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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past decade, attention has focused on the effects of calcium antagonists on renal function. When administered in vitro to the isolated perfused kidney, calcium antagonists exhibit consistent actions permitting characterization of their renal effects. Calcium antagonists do not affect the vasodilated isolated perfused kidney, but they do dramatically alter the response of this preparation to vasoconstrictor agents. Our recent studies using the isolated perfused hydronephrotic rat kidney model, which permits direct visualization of afferent and efferent arterioles, have demonstrated that the preferential augmentation of glomerular filtration rate observed in the isolated perfused kidney is attributable to preferential vasodilatation of preglomerular vessels. Although the clinical implications of such observations have not been fully delineated, the results of recent studies indicate that calcium antagonists exert salutary effects on renal function in patients with impaired renal hemodynamics. Such disorders include radiocontrast-induced nephrotoxicity and transplant-associated acute renal insufficiency. It is apparent, however, that the effects of calcium antagonists on renal blood flow commend their use in the management of essential hypertension.
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PMID:Calcium antagonists and the kidney: implications for renal protection. 161 71

The effects of erythropoietin (EPO) on cytosolic free calcium concentration ([Ca2+]i) in platelets of 20 essential hypertensive patients (HT) and of 25 normotensive subjects (NT) were investigated using the fura2 technique. In resting platelets [Ca2+]i were not significantly higher in HT compared to NT (74.3 +/- 7.8 nM vs 59.8 +/- 7.0 nM, mean +/- SEM). Addition of EPO significantly increased [Ca2+]i in HT compared to NT (13.8 +/- 5.3 nM vs 0.9 +/- 1.9 nM, p less than 0.01). EPO increased the amount of calcium in intracellular stores. This was confirmed independently using thrombin-induced changes of [Ca2+]i in a calcium-free medium and using chlorotetracycline as a marker of stored calcium. After preincubation with EPO thrombin-induced changes of [Ca2+]i were significantly lower in HT compared to NT (306.1 +/- 30.0 nM vs 407.7 +/- 35.7 nM, p less than 0.05). In a calcium-free medium after preincubation with EPO thrombin-induced changes of [Ca2+]i were significantly lower in HT compared to NT (54.7 +/- 11.8 nM vs 100.9 +/- 10.5 nM, p less than 0.05) indicating lower storage capacity in HT. It is concluded that elevated response to EPO may provide a powerful tool to evaluate diagnosis and underlying pathophysiological mechanisms in essential hypertension.
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PMID:Erythropoietin induced transmembrane calcium influx in essential hypertension. 161 80

Plasma humoral factors which modulate the transmembrane distribution of sodium and calcium have been identified in hypertensive patients and have been hypothesized to be involved in the etiology of essential hypertension. In cross-incubation experiments, we have found that plasma of hypertensive subjects elevated basal and stimulated intraplatelet calcium levels, while plasma of normal subjects has an opposite effect on platelets from hypertensives. Basal intraplatelet calcium in normal platelets was 108 +/- 5 nmol/L and rose to 142 +/- 3 nmol/L (P less than .001) after incubation in plasma from hypertensive patients. Platelets from hypertensive patients had basal calcium levels of 182 +/- 11 nmol/L which fell to 127 +/- 11 nmol/L (P less than .01) after incubation in normal plasma. Hypertensive plasma potentiated the rise in intraplatelet calcium in response to ADP and PAF. Hypertensive patients treated experimentally with plasmapheresis exhibited a disappearance of the plasma factor responsible for elevating intraplatelet calcium. These results indicate the presence of a plasma humoral factor in hypertensives which elevates intraplatelet calcium and sensitizes platelets to agonist stimuli.
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PMID:Humoral factor, intraplatelet calcium, and hypertension. 163 35

The authors investigated in ten patients with essential hypertension changes in the membrane transport of sodium in red blood cells and the intracellular calcium content of thrombocytes during the control period during treatment of hypertension with central sympatholytics and after three-week treatment with an inhibitor of the angiotensin converting enzyme (ACE), enalapril. The effect of enalapril in hypertonic patients was manifested by a rise of the renin plasma activity and the potassium concentration and a reduction of the sodium plasma concentration which corresponds to the inhibition of angiotensin II. The intracellular calcium and sodium content was unaltered. In 8 of 10 patients after enalapril treatment increased values of Vmax for Na(+)-K+ cotransport occurred, incl. 6 patients where at the same time a rise of Vmax Na(+)-Li+ countertransport was recorded.
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PMID:[Membrane transport of cations in erythrocytes during treatment of essential hypertension with angiotensin-converting enzyme inhibitors]. 163 92

