Modulation of sympathetic nerve activity by perivascular sensory nerves in the arterioles of the guinea-pig small intestine

Coffa, Francis; Kotecha, Neela

doi:10.1016/s0165-1838(99)00043-0

Cited by 19 publications

(16 citation statements)

References 30 publications

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“…A reduction in sensory nerve density with advanced age may have important consequences on integrated vasomotor control. Because perivascular sympathetic and sensory nerves exert reciprocal inhibition (Kawasaki et al 1990;Coffa & Kotecha, 1999;Kawasaki, 2002), the specific decline in sensory nerve density (Figs 5 and 6) may contribute to ageing-related increases in systemic sympathetic nerve activity (Dinenno et al 1999;Seals & Dinenno, 2004) including elevated blood pressure as shown in mice (Gros et al 2002) as well as humans (Lakatta & Levy, 2003). This interpretation is consistent with finding that deletion of the CGRP gene leads to hypertension in mice (Gangula et al 2000).…”

Section: Differential Effects Of Advanced Age On Perivascular Sympathsupporting

confidence: 52%

“…Because perivascular sympathetic and sensory nerves exert reciprocal inhibition (Kawasaki et al . ; Coffa & Kotecha, ; Kawasaki, ), the specific decline in sensory nerve density (Figs and ) may contribute to ageing‐related increases in systemic sympathetic nerve activity (Dinenno et al . ; Seals & Dinenno, ) including elevated blood pressure as shown in mice (Gros et al .…”

Section: Discussionmentioning

confidence: 99%

“…In addition to their effects on vessel diameter and tissue blood flow, PVNs may exert reciprocal negative feedback, with stimulation of either sympathetic or sensory nerves inhibiting neurotransmitter release from the other (Kawasaki et al . ; Coffa & Kotecha, ; Kawasaki, ). Thus age‐related decline in PVN function may be manifested through alterations in the activation of vascular smooth muscle cells (SMCs) and endothelial cells (ECs) and through impaired neuromodulation.…”

Section: Introductionmentioning

confidence: 99%

“…Sensory PVNs are capable of both orthodromic and antidromic signalling, thereby mediating vasodilatation in response to a range of physiological stimuli including changes in temperature, acid-base status, chemical irritation, mechanical stimulation and vasoactive agents (reviewed in Burnstock & Ralevic, 1994). In addition to their effects on vessel diameter and tissue blood flow, PVNs may exert reciprocal negative feedback, with stimulation of either sympathetic or sensory nerves inhibiting neurotransmitter release from the other (Kawasaki et al 1990;Coffa & Kotecha, 1999;Kawasaki, 2002). Thus age-related decline in PVN function may be manifested through alterations in the activation of vascular smooth muscle cells (SMCs) and endothelial cells (ECs) and through impaired neuromodulation.…”

Section: Introductionmentioning

confidence: 99%

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Depressed perivascular sensory innervation of mouse mesenteric arteries with advanced age

Boerman

Segal

2015

The Journal of Physiology

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Key pointsr The dilatory role for sensory innervation of mesenteric arteries (MAs) is impaired in Old (ß24 months) versus Young (ß4 months) mice. We investigated the nature of this impairment in isolated pressurized MAs. Abstract Vascular dysfunction and sympathetic nerve activity increase with advancing age. In the gut, blood flow is governed by perivascular sensory and sympathetic nerves but little is known of how their functional role is affected by advanced age. We tested the hypothesis that functional sensory innervation of mesenteric arteries (MAs) is impaired for Old (24 months) versus Young (4 months) C57BL/6 male mice. In cannulated pressurized MAs preconstricted 50% with noradrenaline and treated with guanethidine (to inhibit sympathetic neurotransmission), perivascular nerve stimulation (PNS) evoked dilatation in Young but not Old MAs while dilatations to ACh were not different between age groups. In Young MAs, capsaicin (to inhibit sensory neurotransmission) blocked dilatation and increased constriction during PNS. With no difference in efficacy, the EC 50 of CGRP as a vasodilator was ß6-fold greater in Old versus Young MAs. Inhibiting nitric oxide (L-NAME) and prostaglandin (indomethacin) synthesis increased CGRP EC 50 in both age groups. Endothelial denudation reduced the efficacy of dilatation to CGRP by ß30% in Old MAs yet increased this efficacy ß15% in Young MAs while all dilatations to ACh were abolished. Immunolabelling revealed reduced density of sensory (CGRP) but not sympathetic (tyrosine hydroxylase) innervation for Old versus Young MAs. Whereas the distribution of CGRP receptor proteins was similar in SMCs, RAMP1 associated with nuclear regions of endothelial cells of Old but not Young MAs. With advanced age, the loss of sensory nerve function and diminished effectiveness of CGRP as a vasodilator is multifaceted and may adversely affect splanchnic perfusion.

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Section: Differential Effects Of Advanced Age On Perivascular Sympathsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Depressed perivascular sensory innervation of mouse mesenteric arteries with advanced age

Boerman

Segal

2015

The Journal of Physiology

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“…In general, the smaller the blood vessel, the larger the purinergic component (McGrath et al, 1990). Both substance P and CGRP decreased the amplitude of neurally evoked EJPs in arterioles of guinea pig small intestine (Coffa and Kotecha, 1999), suggesting that purinergic neurotransmission can be modulated by neurotransmitter released from sensory nerves. Conversely, ATP released from sympathetic nerve varicosities acts on prejunctional adenosine receptors (after ATP breakdown) on both extrinsic sensory and submucosal vasodilator nerves to inhibit transmitter release (Lomax and Vanner, 2010).…”

Section: H Intestinal Vesselsmentioning

confidence: 91%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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Perivascular Adipose Tissue: the Sixth Man of the Cardiovascular System

Cheng

Bakar

Gollasch

et al. 2018

Cardiovasc Drugs Ther

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Perivascular adipose tissue (PVAT) refers to the local aggregate of adipose tissue surrounding the vascular tree, exhibiting phenotypes from white to brown and beige adipocytes. Although PVAT has long been regarded as simply a structural unit providing mechanical support to vasculature, it is now gaining reputation as an integral endocrine/paracrine component, in addition to the well-established modulator endothelium, in regulating vascular tone. Since the discovery of anti-contractile effect of PVAT in 1991, the use of multiple rodent models of reduced amounts of PVAT has revealed its regulatory role in vascular remodeling and cardiovascular implications, including atherosclerosis. PVAT does not only release PVAT-derived relaxing factors (PVRFs) to activate multiple subsets of endothelial and vascular smooth muscle potassium channels and anti-inflammatory signals in the vasculature, but it does also provide an interface for neuron-adipocyte interactions in the vascular wall to regulate arterial vascular tone. In this review, we outline our current understanding towards PVAT and attempt to provide hints about future studies that can sharpen the therapeutic potential of PVAT against cardiovascular diseases and their complications.

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Modulation of sympathetic nerve activity by perivascular sensory nerves in the arterioles of the guinea-pig small intestine

Cited by 19 publications

References 30 publications

Depressed perivascular sensory innervation of mouse mesenteric arteries with advanced age

Depressed perivascular sensory innervation of mouse mesenteric arteries with advanced age

Purinergic Signaling and Blood Vessels in Health and Disease

Perivascular Adipose Tissue: the Sixth Man of the Cardiovascular System

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