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Neurovascular mechanisms underlying augmented cold‐induced reflex cutaneous vasoconstriction in human hypertension

In hypertensive adults (HTN), cardiovascular risk increases disproportionately during environmental cold exposure. Despite ample evidence of dysregulated sympathetic control of the peripheral vasculature in hypertension, no studies have examined integrated neurovascular function during cold stress i... Full description

Journal Title: Journal of Physiology 01 March 2017, Vol.595(5), pp.1687-1698
Main Author: Greaney, Jody L.
Other Authors: Kenney, W. Larry , Alexander, Lacy M.
Format: Electronic Article Electronic Article
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ID: ISSN: 0022-3751 ; E-ISSN: 1469-7793 ; DOI: 10.1113/JP273487
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recordid: wj10.1113/JP273487
title: Neurovascular mechanisms underlying augmented cold‐induced reflex cutaneous vasoconstriction in human hypertension
format: Article
creator:
  • Greaney, Jody L.
  • Kenney, W. Larry
  • Alexander, Lacy M.
subjects:
  • Cold Stress
  • Skin Blood Flow
  • Sympathetic Nerve Activity
  • Vascular Sensitivity
ispartof: Journal of Physiology, 01 March 2017, Vol.595(5), pp.1687-1698
description: In hypertensive adults (HTN), cardiovascular risk increases disproportionately during environmental cold exposure. Despite ample evidence of dysregulated sympathetic control of the peripheral vasculature in hypertension, no studies have examined integrated neurovascular function during cold stress in HTN. The findings of the present study show that whole‐body cold stress elicits greater increases in sympathetic outflow directed to the cutaneous vasculature and, correspondingly, greater reductions in skin blood flow in HTN. We further demonstrate an important role for non‐adrenergic sympathetic co‐transmitters in mediating the vasoconstrictor response to cold stress in hypertension. In the context of thermoregulation and the maintenance of core temperature, sympathetically‐mediated control of the cutaneous vasculature is not only preserved, but also exaggerated in hypertension. Given the increasing prevalence of hypertension, clarifying the mechanistic underpinnings of hypertension‐induced alterations in neurovascular function during cold exposure is clinically relevant.
language:
source:
identifier: ISSN: 0022-3751 ; E-ISSN: 1469-7793 ; DOI: 10.1113/JP273487
fulltext: fulltext
issn:
  • 0022-3751
  • 00223751
  • 1469-7793
  • 14697793
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titleNeurovascular mechanisms underlying augmented cold‐induced reflex cutaneous vasoconstriction in human hypertension
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subjectCold Stress ; Skin Blood Flow ; Sympathetic Nerve Activity ; Vascular Sensitivity
descriptionIn hypertensive adults (HTN), cardiovascular risk increases disproportionately during environmental cold exposure. Despite ample evidence of dysregulated sympathetic control of the peripheral vasculature in hypertension, no studies have examined integrated neurovascular function during cold stress in HTN. The findings of the present study show that whole‐body cold stress elicits greater increases in sympathetic outflow directed to the cutaneous vasculature and, correspondingly, greater reductions in skin blood flow in HTN. We further demonstrate an important role for non‐adrenergic sympathetic co‐transmitters in mediating the vasoconstrictor response to cold stress in hypertension. In the context of thermoregulation and the maintenance of core temperature, sympathetically‐mediated control of the cutaneous vasculature is not only preserved, but also exaggerated in hypertension. Given the increasing prevalence of hypertension, clarifying the mechanistic underpinnings of hypertension‐induced alterations in neurovascular function during cold exposure is clinically relevant.
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descriptionIn hypertensive adults (HTN), cardiovascular risk increases disproportionately during environmental cold exposure. Despite ample evidence of dysregulated sympathetic control of the peripheral vasculature in hypertension, no studies have examined integrated neurovascular function during cold stress in HTN. The findings of the present study show that whole‐body cold stress elicits greater increases in sympathetic outflow directed to the cutaneous vasculature and, correspondingly, greater reductions in skin blood flow in HTN. We further demonstrate an important role for non‐adrenergic sympathetic co‐transmitters in mediating the vasoconstrictor response to cold stress in hypertension. In the context of thermoregulation and the maintenance of core temperature, sympathetically‐mediated control of the cutaneous vasculature is not only preserved, but also exaggerated in hypertension. Given the increasing prevalence of hypertension, clarifying the mechanistic underpinnings of hypertension‐induced alterations in neurovascular function during cold exposure is clinically relevant.
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abstractIn hypertensive adults (HTN), cardiovascular risk increases disproportionately during environmental cold exposure. Despite ample evidence of dysregulated sympathetic control of the peripheral vasculature in hypertension, no studies have examined integrated neurovascular function during cold stress in HTN. The findings of the present study show that whole‐body cold stress elicits greater increases in sympathetic outflow directed to the cutaneous vasculature and, correspondingly, greater reductions in skin blood flow in HTN. We further demonstrate an important role for non‐adrenergic sympathetic co‐transmitters in mediating the vasoconstrictor response to cold stress in hypertension. In the context of thermoregulation and the maintenance of core temperature, sympathetically‐mediated control of the cutaneous vasculature is not only preserved, but also exaggerated in hypertension. Given the increasing prevalence of hypertension, clarifying the mechanistic underpinnings of hypertension‐induced alterations in neurovascular function during cold exposure is clinically relevant.
doi10.1113/JP273487
orcididhttp://orcid.org/0000-0002-9855-3978
pages1687-1698
date2017-03-01