Abstract
The mineralocorticoid - induced blood pressure increase in normotensive man is characterized by an early rise in cardiac output during the 1st week of steroid administration and a persistent increase in total peripheral resistance (TPR), which is observed later on, when cardiac output returns to pretreatment values [1,2]. The initial rise in cardiac output has been linked to sodium and volume retention [3,4]. The mechanism of the persistent increase in TPR in the presence of a normal or subnormal cardiac output remains elusive. Alterations of sympathetic nervous system activity and increased passive membrane permeability for sodium have been observed in animal models of mineralocorticoid hypertension [5, 6]. The present study examined parameters of sympathetic activity and intracellular calcium concentration, which ultimately should be linked to altered cellular sodium transport [7] in normotensive volunteers, in whom a mineralocorticoid-induced blood pressure increase was evoked by oral administration of fludrocortisone.
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© 1986 Springer-Verlag Berlin Heidelberg
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Fritschka, E. et al. (1986). Effect of Fludrocortisone on Adrenoceptors and Free Intracellular Calcium in Man. In: Middeke, M., Holzgreve, H. (eds) New Aspects in Hypertension Adrenoceptors. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71418-4_14
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DOI: https://doi.org/10.1007/978-3-642-71418-4_14
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