Impaired Inhibitory Function of Presynaptic A₁-Adenosine Receptors in SHR Mesenteric Arteries
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- Rocha-Pereira Carolina
- REQUIMTE/FARMA, Department of Drug Science, Laboratory of Pharmacology, Faculty of Pharmacy, Universidade do Porto, Portugal
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- Magdalena Arribas Silvia
- Department of Physiology, Faculty of Medicine, Universidad Autónoma de Madrid, Spain
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- Fresco Paula
- REQUIMTE/FARMA, Department of Drug Science, Laboratory of Pharmacology, Faculty of Pharmacy, Universidade do Porto, Portugal
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- Carmen González Maria
- Department of Physiology, Faculty of Medicine, Universidad Autónoma de Madrid, Spain
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- Gonçalves Jorge
- REQUIMTE/FARMA, Department of Drug Science, Laboratory of Pharmacology, Faculty of Pharmacy, Universidade do Porto, Portugal
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- Diniz Carmen
- REQUIMTE/FARMA, Department of Drug Science, Laboratory of Pharmacology, Faculty of Pharmacy, Universidade do Porto, Portugal
書誌事項
- タイトル別名
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- Impaired Inhibitory Function of Presynaptic A<sub>1</sub>-Adenosine Receptors in SHR Mesenteric Arteries
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In hypertension, vascular reactivity alterations have been attributed to numerous factors, including higher sympathetic innervation/adenosine. This study examined the modulation of adenosine receptors on vascular sympathetic nerves and their putative contribution to higher noradrenaline spillover in hypertension. We assessed adenosine receptors distribution in the adventitia through confocal microscopy, histomorphometry, and their regulatory function on electrically-evoked [3H]-noradrenaline overflow, using selective agonists/antagonists. We found that: i) A1-adenosine receptor agonist (CPA: 100 nM) inhibited tritium overflow to a lower extent in SHR (25% ± 3%, n = 14) compared to WKY (38% ± 3%, n = 14) mesenteric arteries; ii) A2A-adenosine receptor agonist (CGS 21680: 100 nM) induced a slight increase of tritium overflow that was similar in SHR (22% ± 8%, n = 8) and WKY (24% ± 5%, n = 8) mesenteric arteries; iii) A2B- and A3-adenosine receptors did not alter tritium overflow in either strain; iv) all adenosine receptors were present on mesenteric artery sympathetic nerves and/or some adventitial cells of both strains; and v) A1-adenosine receptor staining fractional area was lower in SHR than in WKY mesenteric arteries. We conclude that there is an impaired inhibitory function of vascular presynaptic A1-adenosine receptors in SHR, likely related to a reduced presence of these receptors on sympathetic innervation, which might lead to higher levels of noradrenaline in the synaptic cleft and contribute to hypertension in this strain.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 122 (2), 59-70, 2013
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680158255616
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- NII論文ID
- 10031185398
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- NII書誌ID
- AA11806667
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- COI
- 1:STN:280:DC%2BC3sjktV2itA%3D%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 024637745
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- PubMed
- 23782593
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可