Local and conducted vasomotor responses in isolated rat cerebral arterioles

Dietrich, Hans H.; Kajita, Yasukazu; Dacey, Ralph G.

doi:10.1152/ajpheart.1996.271.3.h1109

Cited by 90 publications

(107 citation statements)

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“…Pial arterioles may also be exposed to CO 2 released into brain tissue by intracortical arterioles and capillaries. Moreover, propagated vasomotor responses to local pH changes, initiated in parenchymal arterioles (2), may contribute to the pial vasodilator response. Thus CSF flow may not totally abolish the dilation response of pial arterioles during hypercapnia.…”

Section: Discussionmentioning

confidence: 99%

“…The intraparenchymal diffusion of metabolites released during neural activity is unlikely to be affected by topical CSF flow but may initiate vasomotor signals in nearby parenchymal vessels that propagate upstream, via gap junctions, to dilate surface vessels (2,17). Alternatively, a pressure drop due to parenchymal vasodilation may induce the myogenic relaxation (4, 16) of pial arterioles.…”

Section: Discussionmentioning

confidence: 99%

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Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

Ngai

Winn

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Ngai, Al C., and H. Richard Winn. Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites. Am J Physiol Heart Circ Physiol 282: H902-H907, 2002; 10.1152/ajpheart.00128.2001.-Pial arterioles supplying the hindlimb somatosensory cortex dilate in response to contralateral sciatic nerve stimulation. The mechanism of this pial vasodilation is not well understood. One possibility is that vasoactive metabolites released during brain activation may diffuse to subarachnoid cerebrospinal fluid (CSF) to dilate pial vessels. To test this hypothesis, we implanted closed cranial windows in rats and measured pial arteriolar dilation to sciatic nerve stimulation during constant rate superfusion of the pial surface with artificial CSF. We reason that flushing the pial surface with CSF should quickly dissipate vasoactive substances and prevent these substances from dilating pial arterioles. CSF flow (1 and 1.5 ml/min) significantly reduced pial arteriole dilation induced by 5% CO 2 inhalation, but the same flow rates did not affect dilator responses to sciatic nerve stimulation. We conclude that brain-to-CSF diffusion of vasoactive metabolites does not play a significant role in the dilation of pial arterioles during somatosensory activity. cerebral blood flow; coupling; hypercapnia CEREBRAL ACTIVATION by sensory stimulation is accompanied by adjustments of vascular resistance and blood flow in the activated region. For example, we (13) have shown that pial arterioles supplying the hindlimb somatosensory cortex dilate in response to contralateral sciatic nerve stimulation. The mechanism of this pial vasodilation remains unclear. One possibility is that neuronal activity evoked by sensory stimulation causes the release of metabolites, which may diffuse to subarachnoid cerebrospinal fluid (CSF) to dilate pial arterioles. Putative vasoactive metabolites released during cortical synaptic activity include adenosine, H ϩ , K ϩ , and nitric oxide (1, 6). A variation of this diffusion mechanism is an arteriolar-venular countercurrent scheme (5) involving 1) the release of a vasodilator substance in the brain parenchyma and 2) the transport of the vasoactive substance by the draining venules to the pial surface.The present study tested this diffusion hypothesis. We reasoned that flushing the pial surface with CSF should quickly dissipate vasoactive substances and prevent these substances from dilating pial arterioles. We also studied the effect of CSF superfusion on dilation induced by hypercapnia. Moving CSF has previously been shown to attenuate hypercapnic vasodilation of pial arterioles, presumably by washing away perivascular CO 2 released locally from the vascular compartment (9). METHODSExperimental protocols in the present study were approved by the Animal Care Committee of the University of Washington. Adult male Sprague-Dawley rats weighing between 350 and 400 g were initially anesthetized with 2% halothane. The right femoral artery was exposed and cannulated for arterial blood ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

Ngai

Winn

2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…5 In pial arterioles, prostaglandin F (PGF)2a elicited local vasoconstriction and simultaneous conducted vasodilatation. Conducted dilations to ATP and PGF2a were interpreted to be mediated via an endothelium-dependent mechanism.…”

