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1 Department of Physiology, Medical College of Georgia, Augusta, GA, USA
2 Vascular Biology Center, Medical College of Georgia, Augusta, GA, USA; Deaprtment of Pharmacology and toxicology, Medical College of Georgia, Augusta, GA, USA
3 Department of Physiology, Medical College of Georgia, Augusta, GA, USA; Vascular Biology Center, Medical College of Georgia, Augusta, GA, USA
* To whom correspondence should be addressed. E-mail: dlee{at}mail.mcg.edu.
Plasma levels of interleukin-6 (IL-6) correlate with high blood pressure under many circumstances, and angiotensin II (AngII) has been shown to stimulate IL-6 production from various cell types. This study tested the role of IL-6 in mediating the hypertension caused by high-dose AngII and a high-salt diet. Male C57BL6 and IL-6 knockout (IL-6 KO) mice were implanted with biotelemetry devices and placed in metabolic cages to measure mean arterial pressure (MAP), heart rate (HR), sodium balance, and urinary albumin excretion. Baseline MAP during the control period averaged 114 ± 1 and 109 ± 1 mmHg for WT and IL-6 KO mice, respectively, and did not change significantly when the mice were placed on a high-salt diet (HS; 4% NaCl). AngII (90 ng/min, s.c.) caused a rapid increase in MAP in both groups, to 141 ± 9 and 141 ± 4 in WT and KO mice, respectively, on day 2. MAP plateaued at this level in KO mice (134 ± 2 mmHg on day 14 of AngII), but began to increase further in WT mice by day 4, reaching an average of 160 ± 4 mmHg from days 10 to 14 of AngII. Urinary albumin excretion on day 4 of AngII was not different between groups (9.18 ± 4.34 and 8.53 ± 2.85 µg/2 days for WT and KO mice). By day 14 albumin excretion was nearly 4-fold greater in WT mice, but MAP dropped rapidly back to control levels in both groups when the AngII was stopped after 14 days. Thus, the ~ 30 mmHg greater AngII hypertension in the WT mice suggests that IL-6 contributes significantly to AngII-Salt hypertension. In addition, the early separation in MAP, the albumin excretion data, and the rapid, post-AngII recovery of MAP suggest an IL-6-dependent mechanism that is independent of renal injury.
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