Effect of forced titration of nebivolol on response rate in obese hypertensive patients.

tain low (Mg )i in cytotrophoblast cells. In addition (Mg )i is acutely regulated by (Mg 2 )o. Because placental trophoblasts are sites of maternal–fetal ion exchange, and (Mg )o is altered in preeclampsia, derangements in or modulation of this exchanger may contribute to complications of pregnancy such as pregnancy-induced hypertension, preeclampsia, and preterm labor. If a Na /Mg antiporter is defective in the preeclamptic placenta, it may contribute to the hypomagnesemia and vasoconstriction observed in these patients. Future studies are needed to characterize a Na /Mg antiporter in isolated term trophoblast cells. In this context we found lowered plasma, intracellular, and membrane Mg concentrations in preeclampsia contributing to the development of hypertension in pregnancy similar to investigations by Kisters and Bardicef and their colleagues. In another study performed by our group, we measured decreased intracellular Na and increased Mg concentrations in smooth muscle cells in spontaneously hypertensive rats determined by electron-probe X-ray microanalysis. The Mg deficiency hypothesis in essential hypertension has been studied at both the extracellular and intracellular level. At the extracellular level, serum Mg values have been reported higher, lower, or unchanged in hypertensive patients, compared with normotensive subjects. Nevertheless, several investigations have found a decreased intracellular Mg content in red blood cells in essential hypertensive patients and animals. One of the most important mechanisms contributing to the intracellular Mg homeostasis is a Na -dependent Mg efflux through the plasmalemmal membranes. This mechanism was described by Feray and Garay in human and rat erythrocytes. Evidence for a Mg /Na exchanger has been obtained in giant squid axon, and the existence of a similar mechanism in liver cells, thymocytes, and myocardiocytes has been suggested. The increased Na concentration in different hypertensive cells has been previously attributed to a reduced Na -K -ATPase activity, and increased activity of the Na -H exchanger. In conclusion, the excellent study of Stantley et al is similar to our results, showing the existence of a human Na /Mg exchanger. Concerning hypertension in pregnancy, further investigations in other cell models should be performed, to stress the importance of the Na /Mg exchanger in hypertension.