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. Author manuscript; available in PMC: 2017 May 1.
Published in final edited form as: Hypertension. 2016 Mar 28;67(5):970–976. doi: 10.1161/HYPERTENSIONAHA.115.06736

Figure 5.

Figure 5

Augmented pressor effects induced by Ang II during the expression (E) period in rats after central treatment with leptin during the induction (I) period (Fig. 5A). The sensitizing effect of leptin was attenuated by central (ICV) inhibition of TNF-α synthesis, AT1-R or microglial activation. Figure 5B shows the changes in MAP after infusion of Ang II during E in all groups. ICV V = central treatment with vehicle during I; ICV leptin = central treatment with leptin during I; I-ICV leptin/PTX = central concurrent treatment with leptin and TNF-α synthesis inhibitor pentoxifylline during I; ICV leptin/Irbe = central concurrent treatment with leptin and AT1-R blocker irbesartan during I; I-ICV leptin/Mino = central concurrent treatment with leptin and inhibitor of microglial activation minocycline during I; E-Ang II = peripheral treatment with a pressor dose of Ang II during E. (* p<0.05 vs baseline; # p<0.05 vs I-ICV V + E-Ang II and other groups treated with central blockers during I).