Expression of endothelial nitric oxide synthase in human eccrine clear cells

Shimizu, Yoshinori; Sakai, Masao; Umemura, Yoshiki; Ueda, Hiroshi

doi:10.1046/j.1365-2133.1997.d01-1237.x

Cited by 15 publications

(13 citation statements)

References 15 publications

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“…28,29 We found iNOS and NT reactivity in eccrine glands both in leprosy lesions and in control skin, which indicate that iNOS and NT expression is not specific for leprosy. Eccrine glands have previously been shown to be positive for neuronal nitric oxide synthase (nNOS) 30 and endothelial nitric oxide synthase (eNOS), 31 depending on the method of fixation. Interestingly, in an AFB-positive nerve biopsy from a BT/RR patient we found strong NT reactivity in the macrophages and fusiform cells surrounding and infiltrating the nerve.…”

Section: Discussionmentioning

confidence: 99%

Expression of inducible nitric oxide synthase and nitrotyrosine in borderline leprosy lesions.

et al. 2001

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Section: Discussionmentioning

confidence: 99%

Expression of inducible nitric oxide synthase and nitrotyrosine in borderline leprosy lesions.

et al. 2001

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“…eNOS is present in the sweat glands. Interestingly, eNOS-immunoreactive cells coincided with clear cells in the eccrine secretory gland (57). NO is associated with Cav-activated K+ channels in various cell types such as human dermal papilla cells (58), bovine aortic smooth muscle cells (59), porcine coronary artery smooth muscle cells (60), rabbit cerebral artery smooth muscle cells (61) and guinea pig vascular and tracheal smooth muscle cells (62).…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Localization of Nitric Oxide Synthase in Normal Human Skin: Expression of Endothelial‐type and Inducible‐type Nitric Oxide Synthase in Keratinocytes

Shimizu

Sakai

Umemura

et al. 1997

The Journal of Dermatology

105

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Nitric oxide (NO) is a critical mediator of various biological functions. NO is generated from L-arginine by nitric oxide synthase (NOS), which has three isoforms; endothelial-type NOS (eNOS) and brain-type NOS (bNOS) are constitutive enzymes, and inducible-type NOS (iNOS) is expressed after stimulation. We investigated the expression of NOS in normal human skin by an immunohistochemical technique and western blotting analysis. In human skin, epidermal keratinocytes and the outer root sheath were labeled with not only eNOS antibody but also with iNOS antibody. Both eNOS and iNOS protein in epidermal keratinocytes were confirmed by western blotting. eNOS immunoreactivity was observed in endothelial cells, fibroblasts, the arrector pili muscle, apocrine secretory gland, eccrine coiled duct, and eccrine secretory gland. bNOS immunoreactivity was observed in mast cells. No staining with anti-bNOS antibody was observed in any other cell type. Our present findings suggest that epidermal keratinocytes in normal human skin contain both eNOS and iNOS.

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“…Since COX-derived prostanoids can increase cAMP (O'Keefe et al 1992;Smyth et al 2009), it is plausible that COX may contribute to the β-adrenergic sweating. In addition, NOS in sweat glands (Shimizu et al 1997) may be stimulated by β-adrenergic receptor activation, as observed in the above-mentioned studies using human conduit artery (Cardillo et al 1997;Casey et al 2011), and this ultimately would induce an increase in cGMP. However, an earlier study reported that elevations in cGMP did not directly increase sweat rate in eccrine sweat glands of the monkey palm under in vitro conditions (Sato & Sato, 1984a).…”

Section: Introductionmentioning

confidence: 88%

Nitric oxide synthase and cyclooxygenase modulate β‐adrenergic cutaneous vasodilatation and sweating in young men

Fujii

McNeely

Kenny

2016

The Journal of Physiology

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Key pointsr β-Adrenergic receptor agonists such as isoproterenol induce cutaneous vasodilatation and sweating in humans, but the mechanisms underpinning this response remain unresolved.r Using intradermal microdialysis, we evaluated the roles of nitric oxide synthase (NOS) and cyclooxygenase (COX) in β-adrenergic cutaneous vasodilatation and sweating elicited by administration of isoproterenol.r We show that while NOS contributes to β-adrenergic cutaneous vasodilatation, COX restricts cutaneous vasodilatation.r We also show that combined inhibition of NOS and COX augments β-adrenergic sweating r These new findings advance our basic knowledge regarding the physiological control of cutaneous blood flow and sweating, and provide important and new information to better understand the physiological significance of β-adrenergic receptors in the skin.Abstract β-Adrenergic receptor agonists such as isoproterenol can induce cutaneous vasodilatation and sweating in humans, but the mechanisms underpinning this response remain unresolved. We evaluated the hypotheses that (1) nitric oxide synthase (NOS) contributes to β-adrenergic cutaneous vasodilatation, whereas cyclooxygenase (COX) limits the vasodilatation, and (2) COX contributes to β-adrenergic sweating. In 10 young males (25 ± 5 years), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm skin sites infused with (1) lactated Ringer solution (control), (2) 10 mM N ω -nitro-L-arginine (L-NNA), a non-specific NOS inhibitor, (3) 10 mM ketorolac, a non-specific COX inhibitor, or (4) a combination of L-NNA and ketorolac. All sites were co-administered with a high dose of isoproterenol (100 μM) for 3 min to maximally induce β-adrenergic sweating (β-adrenergic sweating is significantly blunted by subsequent activations). Approximately 60 min after the washout period, three incremental doses of isoproterenol were co-administered (1, 10 and 100 μM each for 25 min). Increases in CVC induced by the first and second 100 μM isoproterenol were attenuated by L-NNA alone, and those in response to all doses of isoproterenol were reduced by L-NNA with co-infusion of ketorolac (all P ࣘ 0.05). Ketorolac alone augmented increases in CVC induced by 10 μM and by the second 100 μM isoproterenol (both P ࣘ 0.05). While isoproterenol-induced sweating was not affected by the separate administration of L-NNA or ketorolac (all P > 0.05), their combined administration augmented sweating elicited by the first 3 min of 100 μM isoproterenol (P = 0.05). We show that while NOS contributes to β-adrenergic cutaneous vasodilatation, COX restrains the vasodilatation. Finally, combined inhibition of NOS and COX augments β-adrenergic sweating.

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Expression of endothelial nitric oxide synthase in human eccrine clear cells

Cited by 15 publications

References 15 publications

Expression of inducible nitric oxide synthase and nitrotyrosine in borderline leprosy lesions.

Expression of inducible nitric oxide synthase and nitrotyrosine in borderline leprosy lesions.

Immunohistochemical Localization of Nitric Oxide Synthase in Normal Human Skin: Expression of Endothelial‐type and Inducible‐type Nitric Oxide Synthase in Keratinocytes

Nitric oxide synthase and cyclooxygenase modulate β‐adrenergic cutaneous vasodilatation and sweating in young men

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