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Editorial
. 2010 Nov;56(5):819-21.
doi: 10.1161/HYPERTENSIONAHA.110.159350. Epub 2010 Oct 4.

Does interleukin 6 contribute to renal hemodynamic changes during angiotensin II-dependent hypertension?

Editorial

Does interleukin 6 contribute to renal hemodynamic changes during angiotensin II-dependent hypertension?

Michael J Ryan. Hypertension. 2010 Nov.
No abstract available

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Figures

Figure 1
Figure 1
Proposed role for inflammatory cytokines in angiotensin II dependent hypertension. Direct renal vascular effects of angiotensin II (and TNF-α) reduce renal blood flow (RBF) and glomerular filtration rate (GFR) to promote sodium retention. IL-6, stimulated directly by angiotensin II or indirectly through an angiotensin II mediated increase in TNF-α, activates JAK2/STAT3 signaling in the renal cortex which augments ENaC expression and sodium retention. The natriuretic actions of TNF-α partially counter the effects of impaired renal hemodynamics and IL-6 mediated increases in tubular reabsorption of sodium. The shaded boxes represent relationships that are directly tested, or supported indirectly as an association, in Brands et al .

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