Angiotensin peptides play an important role in the physiological processes regulating blood pressure. Angiotensin 1-7 (Ang 1-7), the heptapeptide formed from Ang I or Ang II, has been reported to have opposing actions to angiotensin II (Le Tran & Forster, 1997). The actions of Ang 1-7 have been shown to be mediated by its own receptor (Le Tran & Forster, 1997) and the AT₁ receptor (Ferrario et al., 1997). Earlier work conducted in our laboratory demonstrated that Ang 1-7 (10^-7M) attenuated the vasopressor responses to Ang II in the renal vasculature of Spontaneously Hypertensive Rats (SHR). The vasopressor action of the heptapeptide is mediated by Ang 1-7 receptor that is coupled to a cyclo-oxygenase dependent pathway and nitric oxide release (Dharmani et al., 2007). The present study investigated the involvement of AT₁ receptor on the vasomodulatory action of Ang 1-7 in the isolated perfused kidneys of SHR using receptor binding assay, semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. Ninety min perfusion with Ang 1-7 (10^-7M) lowered the renal AT₁ receptor density compared to the vehicle control (534 ± 22.05 fmole/mg v.s. 739.6 ± 44 fmole/mg protein, P < 0.05). No significant changes in the mRNA and protein expression of the AT₁ receptor in the SHR kidney were observed following perfusion of the angiotensin peptide. In summary, the vasomodulatory action of Ang 1-7 in the isolated SHR kidney is partly mediated via the AT₁ receptor. Furthermore, the result suggests that Ang 1-7 induces AT₁ receptor internalisation to compensate the ongoing vascular changes in the hypertensive state.