Abstract
The mechanism of salt-dependent, volume-overloaded hypertension is particularly troublesome (1–3). Renin levels are low, and the responses to converting enzyme inhibitors and angiotensin antagonists are minimal. Catecholamine levels are not helpful; in fact, plasma catecholamine levels decrease as a function of salt intake in normal subjects. Long-term autoregulation subsequent to increased cardiac output and overperfusion of tissues has been considered, but increase in total peripheral resistance and blood pressure have been observed in the absence of increased cardiac output.
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Haddy, F.J., Pamnani, M.B., Clough, D.L. (1981). Position Paper: Sodium Metabolism: The Sodium-Potassium Membrane Pump and Volume Overload Hypertension. In: Laragh, J.H., Bühler, F.R., Seldin, D.W. (eds) Frontiers in Hypertension Research. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-5899-5_15
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DOI: https://doi.org/10.1007/978-1-4612-5899-5_15
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