Publications by authors named "Francis J Haddy"

Background: The kidney's role in the pathogenesis of salt-induced hypertension remains unclear. However, it has been suggested that inherited morphological renal abnormalities may cause hypertension. We hypothesized that functional, not morphological, derangements in Dahl salt-sensitive rats' kidneys cause NaCl retention that leads to hypertension accompanied by renal pathologic changes and proteinuria.

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In a 1991 editorial in The FASEB Journal, Robert W. Krauss commented on a recent report of the Presidential Advisory Committee on the Future of the U.S.

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Certain things have not changed since my colleague and I last reviewed the role of dietary salt in hypertension [Haddy, F.J., Pamnani, M.

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Unlike sodium, potassium is vasoactive; for example, when infused into the arterial supply of a vascular bed, blood flow increases. The vasodilation results from hyperpolarization of the vascular smooth muscle cell subsequent to potassium stimulation by the ion of the electrogenic Na+-K+ pump and/or activating the inwardly rectifying Kir channels. In the case of skeletal muscle and brain, the increased flow sustains the augmented metabolic needs of the tissues.

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