Abstract: Objective Excessive vasoconstriction of interlobar renal artery (IRA) is one of preliminary manifestations of renal damage in hypertension, during which caveolin-1 plays an important role. Atorvastatin (ATVS) represses cholesterol (CHO) synthesis to down-regulate the expression of caveolin-1, so we aimed to investigate whether the ATVS inhibited vasoconstriction of IRA to angiotensin Ⅱ (Ang Ⅱ) by regulating caveolin-1 in spontaneously hypertensive rats (SHR).Methods Twelve SHR were randomly divided into two groups:SHR control group, and SHR ATVS-treated group. Six Wistar Kyoto (WKY) rats weighing the same were employed as control group. Systolic blood pressure (SBP) was measured with the tail-cuff technique before and 2 or 4 weeks after ATVS treatment. Isometric force recording system was used to detect the vascular function. Western blotting was conducted to examine the protein abundance of caveolin-1 or angiotensin Ⅱ type 1 receptor (AT₁). Immumoprecipitation was carried out to assess the binding of caveolin-1 and AT₁.Results SBP, and intensity and sensitivity of vasoconstriction of IRA to Ang Ⅱ were significantly increased in SHR as compared to WKY rats (P<0.05). At 4th week, ATVS treatment could significantly reduce SPB(P<0.05), and the intensity and sensitivity of vasoconstriction of IRA to Ang Ⅱ (P<0.05) in SHR control group. Meanwhile, the protein expression of caveolin-1 or AT₁ as well as Ang Ⅱ elicited binding of caveolin-1 or AT₁ in IRA was higher in SHR than in WKY rats, which could also be reduced by ATVS (P<0.05). The ex vivo incubation of CHO raised the caveolin-1 protein content and promoted the binding of caveolin-1 and AT₁ in IRA of ATVS-treated SHR (P<0.05). At the same time, CHO enhanced the intensity and sensitivity of vasoconstriction of IRA to Ang Ⅱ (P<0.05).Conclusions ATVS mitigated the vasoconstriction of IRA to Ang Ⅱ in SHR, which was mediated by reducing caveolin-1 expression and inhibiting the binding of caveolin-1 and AT₁.