Tumor necrosis factor-α-angiotensin interactions and regulation of blood pressure
NR Ferreri, Y Zhao, H Takizawa… - Journal of …, 1997 - journals.lww.com
NR Ferreri, Y Zhao, H Takizawa, JC McGiff
Journal of hypertension, 1997•journals.lww.comObjectives To compare the levels of tumor necrosis factor-α (TNF) produced by medullary
thick ascending limb tubules (MTAL) obtained from normotensive and angiotensin II (Ang II)-
dependent hypertensive rats and determine whether TNF participates in a mechanism that
opposes elevation of blood pressure by Ang II. Design We have previously demonstrated
that in-vitro administration of Ang II increases production of TNF and prostaglandin E 2 (PGE
2) by the MTAL. We hypothesize that production of TNF and PGE 2 by the MTAL is elevated …
thick ascending limb tubules (MTAL) obtained from normotensive and angiotensin II (Ang II)-
dependent hypertensive rats and determine whether TNF participates in a mechanism that
opposes elevation of blood pressure by Ang II. Design We have previously demonstrated
that in-vitro administration of Ang II increases production of TNF and prostaglandin E 2 (PGE
2) by the MTAL. We hypothesize that production of TNF and PGE 2 by the MTAL is elevated …
Abstract
Objectives
To compare the levels of tumor necrosis factor-α (TNF) produced by medullary thick ascending limb tubules (MTAL) obtained from normotensive and angiotensin II (Ang II)-dependent hypertensive rats and determine whether TNF participates in a mechanism that opposes elevation of blood pressure by Ang II.
Design
We have previously demonstrated that in-vitro administration of Ang II increases production of TNF and prostaglandin E 2 (PGE 2) by the MTAL. We hypothesize that production of TNF and PGE 2 by the MTAL is elevated in in-vivo models of Ang II-dependent hypertension and acts to modulate the pressor effects of Ang II. Thus, inhibition of TNF should disclose whether this cytokine acts to modulate Ang II-induced hypertension.
Methods
MTAL tubules obtained from normotensive and Ang II-dependent hypertensive rats were isolated by enzymatic digestion and sieving. Tubules were cultured in the absence of exogenous Ang II. TNF and PGE 2 levels were measured by enzyme-linked immunosorbent assay. Anti-TNF antiserum was administered intravenously to normotensive and Ang II-dependent hypertensive rats and their mean arterial pressures were measured.
Results
Production of TNF and PGE 2 was significantly greater in MTAL tubules isolated from Ang II hypertensive rats than it was in those from normotensive controls. Administration of anti-TNF antiserum exacerbated the Ang II-mediated increase in mean arterial pressure.
Conclusions
The higher levels of production of TNF and PGE 2 by MTAL tubules isolated from Ang II hypertensive rats compared with those of normotensive controls are consistent with results of in-vitro experiments showing that administration of Ang II increases production of TNF and PGE 2 by the MTAL. TNF and PGE 2 participate in a counter-regulatory mechanism that opposes the pressor actions of Ang II.
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