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Publication : Angiotensin II-induced natriuresis is attenuated in knockout mice lacking the receptors for tumor necrosis factor-α.

First Author  Majid DSA Year  2021
Journal  Physiol Rep Volume  9
Issue  15 Pages  e14942
PubMed ID  34337896 Mgi Jnum  J:320575
Mgi Id  MGI:6766129 Doi  10.14814/phy2.14942
Citation  Majid DSA, et al. (2021) Angiotensin II-induced natriuresis is attenuated in knockout mice lacking the receptors for tumor necrosis factor-alpha. Physiol Rep 9(15):e14942
abstractText  Intravenous infusion of relatively higher doses of angiotensin II (AngII) elicits natriuresis as opposed to its usual anti-natruretic response. As AngII can induce tumor necrosis factor-alpha (TNFalpha) production which elicits natriuresis via its action on TNFalpha receptor type 1 (TNFR1), we hypothesize that the concomitant release of TNFalpha contributes to the natriuretic response to AngII. Responses to AngII infusion (1 ng min(-1) g(-1) for 75 min, iv) were evaluated in anesthetized knockout (KO) mice lacking TNFR1 (n = 6) and TNFR2 (TNFalpha receptor type 2; n = 6) and compared these responses with those in wild type (WT; n = 6) mice. Arterial pressure (AP) was recorded from a cannula placed in the carotid artery. Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by PAH and inulin clearances, respectively. Urine was collected from a catheter placed in the bladder. AngII caused similar increases (p < 0.05 vs basal values) in AP (WT, 37 +/- 5%; TNFR1KO, 35 +/- 4%; TNFR2KO, 30 +/- 4%) and decreases (p < 0.05) in RBF (WT, -39 +/- 5%; TNFR1KO, -28 +/- 6%; TNFR2KO, -31 +/- 4%) without significant changes in GFR (WT, -17 +/- 7%; TNFR1KO, -18 +/- 7%; TNFR2KO, -12 +/- 7%). However, despite similar changes in AP and renal hemodynamics, AngII induced increases (p < 0.05) in urinary sodium excretion in WT (3916 +/- 942%) were less in the KO strains, more or less in TNFR1KO (473 +/- 170%) than in TNFR2KO (1176 +/- 168%). These data indicate that TNF-alpha receptors, particularly TNFR1 are involved in the natriuretic response that occur during acute infusion of AngII and thus, plays a protective role in preventing excessive salt retention at clinical conditions associated with elevated AngII level.
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