ArticleActa pharmacologica Sinica2009
Alpha(1D)-adrenergic receptor insensitivity is associated with alterations in its expression and distribution in cultured vascular myocytes.
Article in Acta pharmacologica Sinica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
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- Arterial relaxation is coupled to inhibition of mitochondrial fission in arterial smooth muscle cells: comparison of vasorelaxant effects of verapamil and phentolamine.Acta pharmaceutica Sinica. B · 2017Article
- Endogenous N-terminal Domain Cleavage Modulates α1D-Adrenergic Receptor Pharmacodynamics.The Journal of biological chemistry · 2016Article
- Bladder smooth muscle organ culture preparation maintains the contractile phenotype.American journal of physiology. Renal physiology · 2012Article
- Alpha-dystrobrevin-1 recruits alpha-catulin to the alpha1D-adrenergic receptor/dystrophin-associated protein complex signalosome.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimIt is unclear why alpha(1D)-adrenergic receptors (alpha(1D)-ARs) play a critical role in the mediation of peripheral vascular resistance and blood pressure in situ but function inefficiently when studied in vitro. The present study examined the causes for these inconsistencies in native alpha(1)-adrenergic functional performance between the vascular smooth muscle and myocytes.
methodsThe alpha(1)-adrenergic mediated contraction, Ca(2+) signaling and the subcellular receptor distribution were evaluated using the Fluo-4, BODIPY-FL prazosin and subtype-specific antibodies.
resultsRat aortic rings and freshly dissociated myocytes displayed contractile and increased intracellular Ca(2+) responses to stimulation with phenylephrine (PE, 10 micromol), respectively. However, the PE-induced responses disappeared completely in cultured aortic myocytes, whereas PE-enhanced Ca(2+) transients were seen in cultured rat cardiac myocytes. Further studies indicated that alpha(1D)-ARs, the major receptor subtype responsible for the alpha(1)-adrenergic regulation of aortic contraction, were distributed both intracellularly and at the cell membrane in freshly dispersed aortic myocytes, similar to the alpha(1A)-AR subcellular localization in the cultured cardiomyocytes. In the cultured aortic myocytes, however, in addition to a marked decrease in their protein expression relative to the aorta, most labeling signals for alpha(1D)-ARs were found in the cytoplasm. Importantly, treating the culture medium with charcoal/dextran caused the reappearance of alpha(1D)-ARs at the cell surface and a partial restoration of the Ca(2+) signal response to PE in approximately 30% of the cultured cells.
conclusionReduction in alpha(1D)-AR total protein expression and disappearance from the cell surface contribute to the insensitivity of cultured vascular smooth muscle cells to alpha(1)-adrenergic receptor activation.
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