Abstract
The mechanisms by which diuretics cause vasodilation in hypertension associated with early renal disease are still not completely understood. Reduction of the expanded extracellular fluid volume and removal of accumulated sodium are undoubtedly vital elements in their therapeutic profile (1,2). Nevertheless, the dissociation between the natriuretic and hypotensive efficacy of a thiazide diuretic in patients with severe renal failure points to additional extrarenal factors (3). Moreover, the diuretic-aggravated release of renin can be expected to oppose the blood pressure lowering effects of these agents.
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© 1987 Martinus Nijhoff Publishing, Boston
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Schiffl, H. (1987). Modifications in Cardiovascular Norepinephrine Responsiveness by Diuretic Treatment in Mild Renal Parenchymal Disease. In: Andreucci, V.E., Dal Canton, A. (eds) Diuretics: Basic, Pharmacological, and Clinical Aspects. Developments in Nephrology, vol 18. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2067-8_64
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DOI: https://doi.org/10.1007/978-1-4613-2067-8_64
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