Involvement of Na+ Transport and Natriuretic Hormones in the Antihypertensive Mechanism of Canrenone
A key step in the development of some forms of primary hypertension appears to be the disturbance in cell Na+ homeostasis induced by the interaction of endogenous “ouabain-like” factors (EOLF) with vascular cells having genetic abnormalities in membrane Na+ transport. Several arguments have suggested to us that Canrenone, an antihypertensive antialdosterone drug, may interfere with this mechanism (1). In vitro, this drug behaves like a partial agonist at the digitalis receptor site of the Na+, K+-pump (see for instance ref.1, 2): (i) under basal conditions, canrenone slightly inhibits Na+, K+-pump activity. An effect which can explain the previous observation that canrenone administration potentiates the inotropic effect of digitalis in dogs (3), (ii) canrenone is able to resti mulate a pump blocked by high doses of ouabain. This effect is likely correlated with its ability to protect against digitalis-induced cardiac toxicity (4) and to reverse the inhibitory effect of digoxin on basal and furosemide-stimulated renin secretion (5).
KeywordsToxicity Catheter Glycoside Digoxin Renin
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