Figure 3.
NA contracts capillary pericytes via activation of α2 adrenergic receptors. (a) Left: time course of normalised capillary diameter at the pericyte soma in the absence or presence of the α2 receptor blocker atipamezole in acute cortical slices of P21 rats. Right: blocking α2 receptors with atipamezole had no effect on capillary diameter (n = 9 pericytes for aCSF from 6 rats; n = 4 for atipamezole from 3 rats). (b) Blocking α2 receptors with atipamezole greatly reduced the NA-evoked capillary constriction (n = 9 for NA from 6 rats; n = 4 for NA + atipamezole from 3 rats). (c) Stimulating α2 receptors with xylazine or clonidine induced a capillary constriction similar to that evoked by application of NA (aCSF 3 pericytes from 3 rats; clonidine 10 pericytes from 4 rats; xylazine 10 pericytes from 3 rats). (d) Imaging of somatosensory cortex through a cranial window in NG2-dsRed mice with penetrating arteriole (PA) and capillary pericytes indicated. (e) In vivo application of atipamezole (100 µM) to the cortical surface evoked a tonic dilation of capillaries at pericytes (n = 19 from 3 mice), and of penetrating arterioles and pial arteries (n = 7 from 3 mice) and (f) Proposed mechanism by which NA released from LC axons confers contractile tone via Gi protein-coupled α2 receptors, which lower [cAMP], thus reducing the dephosphorylation of myosin by myosin light chain phosphatase (MLCP).