01) but the Ca2+- and ATP-dependency are similar in the two groups. In order to study the relative roles of hypertension and cardiac hypertrophy in the depression of SHR function, 20-week old SHRs and normotensive rats were treated for 10 weeks with either hydralazine (100 mg X litre-1) or alpha-methyldopa (8 g X litre-1). Both therapeutic regimens resulted in near normalisation of blood pressure of SHRs (hydralazine: 18.1 +/- 0.5 kPa [136 +/- 4 mmHg]; alpha-methyldopa 17.6 +/- kPa [132 +/- 3 mmHg]). Regression of cardiac hypertrophy, however, was seen only in the alpha-methyldopa-treated group, as judged by changes in left ventricular weight, RNA/DNA ratio, and hydroxyproline content. Furthermore, improvement in calcium transport capacity by the SHR, as reflected in higher calcium uptake and stoichiometric ratio between uptake and ATP hydrolysis, was found after alpha-methyldopa, but not hydralazine treatment. These results indicate that reversal of cardiac hypertrophy is required for improvement in calcium transport by cardiac SR after antihypertensive therapy of SHRs.
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PMID:Effect of antihypertensive therapy on calcium transport by cardiac sarcoplasmic reticulum of SHRs. 645 96

Samples of amniotic fluid were obtained at caesarean section from 33 of 80 consecutive unselected patients in whom the membranes were intact. Concentrations of the ATP metabolites, hypoxanthine and xanthine, as well as uridine and urate were determined using high pressure liquid chromatography. Independent 'clinical' factors associated with reduced fetal growth and well-being were identified and the patients were assigned to one of three groups: those with no recognized risk, those with moderate risk and a small group of four patients with high risk. The mean hypoxanthine concentration was higher in the moderate-risk group than in the group with no risk. Two of the three patients with proteinuric hypertension in the high-risk group had normal hypoxanthine concentrations. There were seven patients with fetal distress, and concentrations of hypoxanthine, xanthine, uridine and urate were significantly higher in the three patients who had meconium stained amniotic fluid in addition to abnormal fetal heart rate tracings than in the remaining four who had fetal heart rate abnormalities only. It is suggested that fetal distress at emergency caesarean sections might be quantitated by such analysis.
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PMID:Concentrations of hypoxanthine, xanthine, uridine and urate in amniotic fluid at caesarean section and the association of raised levels with prenatal risk factors and fetal distress. 661 38

Hypertensive disease is known to increase the risks in connection with acute changes in blood pressure due to the presence of pronounced structural as well as functional changes in the cardiovascular system. In the present study the metabolic consequences of fixed haemorrhagic hypotension [mean arterial pressure (MAP) 70 and 45 mmHg] were studied in spontaneously hypertensive (SHR) and in normotensive rats (WKY). Blood gases and acid-base balance, blood glucose, liver (ATP, glucose, lactate) and brain (ATP, ADP, AMP, CP, glucose, lactate) metabolites were determined in unbled animals and after 35 min hypotension in bled animals. In the liver haemorrhage to MAP 70 mmHg resulted in a 70% reduction of the ATP content in SHR while that in WKY remained unchanged. At MAP 45 mmHg reduced liver ATP levels (35% reduction) were observed in WKY as well. In the brain metabolic changes indicative of tissue ischaemia (reduced CP, increased AMP and lactate, decreased energy charge potential) were present only in SHR at MAP 45 mmHg. The more pronounced metabolic disturbances in SHR than in WKY indicate that blood loss is more deleterious for the hypertensive individual.
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PMID:Effects of haemorrhagic hypotension on brain and liver metabolism in normotensive (WKY) and spontaneously hypertensive rats (SHR). 668 Oct 40

Microsomal fractions were isolated from the smooth muscle of gastric fundus, vasa deferentia and mesenteric arteries of rats made hypertensive by deoxycorticosterone-salt treatment. Several enzymatic activities, Ca2+ binding and ATP-dependent Ca2+ accumulation of the microsomal fractions from these hypertensive rats were compared with those from the control of rats which remained normotensive under similar treatment. Altered membrane properties were observed in microsomal fractions isolated from vascular smooth muscle but not in those isolated from non-vascular smooth muscles in this form of experimental hypertension. These alterations included decreased Mg2+ ATPase activity, enhanced alkaline phosphatase activity, decreased Ca2+ binding in the absence of ATP and decreased ATP-dependent Ca2+ accumulation. This result is in contrast to our previous findings that decreased ATP-dependent Ca2+ accumulation was observed in microsomal fraction isolated from non-vascular smooth muscles of rats with genetic hypertension. The present study, together with our previous findings, support the contention that altered Ca2+ handling by vascular smooth muscle is associated with the pathogenesis of hypertension, whereas altered Ca2+ handling by non-vascular smooth muscles previously observed in spontaneous hypertension may be associated with genetic factors not related to hypertension.
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PMID:Membrane abnormalities occur in vascular smooth muscle but not in non-vascular smooth muscle from rats with deoxycorticosterone-salt induced hypertension. 668 Oct 43

