ArticleThe Journal of physiology2002
Growth hormone-releasing peptide-2 reduces inward rectifying K+ currents via a PKA-cAMP-mediated signalling pathway in ovine somatotropes.
Article in The Journal of physiology, 2002. 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, 17 citations in OpenAlex.
- Cantú syndrome resulting from activating mutation in the KCNJ8 gene.Human mutation · 2014Article
- Inward rectifier potassium (Kir) current in dopaminergic periglomerular neurons of the mouse olfactory bulb.Frontiers in cellular neuroscience · 2014Article
- Potassium Current Is Not Affected by Long-Term Exposure to Ghrelin or GHRP-6 in Somatotropes GC Cells.Journal of biophysics (Hindawi Publishing Corporation : Online) · 2013Article
- Dependence of the excitability of pituitary cells on cyclic nucleotides.Journal of neuroendocrinology · 2012Review
- Ion channels and signaling in the pituitary gland.Endocrine reviews · 2010Review
- Integrating GHS into the Ghrelin System.International journal of peptides · 2010Article
- Ghrelin reduces voltage-gated potassium currents in GH3 cells via cyclic GMP pathways.Endocrine · 2005Article
- Review
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Inward-rectifying potassium (Kir) channels are essential for maintaining the resting membrane potential near the K(+) equilibrium and they are responsible for hyperpolarisation-induced K(+) influx. We characterised the Kir current in primary cultured ovine somatotropes and examined the effect of growth hormone-releasing peptide-2 (GHRP-2) on this current and its related intracellular signalling pathways. The Kir current was, in most cases, isolated using nystatin-perforated patch-clamp techniques. In bath solution containing 5 mM K(+), the Kir current was composed of both transient (fast activated) and delayed (slowly activated) components. An increase in the external K(+) concentration from 5 to 25 mM induced an augmentation of approximately 4-fold in the delayed part of the Kir current and both BaCl(2) and CsCl dose-dependently inhibited this current, confirming the presence of the Kir current in ovine somatotropes. Moreover, this specific effect of high K(+) on the Kir current was only observed in the cells that showed positive staining with anti-growth hormone (GH) antibodies, or in GC cells that belong to a rat somatotrope cell line. Application of GHRP-2 (100 nM) reversibly and significantly reduced the Kir current in bath solutions with 5 or 25 mM K(+) in ovine somatotropes. In addition, we found that the reduction in the Kir current mediated by GHRP-2 was totally abolished by the pretreatments with H89 (1 microM) or Rp-cAMP (100 microM) or by intracellular dialysis of a specific protein kinase A (PKA) inhibitory peptide PKI (10 microM). The specific PKC blocker chelerythrine (1 microM) or inhibitory peptide PKC(19-36) (10 microM) did not show any effects on the GHRP-2-induced decrease in the Kir current. These results suggest that the inhibition of Kir current through PKA-cAMP pathways may play an integral role in GHRP-2-induced depolarisation and GH release in ovine somatotropes.
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