Objective: We hypothesize that cerebral ischemia leads to enhanced expression of endothelin (ET), 5-hydroxytryptamine (5-HT) and angiotensin (AngII) receptors in the vascular smooth muscle cells. Our aim is to correlate the upregulation of cerebrovascular receptors and the underlying molecular mechanisms with the reduction in regional and global cerebral blood flow (CBF) after subarachnoid hemorrhage (SAH). Methods: SAH was induced by injecting 250 µl blood into the prechiasmatic cistern in rats. The cerebral arteries were removed 0, 1, 3, 6, 12, 24 and 48 h after the SAH for functional and molecular studies. The contractile responses to endothelin-1 (ET-1), 5-carboxamidotryptamine (5-CT) and Ang II were investigated with myograph. The receptor mRNA and protein levels were analyzed by quantitative real-time PCR and immunohistochemistry, respectively. In addition, regional and global CBF were measured by an autoradiographic method. Results: SAH resulted in enhanced contractions to ET-1 and 5-CT. Ang II (via AT₁ receptors) induced increased contractile responses (in the presence of the AT₂ receptor antagonist PD123319). In parallel the ETB, 5-HT1B and AT₁ receptor mRNA and protein levels were elevated by time. The regional and global CBF showed a successive reduction with time after SAH. Conclusion: The results demonstrate for the first time that SAH induces upregulation of ET_B, 5-HT_1B and AT₁ receptors in a time-dependent manner both at functional, mRNA and protein levels. These changes occur in parallel with a successive decrease in CBF. Thus, there is a temporal correlation between the changes in receptor expression and CBF reduction, suggesting a linkage.