In human red cells, Ca is mainly bound to the inner side of the plasma membrane. A smaller part may be present within intracellular Ca storing vesicles, while only a few percent of total red cell Ca is in ionized form. In some hemolytic anemias (sickle cell anemia, beta-thalassemia), an increased number of endocytotic vesicles storing Ca is probably responsible for the elevation of total red cell Ca content. Red cell Ca inward transport, which is partially susceptible to inhibition by Ca entry blockers, has been reported to be enhanced by physiological shear stress and enrichment in membrane cholesterol, as well as in some hemolytic anemias. Normal intracellular ionized Ca levels have been assessed in several diseases where elevated Ca inward transport rates or decreased Ca efflux through the Ca pump (hemolytic anemias, cystic fibrosis, essential hypertension) had been observed previously. Thus, red cell Ca homeostasis is apparently capable of keeping ionized Ca levels within the physiological range of 20-60 nM under most pathological conditions investigated so far. Conceptually, changes in red cell Ca homeostasis (or also in other red cell membrane parameters) may be of pathophysiological importance in two respects: 1) A disturbance may be directly responsible for some of the symptoms associated with a disease. This is the case in sickle cell anemia, where red cell dehydration is possibly caused by transient elevations of intracellular ionized calcium, which may activate K efflux through the Ca-activated K channel. The presence of dehydrated red cells will, in turn, lead to microvascular occlusion, a pathophysiologically important phenomenon in sickle cell anemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium homeostasis of human erythrocytes and its pathophysiological implications. 164 22

To evaluate the role of calcium and the parathyroid gland in the pathophysiology of essential hypertension, creatinine clearance, urinary excretion of sodium, calcium and nephrogenous cyclic adenosine monophosphate (NcAMP) and serum parathyroid hormone (PTH) levels were measured in 25 newly diagnosed essentially hypertensive patients before institution of any treatment and in 25 age- and sex-matched normal volunteers. While no significant differences in creatinine clearance, serum total calcium levels or 24-hour sodium excretion existed between the two groups, hypertensives had a higher mean (+/- SD) 24-hour calcium excretion rate (199.0 +/- 44.7 vs. 152.8 +/- 33.6 mg, p less than 0.001), a higher mean NcAMP excretion rate (2.54 +/- 0.8 vs. 1.87 +/- 0.5 nmol/100 ml glomerular filtrate, p less than 0.001) and a higher mean serum PTH concentration (1.87 +/- 0.6 vs. 1.53 +/- 0.4 ng/ml, p less than 0.001) than the normotensives. A significant positive correlation existed between calcium and sodium excretion in both hypertensives (r = 0.66, p less than 0.001)) and normotensives (r = 0.67, p less than 0.001), but given the same levels of creatinine clearance and sodium excretion, hypertensives excreted more calcium than normotensives (p less than 0.001)). In both hypertensives and normotensives, serum PTH levels were positively correlated with NcAMP excretion (r = 0.42, p less than 0.05, and r = 0.41, p less than 0.05, respectively) and the ratio of urinary sodium to urinary calcium excretion (r = 0.59, p less than 0.001, and r = 0.75, p less than 0.001), respectively). The above results suggest that in essential hypertension, increased activity of parathyroid glands may occur as a consequence of increased urinary calcium losses which are presumably due to an intrinsic defect in renal calcium handling.
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PMID:Urine calcium excretion, nephrogenous cyclic-adenosine monophosphate and serum parathyroid hormone levels in patients with essential hypertension. 165 70

