Angiotensin II (Ang II) is a potent vasoconstrictor and induces inflammation and end-organ injury through its activation of the proinflammatory transcription factor, nuclear factor–κB (NF-κB). Heat shock (HS) treatment with subsequent expression of heat shock proteins (Hsps) is an effective strategy for tissue protection against oxidative injuries. Recently, HS and Hsps have been shown to interact with NF-κB in tissue injury. In this study, we investigated whether HS could protect against Ang II–induced hypertension and inflammation by inhibiting NF-κB. Sprague-Dawley rats were divided into control and HS groups. Control and 24-hour post–heat shocked rats were treated with Ang II. At days 1, 3, 5, 7, 11, and 14 after Ang II administration, systolic blood pressures were measured by tail-cuff plethysmography, and aorta tissues were collected. Aorta NF-κB deoxyribonucleic acid–binding activity was measured by electrophoretic mobility shift assay, and NF-κB p65 subunit, Hsp70, Hsp27, and interleukin-6 (IL-6) expressions were measured by Western analysis. HS treatment significantly decreased Ang II–induced hypertension. The activation of NF-κB in aorta by Ang II was suppressed by HS treatment. The elevated expression of IL-6 induced by Ang II treatment was also decreased by HS treatment. Although Ang II treatment induced an increase in Hsp70 and Hsp27, HS treatment induced a greater elevation of Hsp70 and Hsp27 expression. HS treatment protects against Ang II–induced hypertension and inflammation. This protection may relate to the interaction of Hsps and the NF-κB pathway.
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