Abstract The aim of the present work was to further characterize intracellular calcium stores released by angiotensin II (Ang II) in spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) vascular smooth muscle cells (VSMCs) and to study their alterations associated with proliferation. Intracellular Ca ²⁺ concentration was monitored by image analysis in aortic myocytes loaded with fura 2. In the presence of extracellular Ca ²⁺ , sensitivity to Ang II in proliferating VSMCs was not different in the two strains, but it increased 10-fold in confluent VSMCs from SHR compared with those from WKY. In Ca ²⁺ -free medium, Ca ²⁺ release induced by thapsigargin (10 μmol/L) was significantly greater (about twofold) in SHR than WKY, in both proliferating and confluent cultures, with responses during proliferation being 0.7-fold smaller. Responses to Ang II were abolished after exposure of the cells to thapsigargin. In proliferating cultures, ryanodine (10 μmol/L) did not modify the rises in intracellular Ca ²⁺ concentration induced by Ang II in VSMCs from both strains. Conversely, in confluent cultures, ryanodine reduced Ang II (100 nmol/L)–induced Ca ²⁺ release to the same level as in proliferating cultures, and it suppressed the difference between SHR and WKY. These results show that the ryanodine-sensitive Ca ²⁺ release induced by Ang II is enhanced in VSMCs from SHR at confluence and is impaired dur-ing proliferation. Thus, they suggest that differences in Ca ²⁺ -induced Ca ²⁺ release from the sarcoplasmic reticulum may participate in increased responsiveness of VSMCs to Ang II in SHR and in phenotypic modulation of vascular myocytes during proliferation.