Effect of Nitric Oxide Synthase Inhibitor on Increase in Nasal Mucosal Blood Flow Induced by Sensory and Parasympathetic Nerve Stimulation in Rats

Ogawa, Fumio; Hanamitsu, Masakazu; Ayajiki, Kazuhide; Aimi, Yoshinari; Okamura, Tomio; Shimizu, Takeshi

doi:10.1177/000348941011900610

Cited by 4 publications

(2 citation statements)

References 25 publications

(3 reference statements)

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“…In the brain, activation of parasympathetic nerves evokes vasodilation and increases cerebral blood flow . In some vascular beds, parasympathetic nerves may play a minor role in vasomotor function , with no presence or functional role in other vessels .…”

Section: Innervation Of Blood Vesselsmentioning

confidence: 99%

Perivascular Innervation: A Multiplicity of Roles in Vasomotor Control and Myoendothelial Signaling

Westcott

Segal

2013

Microcirculation

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The control of vascular resistance and tissue perfusion reflect coordinated changes in the diameter of feed arteries and the arteriolar networks they supply. Against a background of myogenic tone and metabolic demand, vasoactive signals originating from perivascular sympathetic and sensory nerves are integrated with endothelium-derived signals to produce vasodilation or vasoconstriction. PVNs release adrenergic, cholinergic, peptidergic, purinergic, and nitrergic neurotransmitters that lead to SMC contraction or relaxation via their actions on SMCs, ECs, or other PVNs. ECs release autacoids that can have opposing actions on SMCs. Respective cell layers are connected directly to each other through GJs at discrete sites via MEJs projecting through holes in the IEL. Whereas studies of intercellular communication in the vascular wall have centered on endothelium-derived signals that govern SMC relaxation, attention has increasingly focused on signaling from SMCs to ECs. Thus, via MEJs, neurotransmission from PVNs can evoke distinct responses from ECs subsequent to acting on SMCs. To integrate this emerging area of investigation in light of vasomotor control, the present review synthesizes current understanding of signaling events that originate within SMCs in response to perivascular neurotransmission in light of EC feedback. Though often ignored in studies of the resistance vasculature, PVNs are integral to blood flow control and can provide a physiological stimulus for myoendothelial communication. Greater understanding of these underlying signaling events and how they may be affected by aging and disease will provide new approaches for selective therapeutic interventions.

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Section: Innervation Of Blood Vesselsmentioning

confidence: 99%

Perivascular Innervation: A Multiplicity of Roles in Vasomotor Control and Myoendothelial Signaling

Westcott

Segal

2013

Microcirculation

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“…The challenge to provide evidence for the latter forms the ambiguity regarding parasympathetic involvement in vasomotor control. While parasympathetic nerves play an active role in brain vasodilatation 36 , they may have a minute role elsewhere 34 , 37 – 40 . The lack of suitable markers to specify parasympathetic perivascular fibers adds even more complexity, and a potential reason is also the difficulty in interpreting immunological studies of parasympathetic innervation at the perivascular zone such as VIP 41 .…”

Section: Discussionmentioning

confidence: 99%

Peri-arterial Autonomic Innervation of the Human Ear

Cakmak

Cotofana

Jäger

et al. 2018

Sci Rep

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Auricular vasomotor responses are considered to be signs of clinical conditions including migraine. The mechanisms of auricular vasomotor control are still debatable. This study aimed at investigating perivascular co-transmitters of vasomotor control in the auricle. Another aim was to provide three-dimensional arterial maps of the auricle, as a proxy of periarterial autonomic innervation. Twelve paired human auricles were used to visualize the arteries following Spalteholz clearing and μ-CT-based reconstruction. Perivascular innervation staining was conducted using anti-tyrosine hydroxylase (TH), anti-neuropeptide Y (NPY), anti-vasoactive intestinal peptide (VIP) and anti-choline acetyl transferase (ChAT). The combined Spalteholz technique and μ-CT revealed a highly consistent arrangement of the auricular vasculature. The superficial temporal (STA) and posterior auricular artery (PAA) supply the helical rim arcade and arcade, with the STA mainly forming the superior and the PAA forming the middle and inferior auricular artery. Co-existence of sympathetic NPY+ and TH+ terminals mediating vasoconstriction, and VIP+ and ACh+ indicating cholinergic vasodilatation, was found in the perivascular zone. The presence of both sympathetic vasoconstriction and cholinergic co-innervation for active vasodilatation was shown in the perivascular auricular zone. Assuming that the highly-consistent vasculature gives way to these terminals, this periarterial innervation may be found spread out across the helix.

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Recent advances in research on nitrergic nerve-mediated vasodilatation

Toda

Okamura

2014

Pflugers Arch - Eur J Physiol

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Cerebral vascular resistance and blood flow were widely considered to be regulated solely by tonic innervation of vasoconstrictor adrenergic nerves. However, pieces of evidence suggesting that parasympathetic nitrergic nerve activation elicits vasodilatation in dog and monkey cerebral arteries were found in 1990. Nitric oxide (NO) as a neurotransmitter liberated from parasympathetic postganglionic neurons decreases cerebral vascular tone and resistance and increases cerebral blood flow, which overcome vasoconstrictor responses to norepinephrine liberated from adrenergic nerves. Functional roles of nitrergic vasodilator nerves are found also in peripheral vasculature, including pulmonary, renal, mesenteric, hepatic, ocular, uterine, nasal, skeletal muscle, and cutaneous arteries and veins; however, adrenergic nerve-induced vasoconstriction is evidently greater than nitrergic vasodilatation in these vasculatures. In coronary arteries, neurogenic NO-mediated vasodilatation is not clearly noted; however, vasodilatation is induced by norepinephrine released from adrenergic nerves that activates β1-adrenoceptors. Impaired actions of NO liberated from the endothelium and nitrergic neurons are suggested to participate in cerebral hypoperfusion, leading to brain dysfunction, like that in Alzheimer's disease. Nitrergic neural dysfunction participates in impaired circulation in peripheral organs and tissues and also in systemic blood pressure increase. NO and vasodilator peptides, as sensory neuromediators, are involved in neurogenic vasodilatation in the skin. Functioning of nitrergic vasodilator nerves is evidenced not only in a variety of mammals, including humans and monkeys, but also in non-mammals. The present review article includes recent advances in research on the functional importance of nitrergic nerves concerning the control of cerebral blood flow, as well as other regions, and vascular resistance. Although information is still insufficient, the nitrergic nerve histology and function in vasculatures of non-mammals are also summarized.

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Effect of Nitric Oxide Synthase Inhibitor on Increase in Nasal Mucosal Blood Flow Induced by Sensory and Parasympathetic Nerve Stimulation in Rats

Abstract: Nitric oxide released from parasympathetic nitrergic nerves may contribute to an increase in NBF in rats. The afferent impulses induced by sensory nerve stimulation may lead to an increase in mean arterial blood pressure that is partly responsible for the increase in NBF.

Cited by 4 publications

References 25 publications

Perivascular Innervation: A Multiplicity of Roles in Vasomotor Control and Myoendothelial Signaling

Perivascular Innervation: A Multiplicity of Roles in Vasomotor Control and Myoendothelial Signaling

Peri-arterial Autonomic Innervation of the Human Ear

Recent advances in research on nitrergic nerve-mediated vasodilatation

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