Section: Vascular Conducted Responses In the Cerebral Microcirculationmentioning

confidence: 99%

“…2,3 It has been speculated that vascular conducted responses (VCRs) could be such a nonlocal mechanism and thereby assist in coordinating and enhancing the effects of changes in local vascular resistances in brain arteriolar networks and thereby contribute to the effective and highly dynamic distribution of blood flow to areas of the brain undergoing large changes in neuronal activity. 4,5 …”

Section: Introductionmentioning

confidence: 99%

The Vascular Conducted Response in Cerebral Blood Flow Regulation

Jensen¹,

Holstein‐Rathlou

2013

J Cereb Blood Flow Metab

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Despite recent advances in our understanding of the molecular and cellular mechanisms behind vascular conducted responses (VCRs) in systemic arterioles, we still know very little about their potential physiological and pathophysiological role in brain penetrating arterioles controlling blood flow to the deeper areas of the brain. The scope of the present review is to present an overview of the conceptual, mechanistic, and physiological role of VCRs in resistance vessels, and to discuss in detail the recent advances in our knowledge of VCRs in brain arterioles controlling cerebral blood flow. We provide a schematic view of the ion channels and intercellular communication pathways necessary for conduction of an electrical and mechanical response in the arteriolar wall, and discuss the local signaling mechanisms and cellular pathway involved in the responses to different local stimuli and in different vascular beds. Physiological modulation of VCRs, which is a rather new finding in this field, is discussed in the light of changes in plasma membrane ion channel conductance as a function of health status or disease. Finally, we discuss the possible role of VCRs in cerebrovascular function and disease as well as suggest future directions for studying VCRs in the cerebral circulation.

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“…For example, isolated penetrating arterioles are capable of reacting to changes in pH and to a number of chemicals, compounds and peptides [e.g., NO (Furchgott and Zawadzki, 1980), adenosine (Meno et al, 1993), ATP (Dietrich et al, 1996;Janigro et al, 1993), K + (Horiuchi et al, 2002;Kuffler and Potter, 1964), VIP ]. Some of these substances exert their effects selectively with luminal or abluminal application.…”

Section: Physiology Of the Pial And Penetrating Arterial Circulamentioning

confidence: 99%

Regulation of cerebral vasculature in normal and ischemic brain

et al. 2008

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In the present review, we focus on the regulation of cerebral blood flow (CBF) and cerebral vasculature in the normal and ischemic brain, with a special emphasis on the arterial microcirculation of the brain: the pial and penetrating vessels. I. BackgroundThe cerebral circulation can be divided into categories based on a number of criteria. For example, vessel size can be utilized to divide the brain circulation into the macro-circulation and the microcirculation. On the arterial side, the former begins in the neck and extends to pial arteries. The microcirculation consists of the pial and penetrating arterioles, the capillaries and the venules. Within the arterial circulation, the major function of the macro-circulation is conductance of blood whereas the principal activity of the arterial component of the microcirculation is regulation of flow. Although the capillaries and venules are a significant contributor to cerebrovascular resistance, their role in regulation of flow is minimal under physiologic conditions. In addition to size, vessel location can be used to characterize the brain circulation. Thus, the brain vasculature can be divided in relation to the parenchyma into an extrinsic and an intrinsic component. The former encompasses the large conductance vessels (i.e., the macrocirculation) plus the pial circulation, whereas the latter consists of the intracerebral circulation composed of small arterioles, capillaries and venules. Penetrating arterioles represent the transition from the extrinsic to the intrinsic system. Clearly these two systems differ in regard to a number of features, such as proximity to the parenchyma, influence of neuronal and astrocytic activity, and presence and origin of innervation. However, despite these differences, both the extrinsic and intrinsic components of the cerebral circulation have an integrated response to cerebral challenges: co-dependency is the norm under physiologic and most pathologic conditions.

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Local and conducted vasomotor responses in isolated rat cerebral arterioles

Cited by 90 publications

References 0 publications

Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

Pial arteriole dilation during somatosensory stimulation is not mediated by an increase in CSF metabolites

The Vascular Conducted Response in Cerebral Blood Flow Regulation

Regulation of cerebral vasculature in normal and ischemic brain

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