The studies to date on cerebrovascular receptor upregulation have been conducted primarily on males or, in some cases, **data** from males and females have been combined. It is not known whether there are sex differences in this vascular response. To address this question in human cerebral arteries, we utilized an in vitro organ culture model to evoke ischemic-like contractile receptor changes in isolated arteries from human brain. We have established that organ culture, like experimental stroke, increases cerebrovascular expression of contractile GPCRs such as 5hydroxytryptamine type 1B (5-HT 1B ), angiotensin II (Ang II) type 1 (AT 1 ) and endothelin (ET-1) type B (ET B ) receptors in the vascular smooth muscle cells (VSMCs) [11]. Organ culture is not a model for stroke per se, however it has been demonstrated to induce similar changes in vasoconstrictor responses, mRNA and protein expression of GPCRs, and intracellular Ca 2+ levels as observed after focal ischemia [15]. Therefore, organ culture is a convenient method to mimic the changes in vasoconstrictor responses to provide knowledge about vascular receptor upregulation in different tissues and insight into underlying mechanisms. Supporting this approach, the MEK1/2 inhibitor U0126 and Raf inhibitor SB-386023 attenuated upregulation of ET B receptors after organ culture in vitro [16], and after in vivo focal cerebral ischemia [13,14] and subarachnoid hemorrhage [17,18]. In these in vivo studies, attenuated vasoconstrictor responses were associated with increased global cerebral blood flow and improved neurology outcome.