Mechanisms in CBF Control

Some of the mechanisms involved in cerebrovascular control are shown in Figure 2.12. Several of these have been referred to earlier. In addition, the level of free Ca2+ is important in determining vascular tone and arachidonate metabolism can produce prostanoids that are either vasodialators (e.g. PGI2) or vasoconstrictive (e.g. TXA2). Endothelin (ET), produced by endothelin-converting enzyme (ECE) in endothelial cells, balances the vasodilator effects of nitric oxide in a tonic matter by exerting its influences at ETA receptors in the vascular smooth muscle.

Nitric Oxide in the Regulation of Cerebral Haemodynamics37

Recent interest has focused on the role of nitric oxide (NO) in the control of cerebral haemodynamics. NO is synthesized in the brain from the amino acid L-arginine by the constitutive form of enzyme nitric oxide synthase (NOS). This form of the enzyme is calmodulin dependent and requires Ca++ and tetrahydrobiopterin for its activity and differs from the inducible form of the enzyme which is present in mononuclear blood cells and is activated by cytokines. Under basal conditions, endothelial cells synthesize NO which diffuses into the muscular layer and, via a cGMP-mediated mechanism, produces relaxation of vessels. There is strong evidence to suggest that NO exerts a tonic dilatory influence on cerebral vessels. It is important to emphasize that data on NO obtained

Figure 2.12

Mechanisms involved in the regulation of rCBF

in health and disease. The diagram shows a resistance vessel in the brain in the vicinity of a neurone and an astrocyte. E = endothelium; M = muscular layer; PGs = prostaglandins; TXA2 = thromboxane A2; ET = endothelin; ECE = endothelin-converting enzyme; ETa = ETa receptor; NO = nitric oxide; CO = carbon monoxide; DA = dopmaine. The inset box shows the detail of the vessel wall and adjacent glial cell process. See text for details.

Figure 2.12

Mechanisms involved in the regulation of rCBF

in health and disease. The diagram shows a resistance vessel in the brain in the vicinity of a neurone and an astrocyte. E = endothelium; M = muscular layer; PGs = prostaglandins; TXA2 = thromboxane A2; ET = endothelin; ECE = endothelin-converting enzyme; ETa = ETa receptor; NO = nitric oxide; CO = carbon monoxide; DA = dopmaine. The inset box shows the detail of the vessel wall and adjacent glial cell process. See text for details.

from peripheral vessels cannot always be translated to the cerebral vasculature; for example, some of the endothelium-derived relaxant factor (EDRF) activity in cerebral vessels may be due to compounds other than NO. There is growing evidence that carbon monoxide (CO) produced by heme oxygenase may be responsible for significant cerebral vasodilatation, especially when NO production is reduced.124

NO plays an important role in cerebrovascular responses to functional activation, excitatory amino acids, hypercapnia, ischaemia and subarachnoid haemorrhage. Further, it may play an important part in mediating the vasodilatation produced by volatile anaesthetic agents37 although other mechanisms, including a direct effect on the vessel wall, cannot be excluded.

Neurogenic Flow-metabolism Coupling

While the last 10 years have focused on flow-metabolism coupling being effected by a diffusible extracellular mediator, there is now accumulating evidence to suggest that dopaminergic neurones may play a major part in such events125 and, additionally, may control blood-brain barrier permeability.17

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