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(Hypertension. 2006;48:1029.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
From the Department of Internal Medicine, Section of Nephrology, Wake Forest University School of Medicine, Winston Salem, NC.
Correspondence to Vardaman M. Buckalew, Section of Nephrology, Wake Forest University Baptist Medical Center, Medical Center Blvd, Winston Salem, NC 27157. E-mail buckalew@wfubmc.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The demonstration that acute volume expansion released a blood borne natriuretic substance initiated a search for "natriuretic hormone."1 It was initially thought that this factor might regulate blood pressure by regulating blood volume as an endogenous diuretic. Subsequently, it was suggested that natriuretic hormone might be "endogenous digitalis" and cause natriuresis and vasoconstriction by inhibition of renal tubular and vascular Na,K ATPase (NKA), respectively.1 The possibility that this factor might explain the link between sodium intake and hypertension provided an attractive hypothesis, but progress was hampered by difficulties identifying its biochemical structure. "Endogenous digitalis-like factor" has now been identified as multiple cardiotonic steroids of 2 classes, a glycoside indistinguishable from plant derived ouabain and several bufadienolides that are similar if not identical to those found in toads.2 Most of the endogenous cardiotonic steroids that have been studied cause natriuresis; however, none are yet firmly established as natriuretic hormones. On the other hand, endogenous digitalis-like factors have been implicated as causative agents in some experimental and human forms of hypertension, including preeclampsia.13 The exact role of the different types of steroids in the various hypertensive states remains to be determined.
By contrast with endogenous digitalis, the natriuretic factors discovered in cardiac atrial granules were rapidly identified as a family of small peptides derived from a larger precursor. Although the precise role of these peptides in plasma volume and blood pressure regulation is still not entirely clear, they inhibit renal tubular sodium reabsorption in multiple sites, and mice in which the precursor
Related Article:
Hypertension 2006 48: 1160-1168.
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