ObjectivesTo investigate the role of transforming growth factor-β1 (TGF-β1) on Ca2+-dependent mechanisms elicited by angiotensin II in aortic vascular smooth muscle cells (VSMC) of Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).MethodsCai2+release induced by angiotensin II (1 μmol/l) was studied in cultured VSMC isolated from the aortas of 6-week-old WKY rats and SHR. Intracellular Ca2+(Cai2+) was assessed in Fura-2 loaded cells using fluorescent imaging microscopy. Angiotensin II receptors were analysed by binding studies.ResultsPretreatment of VSMC for 24 h with TGF-β1 significantly increased angiotensin II-induced Cai2+mobilization from internal stores in SHR, while Ca2+influx was not altered. This effect involves tyrosine kinase and is not due to an increase in angiotensin II binding sites, or a change in the affinity of the receptors. By contrast, TGF-β1 did not modify the response of VSMC from WKY rats to angiotensin II.ConclusionsThese results help our understanding of the interactions between the pathways activated by TGF-β1 and the G protein-coupled receptor signalling pathway, and their role in genetic hypertension.