This study was designed: (1) to test the hypothesis that the pressor response to sodium chloride loading in patients with essential hypertension is associated with disorder of divalent cations (calcium and magnesium); and (2) to clarify the relationship between intracellular free calcium concentration and serum levels of calcium-regulating factors and intracellular magnesium concentration. With sodium chloride loading, mean blood pressure, urinary calcium and magnesium excretions and platelet calcium concentration were increased, and serum total and ionized calcium, magnesium concentrations and erythrocyte magnesium concentration were decreased. Change in mean blood pressure was correlated with changes in parathyroid hormone (r = 0.49, P less than 0.05), serum total and ionized calcium (r = -0.50, P less than 0.05) and erythrocyte magnesium (r = -0.56, P less than 0.05) and platelet calcium concentrations (r = 0.46, P less than 0.05). In addition, change in platelet calcium concentration was related to changes in parathyroid hormone (r = 0.44, P = 0.05), serum total and ionized calcium (r = -0.66, P less than 0.01) and erythrocyte magnesium concentration (r = -0.49, P less than 0.05). It is concluded that the pressor effect of excessive sodium chloride intake on blood pressure in patients with essential hypertension is associated with a disorder of divalent cations and that alteration of the intracellular free calcium concentration with sodium chloride loading may occur through handling of serum total and ionized calcium, parathyroid hormone and/or intracellular magnesium concentration.
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PMID:Significance of intracellular free calcium and magnesium and calcium-regulating hormones with sodium chloride loading in patients with essential hypertension. 166 59

A10 vascular smooth muscle cells were placed in a flow chamber and exposed to the circulation of foetal calf serum at different rates and pressures. Under unidirectional laminar flow, physiological flow rates and pressures had almost no effect on internal sodium content. Indeed, pressure values greater than 150 mmHg were required to observe modest increases in sodium content. Conversely, a short exposure to turbulent flow (3 min) induced a strong increase in cell sodium content. At flow rates found in large human arteries, the onset of such ionic change required pressure levels of 50-85 mmHg. The restoration of laminar flow allowed the elimination of the excess cell sodium content, with a half-life of 3-4 h. Opening of calcium channels by the turbulent flow was suggested by the following observations: (1) nitrendipine fully prevented sodium uptake, with an inhibitory concentration of 50% of approximately 2 x 10(-7) mol/l; and (2) exposure to turbulent flow increased cytosolic free calcium content by approximately 80%. In addition to sodium uptake, turbulent flow stimulated cell uptake of exogenous cholesterol. Although the restoration of laminar flow allowed the rapid elimination of approximately two-thirds of the excess in cell cholesterol (with a half-life of 30-60 min), one-third of the excess cholesterol remained in the cells for more than 24 h. Finally, cell replication was faster in cells exposed to turbulent flow than in control cells subjected to laminar flow. The results show that turbulent flow provokes membrane ion transport changes in vascular smooth muscle cells, which are associated with enhanced cholesterol uptake and cell hyperplasia. Therefore, the departure from unidirectional laminar flow may be a pathogenic factor in primary hypertension and/or atherosclerosis.
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PMID:Flow-dependent stimulation of sodium and cholesterol uptake and cell growth in cultured vascular smooth muscle. 166 60

High contents of Ca2+ was revealed in thrombocytes' intracellular compartments in patients with essential hypertension. In response to different stimuli, large amount of Ca2+ can be released in the platelets of the patients which makes a considerable contribution to generation of the Ca2+ signal and activation of thrombocytes in cardiovascular diseases.
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PMID:[The compartmentalization of membrane-bound thrombocyte calcium in arterial hypertension]. 166 4

Calcium antagonists are now recommended as monotherapy for the treatment of mild to moderate essential hypertension by the Joint National Committee (JNC) on the Detection, Evaluation, and Treatment of High Blood Pressure. Based on a statement in the 1988 JNC report that black and elderly patients tend to respond better to calcium antagonists, we reviewed the literature to examine the predictive value of age and race to the antihypertensive response of calcium antagonists. The majority of studies we reviewed failed to substantiate the JNC statement and well-promulgated reports in the literature suggesting preferential action of calcium antagonists in the elderly, or their superiority when compared with diuretics, beta-adrenergic blockers, and angiotensin-converting enzyme inhibitors. Although not noted by the JNC, pretreatment blood pressure appeared to be an important predictor of the antihypertensive response to calcium antagonists. The literature reviewed indicates that calcium antagonists have comparable efficacy in black and white hypertensive patients. However, the limited comparative studies reviewed support the JNC statement that, as with diuretics, blacks have a greater antihypertensive response with calcium antagonists than with beta-adrenergic blockers or angiotensin-converting enzyme inhibitors.
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PMID:Calcium antagonists in elderly and black hypertensive patients. Therapeutic controversies. 168 19


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