The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Alterations in intracellular cations and cell membrane ATPase activity in patients with malignant hypertension.

OBJECTIVE: To determine whether cellular cation concentrations and cell membrane ATPase activity are altered in patients with malignant hypertension. DESIGN: Sixteen black patients with malignant hypertension were studied and compared with age- and sex-matched essential hypertensive and normotensive subjects. Calcium, magnesium, sodium and potassium concentrations and cell membrane Na,K-ATPase, Ca-ATPase and Mg-ATPase activities were determined in platelets and erythrocytes. METHODS: Intracellular concentrations of total magnesium and calcium were measured by atomic absorption spectrophotometry, and those of sodium and potassium by flame photometry. Cell membrane ATPase activity was measured by a colorimetric method. RESULTS: The intracellular calcium level was significantly elevated and intracellular magnesium and potassium levels and cell membrane ATPase activity significantly decreased in the hypertensive group. These changes were more marked in patients with malignant hypertension than in patients with benign essential hypertension. In the malignant hypertensive group, mean arterial pressure was negatively correlated with intracellular magnesium and positively correlated with intracellular calcium and sodium levels. CONCLUSIONS: Cellular cation changes in malignant hypertension may be related to altered transmembrane transport mechanisms and activation of the renin-angiotensin system. These alterations may be more pronounced in the malignant than in the benign phase of hypertension.[1]

References

 
WikiGenes - Universities