No independent, but an interactive, role of calcium-activated potassium channels in human cutaneous active vasodilation
Brunt VE, Fujii N, Minson CT
Journal of applied physiology (Bethesda, Md. : 1985) · 39 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- Controlled clinical trial (classified by our AI screen)
- Studied in
- People
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Heart, Lung, and Blood Institute
- Government
- NHLBI NIH HHS
- Grants
- National Heart, Lung, and Blood Institute (HL081671)
Based on 2 listed funder(s).
Publication
- Published
- 2013-08-23 · J Appl Physiol (1985) · vol. 115 · issue 9 · pp. 1290–1296
- Publisher
- American Physiological Society
- Cited
- 46 citations · more than 92% of similar papers · 3.2× the field average
- Impact
- Top 10% most cited in its field
- References
- 51 works
- Access
- Open access (repository copy)
- Research areas
- Thermoregulation and physiological responses · Heart Rate Variability and Autonomic Control · Circadian rhythm and melatonin
- Keywords
- Vasodilation, Tetraethylammonium chloride, Chemistry, Tetraethylammonium, Microdialysis, Potassium channel, Nitric oxide, Potassium, Calcium-activated potassium channel, Nitric oxide synthase, Calcium, Anesthesia, Internal medicine, Pharmacology, Endocrinology, Medicine, Biochemistry, Extracellular
- MeSH
- skin, humans, nitric oxide, tetraethylammonium, ng-nitroarginine methyl ester, potassium channels, calcium-activated, biological factors, laser-doppler flowmetry, microdialysis, regional blood flow, vasodilation, adult, female, male, nitric oxide synthase, hot temperature, young adult
3 authors
From US
- Vienna Elizabeth BruntUniversity of Oregon
- Naoto FujiiUniversity of Oregon
- Christopher Todd Minson · correspondingUniversity of Oregon
Abstract
In human cutaneous microvasculature, endothelium-derived hyperpolarizing factors (EDHFs) account for a large portion of vasodilation associated with local stimuli. Thus we sought to determine the role of EDHFs in active vasodilation (AVD) to passive heating in two protocols. Whole body heating was achieved using water-perfused suits (core temperature increase of 0.8-1.0°C), and skin blood flow was measured using laser-Doppler flowmetry. In the first protocol, four sites were perfused continuously via microdialysis with: 1) control; 2) tetraethylammonium (TEA) to block calcium-activated potassium (KCa) channels, and thus the actions of EDHFs; 3) N-nitro-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase (NOS); and 4) TEA + l-NAME (n = 8). Data are presented as percent maximal cutaneous vascular conductance (CVC). TEA had no effect on AVD (CVC during heated plateau: control 57.4 ± 4.9% vs. TEA 63.2 ± 5.2%, P = 0.27), indicating EDHFs are not obligatory. l-NAME attenuated plateau CVC to 33.7 ± 5.4% (P < 0.01 vs. control); while TEA + l-NAME augmented plateau CVC compared with l-NAME alone (49.7 ± 5.3%, P = 0.02). From these data, it appears combined blockade of EDHFs and NOS necessitates dilation through other means, possibly through inward rectifier (KIR) and/or ATP-sensitive (KATP) potassium channels. To test this second hypothesis, we measured AVD at the following sites (n = 8): 1) control, 2) l-NAME, 3) l-NAME + TEA, and 4) l-NAME + TEA + barium chloride (BaCl2; KIR and KATP blocker). The addition of BaCl2 to l-NAME + TEA reduced plateau CVC to 32.7 ± 6.6% (P = 0.02 vs. l-NAME + TEA), which did not differ from the l-NAME site. These data combined demonstrate a complex interplay between vasodilatory pathways, with cross-talk between NO, KCa channels, and KIR and/or KATP channels.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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