Dual Action of Serotonin on Pial Arterioles &lt;i&gt;in situ&lt;/i&gt; and the Effect of Propranolol on the Response

Edvinsson, Lars; Hardebo, Jan Erik; MacKenzie, Eric T.; Stewart, Margaret

doi:10.1159/000158144

Cited by 9 publications

(4 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a similar system this increase in vascular diameter was blocked by the betaadrenergic antagonist, propranolol. 37 The evidence suggests that alpha-adrenergic receptors mediating constriction and beta-adrenergic or cholinergic receptors mediating dilation of pial arteries can be demonstrated under in vivo conditions. Also, the fact that the constrictor effect of norepinephrine is attenuated by a decrease in K + or H + concentration or increased H + concentration suggests one basis for the effect of carbon dioxide on visual symptoms in migraine described above.…”

Section: Discussionmentioning

confidence: 99%

Isoproterenol treatment of visual symptoms in migraine.

Kupersmith¹,

Hass²,

Chase³

1979

Stroke

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Isoproterenol treatment of visual symptoms in migraine.

Kupersmith¹,

Hass²,

Chase³

1979

Stroke

View full text Add to dashboard Cite

“…Although most studies reported vasoconstriction of the pial vasculature in response to serotonin, 75,76 some studies reported a tone-dependent effect. 45,77,78 Specifically, Harper and MacKenzie 77 demonstrated that small pial arterioles (<70 lm in their study), which have the highest tone within the pial microcirculation, respond with dilation to locally applied serotonin whereas larger vessels respond with constriction.…”

Section: Effects Of Blast On Cerebral Microvasculature 3149mentioning

confidence: 92%

Exposure to Blast Overpressure Impairs Cerebral Microvascular Responses and Alters Vascular and Astrocytic Structure

Abutarboush

Kawoos

et al. 2019

Journal of Neurotrauma

View full text Add to dashboard Cite

Exposure to blast overpressure may result in cerebrovascular impairment, including cerebral vasospasm. The mechanisms contributing to this vascular response are unclear. The aim of this study was to evaluate the relationship between blast and functional alterations of the cerebral microcirculation and to investigate potential underlying changes in vascular microstructure. Cerebrovascular responses were assessed in sham- and blast-exposed male rats at multiple time points from 2 h through 28 days after a single 130-kPa (18.9-psi) exposure. Pial microcirculation was assessed through a cranial window created in the parietal bone of anesthetized rats. Pial arteriolar reactivity was evaluated in vivo using hypercapnia, barium chloride, and serotonin. We found that exposure to blast leads to impairment of arteriolar reactivity >24 h after blast exposure, suggesting delayed injury mechanisms that are not simply attributed to direct mechanical deformation. Observed vascular impairment included a reduction in hypercapnia-induced vasodilation, increase in barium-induced constriction, and reversal of the serotonin effect from constriction to dilation. A reduction in vascular smooth muscle contractile proteins consistent with vascular wall proliferation was observed, as well as delayed reduction in nitric oxide synthase and increase in endothelin-1 B receptors, mainly in astrocytes. Collectively, the data show that exposure to blast results in delayed and prolonged alterations in cerebrovascular reactivity that are associated with changes in the microarchitecture of the vessel wall and astrocytes. These changes may contribute to long-term pathologies involving dysfunction of the neurovascular unit, including cerebral vasospasm.

show abstract

“…The results of the present study do, however, indicate that serotoner gic nerves may have a role to play in the regulation of LCBF under hypercapnic conditions and would be consistent with an intact serotonergic system providing a constrictor influence that moderates ce rebrovascular dilatation induced by hypercapnia. Such a limited physiological role for 5-HT would be in keeping with the constrictor influence of 5-HT being most pronounced in vessels with low tone (Edvinsson et al, 1977;Rosenblum and Nelson, 1990), as will be the case with hypercapnia.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Cerebrovascular Responsiveness to Hypercapnia following Depletion of Central Serotonergic Terminals

Kelly

Ritchie

McBean

et al. 1995

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: Serotonin-containing nerve fibres innervate cerebral blood vessels, but the source of this innervation and the physiological effects of perivascular serotonin re lease remain controversial, The purpose of the present study was to examine the effects of central serotonergic depletion upon the relationship between CBF and glucose utilization under both normo-and hypercapnic condi tions. To induce the loss of serotonergic terminals, rats were injected twice daily for 4 consecutive days with 20 mg/kg of the specific serotonergic neurotoxin methylene dioxyamphetamine (MDA). Between 4 and 6 weeks later, local CBF and glucose utilization were measured using the fully quantitative [14C]iodoantipyrine and [14C]2_ deoxyglucose auto radiographic techniques, respectively, and the efficacy of the lesioning protocol was assessed using [3H]paroxetine radio ligand binding analysis. In all animals treated with MDA, there was a significant de crease in serotonin uptake sites throughout the brain, fall ing from 223 ± 20 to 40 ± 16 fmol/mg tissue in parietal cortex, for example, although the raphe nuclei themThere is now compelling evidence that cerebral blood vessels are innervated by serotonergic neu rones arising from mesencephalic sites within the brain (Steinbusch, 198 1; Edvinsson et ai. , 1983;

show abstract

Dual Action of Serotonin on Pial Arterioles <i>in situ</i> and the Effect of Propranolol on the Response

Cited by 9 publications

References 4 publications

Isoproterenol treatment of visual symptoms in migraine.

Isoproterenol treatment of visual symptoms in migraine.

Exposure to Blast Overpressure Impairs Cerebral Microvascular Responses and Alters Vascular and Astrocytic Structure

Enhanced Cerebrovascular Responsiveness to Hypercapnia following Depletion of Central Serotonergic Terminals

Contact Info

Product

Resources

About