ArticlePharmacological research2012
Impaired β-adrenoceptor-induced relaxation in small mesenteric arteries from DOCA-salt hypertensive rats is due to reduced K(Ca) channel activity.
Article in Pharmacological research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- A KBiomolecules · 2026Article
- The renal vasodilatation from β-adrenergic activation in vivo in rats is not driven by KExperimental physiology · 2024Article
- Mechanisms underlying suppression of noradrenaline-induced contraction by prolonged treatment with advanced glycation end-products in organ-cultured rat carotid artery.Pflugers Archiv : European journal of physiology · 2020Article
- Role of the endothelial caveolae microdomain in shear stress-mediated coronary vasorelaxation.The Journal of biological chemistry · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Kv7 Channel Activation Underpins EPAC-Dependent Relaxations of Rat Arteries.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Overview of Antagonists Used for Determining the Mechanisms of Action Employed by Potential Vasodilators with Their Suggested Signaling Pathways.Molecules (Basel, Switzerland) · 2016Review
- Inhibition of TLR4 attenuates vascular dysfunction and oxidative stress in diabetic rats.Journal of molecular medicine (Berlin, Germany) · 2015Article
- BK Channels in Cardiovascular Diseases and Aging.Aging and disease · 2013Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
β-Adrenoceptor (β-AR)-mediated relaxation plays an important role in the regulation of vascular tone. β-AR-mediated vascular relaxation is reduced in various disease states and aging. We hypothesized that β-AR-mediated vasodilatation is impaired in DOCA-salt hypertension due to alterations in the cAMP pathway. β-AR-mediated relaxation was determined in small mesenteric arteries from DOCA-salt hypertensive and control uninephrectomized (Uni) rats. To exclude nitric oxide (NO) and cyclooxygenase (COX) pathways, relaxation responses were determined in the presence of l-NNA and indomethacin, NO synthase inhibitor and COX inhibitors, respectively. Isoprenaline (ISO)-induced relaxation was reduced in arteries from DOCA-salt compared to Uni rats. Protein kinase A (PKA) inhibitors (H89 or Rp-cAMPS) or adenylyl cyclase inhibitor (SQ22536) did not abolish the difference in ISO-induced relaxation between the groups. Forskolin (adenylyl cyclase activator)-induced relaxation was similar between the groups. The inhibition of IK(Ca)/SK(Ca) channels (TRAM-34 plus UCL1684) or BK(Ca) channels (iberiotoxin) reduced ISO-induced relaxation only in Uni rats and abolished the relaxation differences between the groups. The expression of SK(Ca) channel was decreased in DOCA-salt arteries. The expression of BK(Ca) channel α subunit was increased whereas the expression of BK(Ca) channel β subunit was decreased in DOCA-salt arteries. The expression of receptor for activated C kinase 1 (RACK1), which is a binding protein for BK(Ca) channel and negatively modulates its activity, was increased in DOCA-salt arteries. These results suggest that the impairment of β-AR-mediated relaxation in DOCA-salt mesenteric arteries may be attributable to altered IK(Ca)/SK(Ca) and/or BK(Ca) channels activities rather than cAMP/PKA pathway. Impaired β-AR-stimulated BK(Ca) channel activity may be due to the imbalance between its subunit expressions and RACK1 upregulation.
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