Intracranial pressure (ICP) was measured during induced hypotension with increasing doses of adenosine triphosphate (1-5 mg X kg-1 X min-1 ATP) in dogs without (group I) and with (group II) intracranial hypertension. After administration of 1 mg X kg-1 X min-1 ATP, ICP increased significantly from 11 +/- 4 mm Hg to 14 +/- 5 mm Hg (mean +/- SEM) (P less than 0.05; group I) and from 27 +/- 2 mm Hg to 38 +/- 6 mm Hg (P less than 0.05; group II), while mean arterial pressure (MAP) decreased from 103 +/- 10 mm Hg to 86 +/- 6 mm Hg (P less than 0.05; group I) and from 110 +/- 11 mm Hg to 90 +/- 11 mm Hg (P less than 0.05; group II). In both groups a slow decrease of ICP after the initial increase occurred with further lowering of MAP, but ICP remained significantly above control values even with a dose of 5 mg X kg-1 X min-1 ATP (P less than 0.05). Ventricular volume-pressure response curves (VPR) before and during intravenous infusion of 3 mg X kg-1 X min-1 ATP were constructed to determine changes in intracranial compliance (ICC). In both groups I and II ATP decreased ICC. On the basis of these results it is recommended that in the presence of intracranial mass lesions ATP should not be given to induce arterial hypotension before the dura is opened.
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PMID:Changes in intracranial pressure and compliance during adenosine triphosphate-induced hypotension in dogs. 670 64

Female Long-Evans hooded rats received Schroeder's rye-based diet and 0 or 1 microgram/ml cadmium, or cadmium plus lead in mineral fortified drinking water from weaning to 18 months. The heavy metal-fed rats were normal with respect to control, including growth rates and final body weights. Rats receiving added cadmium and cadmium plus lead in the diet were characterized by a persistent hypertension which was evident after 2 months. Cardiac conduction system excitability was depressed preferentially in cadmium-(atrioventricular nodal region) and cadmium plus lead-(His-Purkinje system) fed rats. Although heart rates were comparable to control, myocardial contractile activity (peak active tension and dT/dt) was significantly decreased in intact perfused heart preparations from both heavy metal-treated groups. In conjunction with the observed physiologic changes, various tissue-specific metabolic alterations were detected in heart, kidney, and liver. Generally, prolonged heavy-metal ingestion at these levels resulted in impaired energy metabolism (e.g., decreased ATP, PCr; increased Pj, ADP concentrations) and altered essential mineral composition (e.g., calcium, magnesium, zinc, and to a lesser extent, sodium and potassium; copper levels were unaffected) that varied in severity according to the tissue. The addition of lead to the cadmium diet had little additive effect on the cardiovascular system; however, renal and hepatic tissues did exhibit apparent additive effects further suggesting that cadmium and lead actions and interactions may be tissue dependent. These experimental findings and the biologic inferences derived are consonant with the hypothesis that chronic, life-long cadmium exposure approximating environmental levels may have significant adverse effects on mammalian systems, that include effects on cardiovascular tissues.
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PMID:Cardiac physiologic and tissue metabolic changes following chronic low-level cadmium and cadmium plus lead ingestion in the rat. 685 84

Serial ECG's were reviewed in 93 consecutive patients who were proven to be susceptible to malignant hyperthermia by caffeine contracture and ATP depletion tests on skeletal muscle biopsies, but who were without a history of pyrexic crises. There were 46 males and 47 females with a mean age of 33 years. Abnormal ECG's were found in 26 of the patients, with conduction defects in 14, repolarization abnormalities (non-specific ST-T changes) or "Q" waves in nine and increased voltages suggesting left ventricular hypertrophy in three (in the absence of hypertension). An abnormal ECG in a young patient may reflect malignant hyperthermia susceptibility.
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PMID:Electrocardiographic abnormalities associated with malignant hyperthermia susceptibility. 706 30

Alkaline phosphatase activity and Ca2+ accumulation were examined in the plasma membrane enriched fractions isolated from mesenteric arteries of spontaneously hypertensive (SHR) and Kyoto-Wistar normotensive (WKY) rats after a long-term antihypertensive treatment with hydralazine. The membrane biochemical abnormalities of arterial smooth muscle such as enhanced alkaline phosphatase activity and reduced ATP-dependent Ca2+ transport previously observed in untreated SHR were persistently observed in hydralazine treated SHR with normalized systolic blood pressure. Our results suggest that the antihypertensive effects of hydralazine do not involve the reversal or modification of the altered Ca2+ handling by vascular muscle membrane in hypertension.
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PMID:Arterial muscle membrane abnormalities of hydralazine-treated spontaneously hypertensive rats. 712 85

The 133Xe single bolus injection technique was used for measuring the cerebral blood flow (CBF) in spontaneously hypertensive (SHR) and normotensive rats. Their age was from 5 to 25 weeks and corresponded to the time before the initiation of the arterial blood pressure (BP) increase to the constant phase of hypertension. CBF in SHR 5 and 10 weeks of age was significantly higher than in all other groups being 155 +/- 7.2 and 151 +/- 9.3 ml/min/100 g, respectively. At 15 weeks of age the localization of the reactive products of ATP and CTP became scanty and spread over the endothelial cytoplasm. Further, at 25 weeks an enlarged number of empty pinocytic vesicles and astrocytic foot processes filled with flocculent electron dense material was found. These data suggest that the initial high CBF preceding the increase of BP can initiate the irreversible disorder of endothelial cells in brain capillaries.
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PMID:Cerebral blood flow and ultrastructural studies of the brain capillaries in the early state of hypertension in SHR+. 721 70


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