ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010
beta-Adrenergic activation of electrogenic K+ and Cl- secretion in guinea pig distal colonic epithelium proceeds via separate cAMP signaling pathways.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Role of brain-gut-muscle axis in human health and energy homeostasis.Frontiers in nutrition · 2022Review
- Effect of Soluble Adenylyl Cyclase (ADCY10) Inhibitors on the LH-Stimulated cAMP Synthesis in Mltc-1 Leydig Cell Line.International journal of molecular sciences · 2021Article
- The functional association between the sodium/bicarbonate cotransporter (NBC) and the soluble adenylyl cyclase (sAC) modulates cardiac contractility.Pflugers Archiv : European journal of physiology · 2020Article
- Segmental differences in ion transport in rat cecum.Pflugers Archiv : European journal of physiology · 2019Article
- Pharmacological modulation of the COPharmacology & therapeutics · 2018Review
- Intracellular cAMP Sensor EPAC: Physiology, Pathophysiology, and Therapeutics Development.Physiological reviews · 2018Review
- Endocrinology and the brain: corticotropin-releasing hormone signaling.Endocrine connections · 2017Review
- Pilot study of small bowel mucosal gene expression in patients with irritable bowel syndrome with diarrhea.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Different cAMP sources are critically involved in G protein-coupled receptor CRHR1 signaling.The Journal of cell biology · 2016Article
- Glucose-dependent insulinotropic polypeptide-mediated signaling pathways enhance apical PepT1 expression in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Hydrogen peroxide stimulation of CFTR reveals an Epac-mediated, soluble AC-dependent cAMP amplification pathway common to GPCR signalling.British journal of pharmacology · 2015Article
- The role of soluble adenylyl cyclase in neurite outgrowth.Biochimica et biophysica acta · 2014Review
- Pharmacological distinction between soluble and transmembrane adenylyl cyclases.The Journal of pharmacology and experimental therapeutics · 2013Article
- cAMP-stimulated Cl- secretion is increased by glucocorticoids and inhibited by bumetanide in semicircular canal duct epithelium.BMC physiology · 2013Article
- Dual activation of CFTR and CLCN2 by lubiprostone in murine nasal epithelia.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Role of the BK channel (KCa1.1) during activation of electrogenic K+ secretion in guinea pig distal colon.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Activation of soluble adenylyl cyclase protects against secretagogue stimulated zymogen activation in rat pancreaic acinar cells.PloS one · 2012Article
- Intracellular cAMP signaling by soluble adenylyl cyclase.Kidney international · 2011Review
- Activation of the basolateral membrane Cl- conductance essential for electrogenic K+ secretion suppresses electrogenic Cl- secretion.Experimental physiology · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Adrenergic stimulation of isolated guinea pig distal colonic mucosa produced transient Cl(-) and sustained K(+) secretion. Transient short-circuit current (I(sc)) depended on beta(2)-adrenergic receptors (beta(2)-AdrR), and sustained I(sc) relies on a beta(1)-AdrR/beta(2)-AdrR complex. Epinephrine (epi) increased cAMP content with a biphasic time course similar to changes in epi-activated I(sc) ((epi)I(sc)). Inhibition of transmembrane adenylyl cyclases (tmACs) reduced peak (epi)I(sc) and cAMP to near zero without decreasing sustained (epi)I(sc), consistent with cAMP from tmAC signaling for only Cl(-) secretion. Inhibition of soluble adenylyl cyclase (sAC) reduced sustained (epi)I(sc) and cAMP to near zero without decreasing peak (epi)I(sc) or cAMP, consistent with cAMP from sAC signaling for K(+) secretion. Sensitivity to phosphodiesterase (PDE) inhibitors and peptide YY (PYY) stimulation further supported separate signaling for the two components. PDE3 or PDE4 inhibitors enhanced peak (epi)I(sc) but not sustained (epi)I(sc), consistent with these PDEs as part of the beta(2)-AdrR signaling domain. PYY suppressed peak (epi)I(sc) in a pertussis toxin (PTx)-sensitive manner, supporting Galpha(i)-dependent inhibition of tmACs producing cAMP for Cl(-) secretion. Since PYY or PTx did not alter sustained (epi)I(sc), signaling for K(+) secretion occurred via a Galpha(i)-independent mechanism. Presence of multiple sAC variants in colonic epithelial cells was supported by domain-specific antibodies. Responses to specific activators and inhibitors suggested that protein kinase A was not involved in activating peak or sustained components of (epi)I(sc), but the cAMP-dependent guanine nucleotide exchange factor, Epac, may contribute. Thus beta-adrenergic activation of electrogenic Cl(-) and K(+) secretion, respectively, required tmAC- and sAC-dependent signaling pathways.
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