Abstract
Active nerve cells release vasodilators that increase their energy supply by dilating local blood vessels, a mechanism termed neurovascular coupling and the basis of BOLD functional neuroimaging signals. Here, we reveal a mechanism for cerebral blood flow control, a precapillary sphincter at the transition between the penetrating arteriole and first order capillary, linking blood flow in capillaries to the arteriolar inflow. The sphincters are encircled by contractile mural cells, which are capable of bidirectional control of the length and width of the enclosed vessel segment. The hemodynamic consequence is that precapillary sphincters can generate the largest changes in the cerebrovascular flow resistance of all brain vessel segments, thereby controlling capillary flow while protecting the downstream capillary bed and brain tissue from adverse pressure fluctuations. Cortical spreading depolarization constricts sphincters and causes vascular trapping of blood cells. Thus, precapillary sphincters are bottlenecks for brain capillary blood flow.
Highlights
Active nerve cells release vasodilators that increase their energy supply by dilating local blood vessels, a mechanism termed neurovascular coupling and the basis of BOLD functional neuroimaging signals
The activity-induced flow increase is based on coordinated changes in vessel diameters, which are regulated by Ca2+ fluctuations within the vascular smooth muscle cells (VSMCs) that circumscribe arteries and larger arterioles and the pericytes that ensheathe capillaries close to the PA5–8
We characterized the precapillary sphincter as a mural cell encircling an indentation of the capillary where it emerges from the penetrating arterioles (PAs)
Summary
Active nerve cells release vasodilators that increase their energy supply by dilating local blood vessels, a mechanism termed neurovascular coupling and the basis of BOLD functional neuroimaging signals. 1234567890():,; Neurovascular coupling (NVC) is the signaling mechanism that links neuronal activity to local increases in cerebral blood flow[1,2,3,4]. The activity-induced flow increase is based on coordinated changes in vessel diameters, which are regulated by Ca2+ fluctuations within the vascular smooth muscle cells (VSMCs) that circumscribe arteries and larger arterioles and the pericytes that ensheathe capillaries close to the PA5–8. We reveal the structure and function of brain precapillary sphincters, which may serve to protect capillaries from high blood pressure while preserving blood supply to all bifurcations along the PA. This study provides unequivocal structural and functional evidence of brain precapillary sphincters and examines their role in NVC and during cortical spreading depolarization (CSD)
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