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

Cardiac hypertrophy in hypertensive subjects, its biochemical markers, and functional consequences are of great clinical importance but still unclear. We observed a shift of the ventricular isomyosin of adult spontaneously hypertensive (H) rats of both sexes to the V3 form and a decreased myofibrillar ATPase activity in the H animals when compared to normotensive (N) controls. Compared to the male H rats, age-matched female H animals revealed a lower blood pressure, the same or even an elevated magnitude of cardiac hypertrophy, a different ventricular isomyosin pattern, and a higher myofibrillar ATPase activity. In female H rats the V1 and V3 isomyosins were equally distributed (35% V1 and 35% V3), but in male H animals the V3 was predominant (24% V1 and 45% V3). The Ca2+-regulated Mg2+-dependent myofibrillar ATPase of the rat ventricle correlated positively with the amount of V1 when measured at pCa 5 (maximum activation). At submaximum Ca2+-concentrations (pCa 6.9-5.9) the myofibrillar ATPase activities were not changed with the proportion of V1. The cooperativity of the Ca2+-activation of the myofibrillar ATPase increased with increasing amount of V1 (Hill-coefficient 3.7 with 100% V1) and decreased with increased proportion of V3 (Hill-coefficient 1.3 at 45% V3). Two myosin isoenzymes were detected in the aorta of rats, a slow migrating (S2) and a fast migrating (S1) form having both a higher mobility than the ventricular isomyosins. Only one band was observed in the portal vein, which revealed the same mobility as S2. Hypertension did not change the appearance of these vascular smooth muscle isomyosins neither in male nor in female animals.
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PMID:Myosin isoenzymes of vascular smooth and cardiac muscle in the spontaneously hypertensive and normotensive male and female rat: a comparative study. 294 38

1. The effect of oral magnesium aspartate hydrochloride on monocrotaline (MCT)-induced pulmonary arterial hypertension was evaluated in rats. 2. A single subcutaneous injection of MCT, a pyrrolizidine alkaloid of plant origin, induces significant morphological changes in pulmonary vessels, pulmonary arterial hypertension and right ventricular hypertrophy in rats by 3 weeks. 3. Two groups of rats (Mg2+ control and Mg2+ + MCT) were started on oral Mg2+ (15.4 g/l magnesium aspartate hydrochloride dissolved in deionized water) 2 weeks before the MCT injection. The rest were given deionized water. At the start of the experiment, the control groups (deionized water and Mg2+) were given normal saline subcutaneously; the other groups (deionized water and Mg2+) were given MCT (60 mg/kg) subcutaneously. 4. Pulmonary artery pressure, right ventricular hypertrophy, lung pathology, organ weights and serum electrolytes were assessed 3 weeks after a single subcutaneous injection of MCT. Seventy-five per cent of the rats treated with MCT and oral Mg2+ (12 out of 16) showed significant reduction in pulmonary arterial hypertension, arterial pathology and right ventricular hypertrophy. 5. Our data indicate that Mg2+ attenuates experimentally induced pulmonary hypertension, possibly either by modulating the intracellular Ca2+ level and/or by directly affecting the pulmonary endothelial cell-smooth muscle cell complex involved in metabolism and maintenance of pulmonary vascular resistance.
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PMID:Magnesium aspartate hydrochloride attenuates monocrotaline-induced pulmonary artery hypertension in rats. 297 71

Dispersed cells from the submandibular gland of the male rat were prepared by collagenase treatment to study the mechanism by which immunoreactive tonin is secreted in vitro. Norepinephrine, epinephrine, and phenylephrine stimulated tonin release, an effect that was inhibited by phentolamine but not by propranolol, whereas isoproterenol, carbachol, histamine, and serotonin did not stimulate tonin release. The stimulatory effect elicited by alpha-adrenergic agonists was inhibited by both removal of Ca2+ from the medium and addition of diltiazem and nifedipine, both selective calcium channel blockers. The divalent cation ionophore A23187 stimulated tonin release in the presence of Ca2+, but not in the presence of Mg2+. Dibutyryl cyclic adenosine 3',5'-monophosphate, methylisobutylxanthine, angiotensin II, and vasoactive intestinal peptide had no effect on tonin release. The apparent molecular size of immunoreactive tonin released into the medium under basal and norepinephrine-stimulated conditions was similar to that of standard tonin by gel exclusion chromatography. These data suggest that the in vitro secretion of immunoreactive tonin from rat submandibular gland is initiated by activation of alpha-adrenergic receptors and apparently involves a mechanism dependent not on cyclic adenosine 3',5'-monophosphate, but on the influx of extracellular Ca2+.
Hypertension 1986 Oct
PMID:In vitro secretion of immunoreactive tonin from dispersed rat submandibular gland cells. 301 87

