Cochlear blood flow regulation.
The regulation of cochlear blood flow is crucial for auditory function due to the sensitivity of this sensory organ to hypoxia. Part of the regulation of cochlear blood flow occurs in the spiral modiolar artery, which provides the main blood supply to the cochlea. Blood flow in general is most effectively regulated through the control of the vascular diameter. The vascular diameter is determined by the degree of constriction of the smooth muscle cells in the vascular wall. A constriction of the smooth muscle cells reduces the diameter of the vascular lumen and thereby decreases blood flow, whereas a relaxation of the smooth muscle cells increases blood flow. The degree of constriction of the smooth muscle cells in the spiral modiolar artery is carefully controlled and must be adjusted properly to the demands of the cochlear tissues. To achieve proper control, smooth muscle cells integrate information from various sources. Vasoconstrictors and dilators may originate from the innervation surrounding the vessel, from endothelial cells lining the vascular lumen or from the smooth muscle cells themselves. Recent advances revealed that smooth muscle cells from different arterioles differ widely in their endowment with mechanisms that regulate the degree of smooth muscle cell tone. Signal transduction mechanisms, which mediate these neurogenic, local and paracrine regulations of smooth muscle contractility are now beginning to be understood. This report reviews recently obtained evidence for adrenergic regulation of cochlear blood flow and then focuses on a novel vasodilation mechanism that involves ryanodine receptors, Ca2+ sparks and the activation of Ca2+-activated K+ channels.
Wangemann
Philine
P
Anatomy and Physiology Department, Kansas State University, Manhattan 66506, USA. wange@vet.ksu.edu
D015220:Calcium Channels / Q000378:metabolism; D003051:Cochlea / Q000098:blood supply* / Q000378:metabolism; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000098:blood supply / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D011941:Receptors, Adrenergic / Q000378:metabolism; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D013233:Stellate Ganglion / Q000378:metabolism
D015220:Calcium Channels; D015221:Potassium Channels; D011941:Receptors, Adrenergic; D019837:Ryanodine Receptor Calcium Release Channel