Regulation of Cerebral Microcirculation. Update.

Abstract

Abstract. The present symposium during Brain 99 was convened to explore the current aspects of the neural (extrinsic and intrinsic) and chemical control of the microvasculature in the brain with specific relevance to stimuli and rapid flow responses. N. Suzuki demonstrated the presence of neurokinin-1 receptors along the axons of vasoactive intestinal polypeptide-containing cerebrovascular para sympathetic nerves. Since the receptors were activated by substance P, calcitonin gene-related peptide and neurokinin released from coexisting sensory nerve fibers, the parasympathetic (vasodilating) fibers could effect rapid local flow increases. N. Suzuki, however, considered this as part of an elaborate de fensive network protecting the brain from invasions by noxious substances. E. Hamel discussed the responses of the microvessels to neurotransmitters and suggested that nitric oxide (NO) released from intrinsic neurons may serve as a relay in the flow activation responses by intracerebral cholinergic fi bers originating in the basal forebrain nuclei. D. Busija summarized a vasodilating system of activated N-methyl-D-asparate receptors located on neurons involving Ca influx-NO production, and activated ATP-sensitive potassium channels located in the vascular system. According to Busija, such inter actions were disrupted during hypoxia and ischemia due to cyclooxygenase-derived superoxide anion. M. Lauritzen observed a 10 times larger increase in blood flow on stimulation of the climbing nerve as compared with that following the parallel nerve stimulation. The former transmitters are considered by him to be NO and K, and the latter NO and adenosine. Each speaker singled out NO as a common mediator for the microvasculature in the rapid local flow increases. (Keio J Med 49 (1): 26-34, March 2000)

Intracallosal neuronal nitric oxide synthase neurons colocalize with neurokinin 1 substance P receptor in the rat

“…Therefore, intracallosal blood vessels could be regulated primarily by neighboring neuronal elements (intracallosal neurons) and then by an integrated vascular mechanism, as proposed for other vascular beds in the CNS (Tomita et al, ). How and when intravascular SP gains access to intracallosal perivascular nNOS/NK1 neurons to induce NO release remains to be determined.…”

Vascular remodeling after ischemic stroke: Mechanisms and therapeutic potentials

“…Stimulation of the sphenopalatine ganglion increases intracranial blood flow and induces vasodilation through the parasympathetic innervation in the intracranial blood vessels (Suzuki et al, 1991, Tomita et al, 2000, Ayajiki et al, 2005, Yarnitsky et al, 2005). Data in experimental models of stroke have demonstrated that stimulation of this ganglion increased blood flow, reduced infarct volume and improved functional outcomes (Henninger and Fisher, 2007, Bar-Shir et al, 2010).…”

Prostaglandin H Synthase and Vascular Function

“…For example, nitric oxide is a potent vasodilator of the cerebral circulation, but it has been hypothesized that this vasodilatory pathway is disrupted during ischemia as a result of PGHS-derived superoxide anions. 126 Further studies are necessary to decipher the complexity of these systems.…”