An increase in endogenous Na+,K+-ATPase inhibitor(s) with digitalis-like properties has been reported in chronic renal insufficiency, in Na+-dependent experimental hypertension and in some essential hypertensive patients. The present study specifies some properties and some biochemical characteristics of a semipurified compound from human urine having digitalis-like properties. The urine-derived inhibitor (endalin) inhibits Na+,K+-ATPase activity and [3H]-ouabain binding, and cross-reacts with anti-digoxin antibodies. The inhibitory effect on ATPases of endalin is higher on Na+,K+-ATPase than on Mg2+-ATPase and Ca2+-ATPase. The mechanism of endalin action on highly purified Na+,K+-ATPase was compared to that of ouabain and was similar in that it reversibly inhibited Na+,K+-ATPase activity; it inhibited Na+,K+-ATPase non-competitively with ATP; its inhibitory effect was facilitated by Na+; K+ decreased its inhibitory effect on Na+,K+-ATPase; it competitively inhibited ouabain binding to the enzyme; its binding was maximal in the presence of Mg2+ and Pi; it decreased the Na+ pump activity in human erythrocytes; it reduced serotonin uptake by human platelets; and it was diuretic and natriuretic in rat bioassay. The endalin differed from ouabain in only three aspects: its inhibitory effect was not really specific for Na+,K+-ATPase; its binding to the enzyme was undetectable in the presence of Mg2+ and ATP; it was not kaliuretic in rat bioassay. Endalin is a reversible and partial specific inhibitor of Na+,K+-ATPase, its Na+,K+-ATPase inhibition closely resembles that of ouabain and it could be considered as one of the natriuretic hormones.
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PMID:Further biochemical characterization of an Na+ pump inhibitor purified from human urine. 302 85

7.2 per cent of babies born in England and Wales in 1986 had birthweights below 2,500 g. Low birthweight and hypertension are associated. European trials have reported that oral supplementation with physiological amounts of magnesium during pregnancy reduces pregnancy hypertension and also miscarriage, preterm birth and fetal growth retardation. Magnesium deficiency causes hypertension and low birthweight in animals. In humans deficiency of thiamin and other B vitamins has also been reported to cause pregnancy hypertension and low birthweight. Magnesium and B vitamins are essential for the same biochemical reactions in energy metabolism. There is evidence that magnesium consumption of substantial numbers of women in Europe and North America is too low to support a healthy pregnancy. Magnesium and thiamin are lost in processing many foods. British trials of magnesium supplementation are advocated. It is suggested that more attention should be given to magnesium in nutritional advice.
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PMID:Magnesium and other nutrient deficiencies as possible causes of hypertension and low birthweight. 307

Serum and erythrocyte magnesium concentrations (S-Mg, E-Mg) were measured in 380 Japanese junior high school students, and the relationship to blood pressure and a family history of hypertension were studied. Systolic blood pressure was higher in the subjects with a positive family history of hypertension [FH(+)] than in those with a negative family history [FH(-)], whereas E-Mg was lower in the FH(+) group than in the FH(-) group with a significant different in boys. Furthermore, in the FH(+) group, systolic blood pressure was significantly higher in the subjects with lower S-Mg and E-Mg than in those with higher S-Mg and E-Mg. In the FH(-) group, however, no difference was observed in blood pressure levels between the two subgroups. These findings suggest that magnesium deficiency is partially responsible for a rise of blood pressure in the FH(+) children, and that a genetic predisposition of hypertension may be closely related to magnesium metabolism.
Magnesium 1988
PMID:Serum and erythrocyte magnesium levels in junior high school students: relation to blood pressure and a family history of hypertension. 324 81

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

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

The effects of a dietary magnesium supplementation have been studied both on systolic blood pressure and plasma renin activity in the spontaneously hypertensive rat (SHR). This study has been conducted in young (developing hypertension) and mature (established hypertension) male SHR fed during 6 weeks with a normal magnesium diet or with a high magnesium diet. After 6 weeks of diets, the systolic blood pressure was lower in young and mature SHR fed with an increased dietary amount of magnesium than in the young and mature SHR fed with a normal amount of dietary magnesium. Plasma renin activity was similar after the two different diets in young SHR while it was greater in mature SHR receiving a high magnesium diet than in mature SHR receiving a normal diet. Hence, dietary supplementation with magnesium inhibits the development of hypertension in young SHR, and reduces arterial blood pressure in mature SHR. The hypotensive effect observed during magnesium supplementation is not related to an inhibition of the renin release.
Magnesium 1987
PMID:Blood pressure and plasma renin activity after magnesium supplementation in the spontaneously hypertensive rat: a study during developing and established hypertension. 332 76

Recent interest has centred on the role of divalent cations in hypertension, particularly in relation to the renin-angiotensin system. This study was undertaken to determine the hypotensive effect of magnesium administration in relation to the state of activation of the renin-angiotensin system. The mean blood pressure (MBP) and heart rate (HR) response to either the acute intravenous administration of a pharmacological dose of MgSO4 or vehicle was determined in conscious mineralocorticoid-salt (DOCA-salt, low-renin) and two-kidney, one clip renovascular, high-renin hypertensive rats. Baseline MBP was higher in the renovascular than in the DOCA-salt rats, while there was no difference in HR or serum Mg concentration between the two. Following administration of MgSO4, serum Mg increased equally in both the DOCA-salt (1.4 +/- 0.8 to 4.9 +/- 0.16 mEq/l; P less than 0.001) and in the renovascular rats (1.8 +/- 0.14 to 4.4 +/- 0.27 mEq/l; P less than 0.001). Magnesium administration significantly lowered MBP over the 1-h infusion in the DOCA-salt (167 +/- 8 to 145 +/- 5 mmHg, P less than 0.001) but not the renovascular hypertensive rats (191 +/- 5 to 183 +/- 4, NS). We conclude that the blood pressure lowering effect of Mg is related, in part, to the state of activation of the renin-angiotensin system. The mechanism of this differential effect remains to be determined.
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PMID:Haemodynamic response to magnesium administration in mineralocorticoid-salt and two-kidney, one clip renovascular hypertension. 338 7


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