ArticleAmerican journal of physiology. Cell physiology2010
Elevated Ca2+ sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed, 96 citations in OpenAlex.
- Renin-Angiotensin Signaling and Vascular Function: Insights into Health and Disease.Acta physiologica (Oxford, England) · 2026Review
- TMEM16A channel signalling microdomains in the regulation of vascular function.The Journal of physiology · 2026Review
- Experimental Models for Studying Cardiovascular Dysfunction in Metabolic Syndrome.Handbook of experimental pharmacology · 2026Review
- Arterial Myocyte Pannexin 1 Channel Controls Vascular Reactivity in Diabetic Hyperglycemia.Circulation research · 2025Article
- BK Channels in Tail Artery Vascular Smooth Muscle Cells of Normotensive (WKY) and Hypertensive (SHR) Rats Possess Similar Calcium Sensitivity But Different Responses to the Vasodilator Iloprost.International journal of molecular sciences · 2024Article
- Risk factors associated with intraoperative persistent hypotension in pancreaticoduodenectomy.World journal of gastrointestinal surgery · 2024Article
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- Mechanisms of Vascular CaHandbook of experimental pharmacology · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Spatiotemporal Control of Vascular CaCirculation research · 2022Article
- Mechanisms and physiological implications of cooperative gating of clustered ion channels.Physiological reviews · 2022Review
- Ginsenoside Rg-1 prevents elevated cytosolic CaBMC complementary medicine and therapies · 2022Article
- Functional tuning of Vascular L-type CaFrontiers in physiology · 2022Review
- Lymphatic Collecting Vessel: New Perspectives on Mechanisms of Contractile Regulation and Potential Lymphatic Contractile Pathways to Target in Obesity and Metabolic Diseases.Frontiers in pharmacology · 2022Review
- Ion channel molecular complexes in vascular smooth muscle.Frontiers in physiology · 2022Review
- The combination of dantrolene and nimodipine effectively reduces 5-HT-induced vasospasms in diabetic rats.Scientific reports · 2021Article
- The Calcium Signaling Mechanisms in Arterial Smooth Muscle and Endothelial Cells.Comprehensive Physiology · 2021Article
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- Coronary Large Conductance CaFrontiers in physiology · 2021Review
- Secondhand Smoke Exposure Impairs Ion Channel Function and Contractility of Mesenteric Arteries.Function (Oxford, England) · 2021Article
4 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
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Abstract
Ca(+) sparklets are subcellular Ca(2+) signals produced by the opening of L-type Ca(2+) channels (LTCCs). In cerebral arterial myocytes, Ca(2+) sparklet activity varies regionally, resulting in low and high activity, "persistent" Ca(2+) sparklet sites. Although increased Ca(2+) influx via LTCCs in arterial myocytes has been implicated in the chain of events contributing to vascular dysfunction during acute hyperglycemia and diabetes, the mechanisms underlying these pathological changes remain unclear. Here, we tested the hypothesis that increased Ca(2+) sparklet activity contributes to higher Ca(2+) influx in cerebral artery smooth muscle during acute hyperglycemia and in an animal model of non-insulin-dependent, type 2 diabetes: the dB/dB mouse. Consistent with this hypothesis, acute elevation of extracellular glucose from 10 to 20 mM increased the density of low activity and persistent Ca(2+) sparklet sites as well as the amplitude of LTCC currents in wild-type cerebral arterial myocytes. Furthermore, Ca(2+) sparklet activity and LTCC currents were higher in dB/dB than in control myocytes. We found that activation of PKA contributed to higher Ca(2+) sparklet activity during hyperglycemia and diabetes. In addition, we found that the interaction between PKA and the scaffolding protein A-kinase anchoring protein was critical for the activation of persistent Ca(2+) sparklets by PKA in cerebral arterial myocytes after hyperglycemia. Accordingly, PKA inhibition equalized Ca(2+) sparklet activity between dB/dB and wild-type cells. These findings suggest that hyperglycemia increases Ca(2+) influx by increasing Ca(2+) sparklet activity via a PKA-dependent pathway in cerebral arterial myocytes and contributes to vascular dysfunction during diabetes.
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