Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Effects of neuropeptides of the vasopressin family on Cl(-) secretion have not yet been reported in lung. Using the 16HBE14o- bronchial epithelial cell line, we investigated their action on Cl(-) secretion. 2. In symmetrical Cl(-) solutions, basolateral application of arginine vasotocin (AVT), oxytocin or isotocin induced a transient I(sc) stimulation (I(peak)), whereas arginine vasopressin (AVP) did not. The effects of different Cl(-) channel blockers and of a protein kinase C (PKC) inhibitor suggest that CFTR is involved in I(peak). The calcium-activated K(+) channel (SK4) and the Cl(-)/HCO(-)(3) exchanger favor the driving force for AVT-mediated Cl(-) secretion. The antagonists of V1a (SR49059)- and V1b (SSR149415)-receptors blocked I(peak), while SR121463B, a V2 receptor antagonist, did not. These results point to the stimulation of a V1-like receptor mediating I(peak) and presenting an efficacy order, AVT>oxytocin>isotocin>>AVP. 3. When a serosal to mucosal Cl(-) gradient was applied, AVT and AVP both stimulated I(sc) according to a biphasic profile, I(peak) being followed by a plateau phase (I(plateau)). The pharmacology of I(plateau) suggests that CFTR channels are involved and that Na(+)/K(+)/2Cl(-) is the only transporter associated with I(plateau). dDAVP, a V2 receptor agonist-induced I(plateau) with the same potency as AVP, suggesting the involvement of V2 receptors in the AVP-induced I(plateau). V2 receptors are present on both opposite membranes, while V1-like receptors are mainly expressed on the basolateral membranes. RT-PCR experiments show the expression of V1a, V1b, V2 and vasopressin-activated calcium-mobilizing (VACM) receptors mRNAs.
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PMID:Vasotocin and vasopressin stimulation of the chloride secretion in the human bronchial epithelial cell line, 16HBE14o-. 1568 10

We address advances in the understanding of myometrial physiology, focusing on excitation and the effects of gestation on ion channels and their relevance to labor. This review moves through pioneering studies to exciting new findings. We begin with the myometrium and its myocytes and describe how excitation might initiate and spread in this myogenic smooth muscle. We then review each of the ion channels in the myometrium: L- and T-type Ca2+ channels, KATP (Kir6) channels, voltage-dependent K channels (Kv4, Kv7, and Kv11), twin-pore domain K channels (TASK, TREK), inward rectifier Kir7.1, Ca2+-activated K+ channels with large (KCNMA1, Slo1), small (KCNN1-3), and intermediate (KCNN4) conductance, Na-activated K channels (Slo2), voltage-gated (SCN) Na+ and Na+ leak channels, nonselective (NALCN) channels, the Na K-ATPase, and hyperpolarization-activated cation channels. We finish by assessing how three key hormones- oxytocin, estrogen, and progesterone-modulate and integrate excitability throughout gestation. Expected final online publication date for the Annual Review of Physiology, Volume 83 is February 10, 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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PMID:Uterine Excitability and Ion Channels and Their Changes with Gestation and Hormonal Environment. 3315 76