ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Interactions between adenosine and K+ channel-related pathways in the coupling of somatosensory activation and pial arteriolar dilation.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Protein kinase Cδ and pharmacomechanical coupling: Re-envisioning cerebral vascular control.The Journal of physiology · 2026Article
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- Connexin and Pannexin Large-Pore Channels in Microcirculation and Neurovascular Coupling Function.International journal of molecular sciences · 2022Review
- Genetic factors for susceptibility to and manifestations of neuromyelitis optica.Annals of clinical and translational neurology · 2020Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Impairment of neurovascular coupling in Type 1 Diabetes Mellitus in rats is prevented by pancreatic islet transplantation and reversed by a semi-selective PKC inhibitor.Brain research · 2017Article
- Potassium Channels in Regulation of Vascular Smooth Muscle Contraction and Growth.Advances in pharmacology (San Diego, Calif.) · 2017Review
- BK Channels in the Central Nervous System.International review of neurobiology · 2016Review
- Neurovascular signaling in the brain and the pathological consequences of hypertension.American journal of physiology. Heart and circulatory physiology · 2014Review
- Astrocyte regulation of cerebral vascular tone.American journal of physiology. Heart and circulatory physiology · 2013Review
- Cellular signalling pathways mediating dilation of porcine pial arterioles to adenosine A₂A receptor activation.Cardiovascular research · 2013Article
- Impairment of neurovascular coupling in type 1 diabetes mellitus in rats is linked to PKC modulation of BK(Ca) and Kir channels.American journal of physiology. Heart and circulatory physiology · 2012Article
- Relative contribution of cyclooxygenases, epoxyeicosatrienoic acids, and pH to the cerebral blood flow response to vibrissal stimulation.American journal of physiology. Heart and circulatory physiology · 2012Article
- An emerging role for adenosine and its receptors in bone homeostasis.Frontiers in endocrinology · 2012Article
- ATP hydrolysis pathways and their contributions to pial arteriolar dilation in rats.American journal of physiology. Heart and circulatory physiology · 2011Article
- Purinergic mechanisms in gliovascular coupling.Seminars in cell & developmental biology · 2011Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Multiple, perhaps interactive, mechanisms participate in the linkage between increased neural activity and cerebral vasodilation. In the present study, we assessed whether neural activation-related pial arteriolar dilation (PAD) involved interactions among adenosine (Ado) A(2) receptors (A(2)Rs), large-conductance Ca(2+)-operated K(+) (BK(Ca)) channels, and inward rectifier K(+) (K(ir)) channels. In rats with closed cranial windows, we monitored sciatic nerve stimulation (SNS)-induced PAD in the absence or presence of pharmacological blockade of A(2)Rs (ZM-241385), ecto-5'-nucleotidase (α,β-methylene-adenosine diphosphate), BK(Ca) channels (paxilline), and K(ir) channels (BaCl(2)). Individually, these interventions led to 53-66% reductions in SNS-induced PADs. Combined applications of these blockers led to little or no further repression of SNS-induced PADs, suggesting interactions among A(2)Rs and K(+) channels. In the absence of SNS, BaCl(2) blockade of K(ir) channels produced 52-80% reductions in Ado and NS-1619 (BK(Ca) channel activator)-induced PADs. In contrast, paxilline blockade of BK(Ca) channels was without effect on dilations elicited by KCl (K(ir) channel activator) and Ado suffusions, indicating that Ado- and NS-1619-associated PADs involved K(ir) channels. In addition, targeted ablation of the superficial glia limitans was associated with a selective 60-80% loss of NS-1619 responses, suggesting that the BK(Ca) channel participation (and paxilline sensitivity) derived largely from channels within the glia limitans. Additionally, blockade of either PKA or adenylyl cyclase caused markedly attenuated pial arteriolar responses to SNS and, in the absence of SNS, responses to Ado, KCl, and NS-1619. These findings suggested a key, possibly permissive, role for A(2)R-linked cAMP generation and PKA-induced K(+) channel phosphorylation in somatosensory activation-evoked PAD.
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