Non-nociceptive capsaicin-sensitive nerve terminal stimulation allows for an original vasodilatory reflex in the human skin

Fromy, Bérengère; Ábrahám, Pierre; Saumet, J. L.

doi:10.1016/s0006-8993(98)00973-1

Cited by 90 publications

(100 citation statements)

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“…This transient pressure-induced vasodilation (PIV) appears to be a protective cutaneous response. This response was observed both on the hand in humans (5,6) and on the skin of the head in rats (7). This mechanism disappears after desensitization of primary afferents by capsaicin in animals and humans (6,7).…”

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confidence: 89%

“…This response was observed both on the hand in humans (5,6) and on the skin of the head in rats (7). This mechanism disappears after desensitization of primary afferents by capsaicin in animals and humans (6,7). Therefore, we speculated that the PIV, relying on unmyelinated afferent excitation, could be a missing link between neuropathy and foot ulcer in diabetes.…”

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confidence: 94%

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Impaired Pressure-Induced Vasodilation at the Foot in Young Adults With Type 1 Diabetes

et al. 2004

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Vascular and neurological mechanisms are both likely to be involved in foot ulcer. We recently reported a pressure-induced vasodilation (PIV), relying on unmyelinated afferent excitation. We previously found that cutaneous blood flow in response to locally applied pressure might be impaired in diabetic patients because of the combined effects of low cutaneous temperature and alterations in microcirculatory function. Therefore, we aimed to analyze whether, at a relatively high cutaneous temperature, PIV is present in type 1 diabetes and to assess endothelial-dependent vasodilation and endothelium-independent vasodilation. We measured cutaneous blood flow using laser Doppler flowmetry on the head of the first metatarsus in response to applied pressure at 5.0 mmHg/min in warm conditions (29.5 ؎ 0.2°C). Responses to iontophoresis of acetylcholine (endothelium dependent) and sodium nitroprusside (endothelium independent) were measured using laser Doppler flowmetry in the forearm. The data indicate that PIV exists at the foot level in normal subjects, whereas it was not found in diabetic patients. In diabetic patients, the nonendothelial-mediated response to sodium nitroprusside was preserved, whereas the endothelial-mediated response to acetylcholine was impaired. These findings might be relevant to the high prevalence of foot ulcer that occurs in diabetic patients. Diabetes 53: [721][722][723][724][725] 2004

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confidence: 89%

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Impaired Pressure-Induced Vasodilation at the Foot in Young Adults With Type 1 Diabetes

et al. 2004

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“…We reported a novel relationship between nerves and vessels involving neural mechanosensitivity and cutaneous vasodilation, referred to as pressure-induced vasodilation (3). The increase in cutaneous blood flow induced by local pressure application delays the occurrence of tissue ischemia, thus protecting the skin against pressure.…”

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confidence: 99%

“…The increase in cutaneous blood flow induced by local pressure application delays the occurrence of tissue ischemia, thus protecting the skin against pressure. The mechanism of pressure-induced vasodilation involves pressure sensing by specialized capsaicin sensory neurons that act at the endothelial level to synthesize and release endothelial factors, such as nitric oxide (NO) (3,4), that induce smooth muscle relaxation. Therefore, neurovascular interaction is crucial for pressure-induced vasodilation development.…”

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Aldose Reductase Pathway Inhibition Improved Vascular and C-Fiber Functions, Allowing for Pressure-Induced Vasodilation Restoration During Severe Diabetic Neuropathy

et al. 2006

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Pressure-induced vasodilation, a neurovascular mechanism relying on the interaction between mechanosensitive Cfibers and vessels, allows skin blood flow to increase in response to locally nonnociceptive applied pressure that in turn may protect against pressure ulcers. We expected that severe neuropathy would dramatically affect pressure-induced vasodilation in diabetic mice, and we aimed to determine whether pressure-induced vasodilation alteration could be reversed in 8-week diabetic mice. Control and diabetic mice received no treatment or sorbinil, an aldose reductase inhibitor, or alagebrium, an advanced glycation end product breaker, the last 2 weeks of diabetes. Laser Doppler flowmetry was used to evaluate pressureinduced vasodilation and endothelium-dependent vasodilation after iontophoretic delivery of acetylcholine (ACh). We assessed the nervous function with measurements of motor nerve conduction velocity (MNCV) as well as the C-fiber-mediated nociception threshold. Pressure-induced vasodilation, endothelial response, C-fiber threshold, and MNCV were all altered in 8-week diabetic mice. None of the treatments had a significant effect on MNCV. Although sorbinil and alagebrium both restored ACh-dependent vasodilation, sorbinil was the sole treatment to restore the C-fiber threshold as well as pressure-induced vasodilation development. Therefore, the inhibition of aldose reductase pathway by sorbinil improved vascular and C-fiber functions that allow pressure-induced vasodilation restoration that could limit neuropathic diabetic cutaneous pressure ulcers.

