5-HT7R stimulation, as mediated by medial smooth muscle, results in vascular relaxation. This is true for large veins [31] and small arterioles [32] in vitro and occurs through activation of the 5-HT7R. In vivo, administration of a low dose of 5-HT causes a hypotension that can last up to a month during administration [33]. Importantly, the hypotension mediated by 5-HT is abolished in the presence of pharmacological blockade by SB269970 [34] or genetic loss of the 5-HT7R in the rat [35]. What is unknown at this point is how the 5-HT7R functions in vivo to carry out these effects. Specifically, is a subset of receptors recruited to stimulate Gs to elicit the hypotension; to stimulate -arrestin to elicit the hypotension, or is a balance of both necessary? Our published collaborative work suggests that a Gs biased, not -arrestin-biased, 5-HT7R ligand would be a beneficial type of drug to develop for treatment of elevated blood pressure (hypertension) or diseases that benefit from a lowering of blood pressure (heart failure). Thus, cardiovascular research, like CNS disorders described above, will benefit from a consortium of researchers that can gather or discover, as Dr. Morisset-Lopez, Dr. Suzenet and Dr. Watts did with serodolin, the right/best tools to answer these important questions and test important ideas.