Bradykinin does not mediate cutaneous active  vasodilation during heat stress in humans

Kellogg, Dean L.; Liu, Y.; McAllister, Kevin H.; Friel, Ciarán P.; Pèrgola, Pablo E.

doi:10.1152/japplphysiol.01142.2001

Cited by 28 publications

(24 citation statements)

References 28 publications

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“…The traditional view that active vasodilatation in the skin is mediated by vasoactive substances released during sudomotor activity (Fox and Hilton 1958;Fox et al 1961;Johnson 1986;Rowell 1977), has been challenged by several studies (Frewin et al 1973;Kellogg et al 1991Kellogg et al , 2002. Our finding of an ischaemia-inhibited vasodilatation in the skin concomitant with a potentiated sweating response concurs with the findings of Bini et al (1980), that in certain situations simultaneous activity in vasoconstrictor and sudomotor fibres can be observed.…”

Section: Non-thermal Local Stimuli For Regulation Of Exercise Heat Losupporting

confidence: 80%

Human temperature regulation during cycling with moderate leg ischaemia

et al. 2005

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The effect of graded ischaemia in the legs on the regulation of body temperature during steady-state exercise was investigated in seven healthy males. It was hypothesised that graded ischaemia in the working muscles increases heat storage within the muscles, which in turn potentiates sweat secretion during exercise. Blood perfusion in the working muscles was reduced by applying a supra-atmospheric pressure (+6.6 kPa) around the legs, which reduced maximal working capacity by 29%. Each subject conducted three separate test trials comprising 30 min of steady-state cycling in a supine position. Exercise with unrestricted blood flow (Control trial) was compared to ischaemic exercise conducted at an identical relative work rate (Relative trial), as well as at an identical absolute work rate (Absolute trial); the latter corresponding to a 20% increase in relative workload. The average (SD) increases in both the rectal and oesophageal temperatures during steady-state cycling was 0.3 (0.2) degrees C and did not significantly differ between the three trials. The increase in muscle temperature was similar in the Control (2.7 (0.3) degrees C) and Absolute (2.4 (0.7) degrees C) trials, but was substantially lower (P < 0.01) in the Relative trial (1.4 (0.8) degrees C). Ischaemia potentiated (P < 0.01) sweating on the forehead in the Absolute trial (24.2 (7.3) g m(-2) min(-1)) compared to the Control trial (13.4 (6.2) g m(-2) min(-1)), concomitant with an attenuated (P < 0.05) vasodilatation in the skin during exercise. It is concluded that graded ischaemia in working muscles potentiates the exercise sweating response and attenuates vasodilatation in the skin initiated by increased core temperature, effects which may be attributed to an augmented muscle metaboreflex.

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Section: Non-thermal Local Stimuli For Regulation Of Exercise Heat Losupporting

confidence: 80%

Human temperature regulation during cycling with moderate leg ischaemia

et al. 2005

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“…Previous studies measured bradykinin either in sweat or in the interstitial fluid during heat stress, which leaves open the possibility that bradykinin is formed by sweat glands but is not involved in the cutaneous vasodilation 16,19,20 . To directly assess the contribution of bradykinin to cutaneous active vasodilation, Kellogg et al 21 . blocked bradykinin B2 receptors via intradermal microdialysis infusion of a specific B2 receptor antagonist.…”

Section: Early Studies Of Human Temperature Regulation and Skin Bloodmentioning

confidence: 99%

“…blocked bradykinin B2 receptors via intradermal microdialysis infusion of a specific B2 receptor antagonist. These authors found that inhibition of B2 receptors had no effect on either the threshold or magnitude of cutaneous vasodilation 21 . The current thinking is that bradykinin formation from sweat gland activity does not contribute to cutaneous active vasodilation; however, whether some other vasodilator(s) produced from sweat gland activity effects cutaneous active vasodilation is unknown.…”

Section: Early Studies Of Human Temperature Regulation and Skin Bloodmentioning

confidence: 99%

Current concepts of active vasodilation in human skin

Wong

Hollowed

2016

Temperature

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In humans, an increase in internal core temperature elicits large increases in skin blood flow and sweating. The increase in skin blood flow serves to transfer heat via convection from the body core to the skin surface while sweating results in evaporative cooling of the skin. Cutaneous vasodilation and sudomotor activity are controlled by a sympathetic cholinergic active vasodilator system that is hypothesized to operate through a co-transmission mechanism. To date, mechanisms of cutaneous active vasodilation remain equivocal despite many years of research by several productive laboratory groups. The purpose of this review is to highlight recent advancements in the field of cutaneous active vasodilation framed in the context of some of the historical findings that laid the groundwork for our current understanding of cutaneous active vasodilation.

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“…Although we did not evaluate the sweat response, it is likely that there was a greater activation of sweat glands during heat stress at ϩ1.0°C T es than at ϩ0.6°C T es . The greater sweat gland activation could, in turn, lead to greater release of bradykinin, which would increase skin blood flow during heat stress (13), although the absence of a bradykinin effect on skin blood flow has also been reported (29). We speculate that bradykinin-mediated vasodilation was greater at ϩ1.0°C T es , counteracting the hypocapnia-induced reduction in forearm skin blood flow.…”

Section: Discussionmentioning

confidence: 78%

Effect of voluntary hypocapnic hyperventilation on cutaneous circulation in resting heated humans

Fujii

Honda

Delliaux

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Hypocapnia attenuates the sweat response normally seen in hyperthermic resting subjects, but its effect on the blood flow response in their nonglabrous skin under the same hyperthermic conditions remains unclear. In the present study, we investigated whether hypocapnia induced by voluntary hyperventilation affects the blood flow response to heat stress in the nonglabrous skin of resting humans. Nine healthy male subjects were passively heated using legs-only hot water immersion and a water-perfused suit, which caused esophageal temperature (T(es)) to increase by as much as 1.0°C. During normothermia and at +0.6°C T(es) and +1.0°C T(es), the subjects performed two voluntary 7-min hyperventilation (minute ventilation = 40 l/min) trials (hypocapnic and eucapnic) in random order. End-tidal CO(2) pressure was reduced by 23-25 torr during hypocapnic hyperventilation, but it was maintained at the spontaneous breathing level during eucapnic hyperventilation. Cutaneous blood flow was evaluated as the cutaneous red blood cell flux in the forearm (CBF(forearm)) or forehead (CBF(forehead)) and was normalized to the normothermic spontaneous breathing value. Hypocapnic hyperventilation at +0.6°C T(es) was associated with significantly reduced CBF(forearm), compared with eucapnic hyperventilation, after 5-7 min of hyperventilation (395 to 429 vs. 487 to 525% baseline, P < 0.05). No significant difference in CBF(forehead) was seen during hypocapnic hyperventilation compared with eucapnic hyperventilation at +0.6°C T(es) or +1.0°C T(es). These results suggest that in resting humans, hypocapnia achieved through voluntary hyperventilation attenuates the increase in cutaneous blood flow elicited by moderate heat stress in the nonglabrous skin of the forearm, but not the forehead.

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Bradykinin does not mediate cutaneous active vasodilation during heat stress in humans

Cited by 28 publications

References 28 publications

Human temperature regulation during cycling with moderate leg ischaemia

Human temperature regulation during cycling with moderate leg ischaemia

Current concepts of active vasodilation in human skin

Effect of voluntary hypocapnic hyperventilation on cutaneous circulation in resting heated humans

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