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“…Different mechanisms in the regulation of responses to a reduction in vessel diameter have already been proposed, although whether these mechanisms contribute to the cardiac contraction-dependent regulation of coronary flow is still an open question. For instance, cell-to-cell communication between smooth muscle and endothelium has been suggested to be essential for the release of endothelial NO elicited by agonist-induced vessel constriction (4), and compression-induced cutaneous vasodilation has been shown to be mediated by an axon reflex (5). It is tempting to speculate that multiple and functionally redundant mechanisms influence the regulation of coronary vessel diameter and consequent coronary perfusion in vivo during cardiac contraction.…”

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confidence: 99%

Mechanical compression elicits NO-dependent increases in coronary flow

Sun

Huang

Kaley

2004

American Journal of Physiology-Heart and Circulatory Physiology

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Our previous studies have demonstrated that a decrease in arteriolar diameter that causes endothelial deformation elicits the release of nitric oxide (NO). Thus we hypothesized that cardiac contraction, via deformation of coronary vessels, elicits the release of NO and increases in coronary flow. Coronary flow was measured at a constant perfusion pressure of 80 mmHg in Langendorff preparations of rat hearts. Hearts were placed in a sealed chamber surrounded with perfusion solution. The chamber pressure could be increased from 0 to 80 mmHg to generate extracardiac compression. To minimize the impact of metabolic vasodilatation and rhythmic changes in shear stress, nonbeating hearts, by perfusing the hearts with a solution containing 20 mM KCl, were used. After extracardiac compression for 10 or 20 s, coronary flow increased significantly, concurrent with an increased release of nitrite into the coronary effluent and increased phosphorylation of endothelial NO synthase in the hearts. Inhibition of NO synthesis eliminated the compression-induced increases in coronary flow. Shear stressinduced dilation could not account for this increased coronary flow. Furthermore, in isolated coronary arterioles, without intraluminal flow, the release of vascular compression elicited a NO-dependent dilation. Thus this study reveals a new mechanism that, via coronary vascular deformation, elicited by cardiac contraction, stimulates the endothelium to release NO, leading to increased coronary perfusion. endothelial deformation; nitric oxide; coronary circulation WE DEMONSTRATED PREVIOUSLY that a brief compression of single isolated mesenteric arterioles elicits an endothelium-dependent, nitric oxide (NO)-mediated dilation. Also, a unidirectional compression of cultured endothelial cells stimulates, time dependently, the release of NO from the cells (26). These studies indicate that vascular deformation coincident with endothelial deformation induced by physical forces stimulates endothelial cells to produce vasoactive substances to regulate vascular tone.Multiple mechanisms are involved in the regulation of the coronary circulation, among them cardiac metabolism (8), as well as local mechanisms including myogenic constriction (12,18,20) and flow-induced dilation (13, 23), all of which have been demonstrated to participate significantly in the control of vascular resistance. It is well known that in the coronary circulation, vessels are rhythmically compressed by contraction of the myocardium. Unlike the physical forces exerted by pulsatile pressure, in which the vessels are subjected to circumferential stretch (1), myocardial contraction provides for circumferential compression of the vessels. Thus studies aimed to evaluate the physiological significance of cardiac contraction in the regulation of the coronary circulation become of considerable interest, because they may implicate this physical force as being a factor in the local regulation of myocardial blood flow.Given that endothelial deformation caused by changes in vascular di...

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Non-nociceptive capsaicin-sensitive nerve terminal stimulation allows for an original vasodilatory reflex in the human skin

Cited by 90 publications

References 9 publications

Impaired Pressure-Induced Vasodilation at the Foot in Young Adults With Type 1 Diabetes

Impaired Pressure-Induced Vasodilation at the Foot in Young Adults With Type 1 Diabetes

Aldose Reductase Pathway Inhibition Improved Vascular and C-Fiber Functions, Allowing for Pressure-Induced Vasodilation Restoration During Severe Diabetic Neuropathy

Mechanical compression elicits NO-dependent increases in coronary flow

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