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Takayama et al. (185) used a non-invasive laser speckle technique they have used before to show regulation of optic nerve blood flow in rabbits, and which they previously validated to correlate with a microsphere method of estimating blood flow (r2 approximately 0.35). In the present work, they raised the IOP to either 40 mmHg or 60 mmHg acutely, and after a short time returned the IOP back to 10 mmHg. The laser speckle signal remained stable (indicating that blood flow was maintained by autoregulation) when the IOP was raised to 40 mmHg, but decreased with IOP was raised to 60 mmHg. In the latter case, the signal returned to normal (with a small brief overshoot) when the IOP was returned to 10 mmHg, the overshoot presumably representing a residual altered chemical environment resulting from ischemia, which cleared fairly quickly. These events are the expected result of metabolic autoregulation in the tissue, as shown before. They also showed that these responses were attenuated and slowed in the presence of an inhibitor of L-type calcium channels, but not by inhibitors of nitric oxide synthesis, prostaglandin synthesis, or of the sympathetic nervous system. Apart from confirming that circulation is autoregulated in the optic nerve region of the rabbit, the authors conclude that blood flow regulation depends on the calcium physiology of smooth muscle cells in the circulation, but it is possible that contractile cells of the capillaries (pericytes) would behave similarly.