Neuropeptide Y Y1 receptors are involved in the vasoconstriction caused by human sympathetic nerve stimulation

Racchi, Héctor; Schliem, Aaron J; Donoso, M. Verónica; Rahmer, A; Zúñiga, Álvaro; Guzmán, Sergio; Rudolf, K; Huidobro‐Toro, J. Pablo

doi:10.1016/s0014-2999(97)00160-x

Cited by 34 publications

(23 citation statements)

References 12 publications

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“…NPY is known to mediate its pressor effects postsynaptically via Y1-receptors located on arterial vascular smooth muscle cells as has been evidenced in various species and vascular beds [34][35][36][37][38][39][40]. In accordance, in rat mesenteric arteries facilitation of adrenergic vasoconstriction induced by NPY has been demonstrated to be abolished by selective NPY Y1-receptor antagonists [41].…”

Section: Discussionmentioning

confidence: 75%

Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Wiest

Jurzik

Moleda

et al. 2006

Journal of Hepatology

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Section: Discussionmentioning

confidence: 75%

Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Wiest

Jurzik

Moleda

et al. 2006

Journal of Hepatology

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“…Vasoconstriction in response to nerve stimulation has been reported for both the human mesenteric artery and vein, although the responses were greater in the vein than in the artery [15]. The constriction was shown to be mediated by sympathetic nerves, involving NA, ATP and NPY as cotransmitters.…”

Section: Discussionmentioning

confidence: 99%

“…There are surprisingly few published morphological studies on the innervation of human vessels. However, light microscope immunohistochemical descriptions of the innervation of human mesenteric artery are available [14], and a functional study showed that the magnitude of the vasomotor response induced by perivascular nerve stimulation was larger in the vein than in the artery [15]. The purpose of this study was to investigate differences in the ultrastructural relationships of the nerves and smooth muscle in human mesenteric arteries and veins and the expression of immunomarkers for neurotransmitters commonly found in perivascular nerves that may relate to their responsiveness and to provide control information for studies of the innervation of human mesenteric vessels in inflammatory bowel disease.…”

Section: Introductionmentioning

confidence: 99%

Sympathetic Innervation of Human Mesenteric Artery and Vein

Birch

Turmaine²,

Boulos³

et al. 2008

J Vasc Res

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Background: Innervation of blood vessels shows inter-species variability. There are few studies on the innervation of human vessels; thus, healthy mesenteric vessels were studied to identify the expression of immunomarkers and the morphology of sympathetic innervation as the basis for a study of mesenteric vessels in inflammatory bowel disease. Methods and Results: Electron microscopy studies examined the relationships of nerves to smooth muscle cells. In veins, nerves were distributed throughout the medial smooth muscle coat, often in close apposition (50 nm) to smooth muscle cells. In arteries, nerves were located at the adventitial-medial border, few closer than 2,000 nm to smooth muscle cells, often with interposing connective tissue and Schwann cell processes. There was a significantly greater nerve density in veins than in arteries (227 vs. 41 mm²; p = 0.03). Immunohistochemical studies revealed the presence of sympathetic and sensory-motor nerves in arteries and veins. Conclusions: It is suggested that in humans with an upright stance, the mesenteric venous system plays a particularly important role in controlling mesenteric capacitance, which is reflected by their dense innervation. It is speculated that transmitters released from perivascular nerves supplying the human mesenteric arteries may play a long-term (trophic) role in addition to short-term signalling roles.

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“…Furthermore, when both NPY and adrenergic inhibition were combined, the cutaneous vasoconstrictor response to cooling was abolished (137), suggesting that both NPY and NE play critical additive roles in reflex cutaneous vasoconstriction. This notion is strengthened by multiple studies indicating a synergistic effect of NPY on adrenergic receptor function in a number of tissues, including human skin (48,54,66,98,115,116,135,137,155).…”

Section: Potential Loci For Deficient Skin Vasoconstriction In Agingmentioning

confidence: 99%

Sympathetic control of reflex cutaneous vasoconstriction in human aging

Greaney

Alexander

Kenney

2015

Journal of Applied Physiology

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This Synthesis highlights a series of recent studies that has systematically interrogated age-related deficits in cold-induced skin vasoconstriction. In response to cold stress, a reflex increase in sympathetic nervous system activity mediates reductions in skin blood flow. Reflex vasoconstriction during cold exposure is markedly impaired in aged skin, contributing to the relative inability of healthy older adults to maintain core temperature during mild cold stress in the absence of appropriate behavioral thermoregulation. This compromised reflex cutaneous vasoconstriction in healthy aging can occur as a result of functional deficits at multiple points along the efferent sympathetic reflex axis, including blunted sympathetic outflow directed to the skin vasculature, reduced presynaptic neurotransmitter synthesis and/or release, and altered end-organ responsiveness at several loci, in addition to potential alterations in afferent thermoreceptor function. Arguments have been made that the relative inability of aged skin to appropriately constrict is due to the aging cutaneous arterioles themselves, whereas other data point to the neural circuitry controlling those vessels. The argument presented herein provides strong evidence for impaired efferent sympathetic control of the peripheral cutaneous vasculature during whole body cold exposure as the primary mechanism responsible for attenuated vasoconstriction.

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Neuropeptide Y Y1 receptors are involved in the vasoconstriction caused by human sympathetic nerve stimulation

Cited by 34 publications

References 12 publications

Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Sympathetic Innervation of Human Mesenteric Artery and Vein

Sympathetic control of reflex cutaneous vasoconstriction in human aging

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