scholarly journals Mechanisms of Arginine-Vasopressin-Induced Ca2+Oscillations in β-Cells (HIT-T15): A Role for Oscillating Protein Kinase C

Endocrinology ◽  
2004 ◽  
Vol 145 (10) ◽  
pp. 4635-4644 ◽  
Author(s):  
Michael Schaefer ◽  
Harald Mischak ◽  
Susanne Schnell ◽  
Anne Griese ◽  
Roman Iakubov ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Arginine Vasopressin ◽  
Β Cells ◽  
Kinase C

scholarly journals Arginine Vasopressin Potentiates the Stimulatory Action of CRH on Pituitary Corticotropes via a Protein Kinase C–Dependent Reduction of the Background TREK-1 Current

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3661-3672 ◽  
Author(s):  
Andy K. Lee ◽  
Frederick W. Tse ◽  
Amy Tse
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Arginine Vasopressin ◽  
Underlying Mechanism ◽  
Sk Channels ◽  
Acth Secretion ◽  
Patch Clamp Technique ◽  
Stimulatory Action ◽  
Kinase C ◽  
Perforated Patch Clamp

The hypothalamic hormone arginine vasopressin (AVP) potentiates the stimulatory action of CRH on ACTH secretion from pituitary corticotropes, but the underlying mechanism is elusive. Using the perforated patch-clamp technique to monitor membrane potentials in mouse corticotropes, we found that AVP triggered a transient hyperpolarization that was followed by a sustained depolarization. The hyperpolarization was caused by intracellular Ca2+ release that in turn activated the small conductance Ca2+-activated K+ (SK) channels. The depolarization was due to the suppression of background TWIK-related K+ (TREK)-1 channels. Direct activation of protein kinase C (PKC) reduced the TREK-1 current, whereas PKC inhibition attenuated the AVP-mediated reduction of the TREK-1 current, implicating the involvement of PKC. The addition of CRH (which stimulates the protein kinase A pathway) in the presence of AVP, or vice versa, resulted in further suppression of the TREK-1 current. In corticotropes with buffered cytosolic Ca2+ concentration ([Ca2+]i), AVP evoked a sustained depolarization, and the coapplication of AVP and CRH caused a larger depolarization than that evoked by AVP or CRH alone. In cells with minimal perturbation of [Ca2+]i and background TREK-1 channels, CRH evoked a sustained depolarization that was superimposed with action potentials, and the subsequent coapplication of AVP and CRH triggered a transient hyperpolarization that was followed by a larger depolarization. In summary, AVP and CRH have additive effects on the suppression of the TREK-1 current, resulting in a more robust depolarization in corticotropes. We suggest that this mechanism contributes to the potentiating action of AVP on CRH-evoked ACTH secretion.

Arginine-Vasopressin Stimulates CRH and ACTH Release by Rat Adrenal Medulla, Acting Via the V 1 Receptor Subtype and a Protein Kinase C-Dependent Pathway

Peptides ◽  
1997 ◽  
Vol 18 (2) ◽  
pp. 191-195 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Ludwik K Malendowicz ◽  
Pierra Rebuffat ◽  
Cinzia Tortorella ◽  
Gastone G Nussdorfer
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Adrenal Medulla ◽  
Arginine Vasopressin ◽  
Receptor Subtype ◽  
Kinase C ◽  
Dependent Pathway ◽  
Acth Release

Regulation of arginine vasopressin mRNA in rat fetal hypothalamic cell culture. Role of protein kinases and glucocorticoids

1993 ◽  
Vol 10 (1) ◽  
pp. 51-57 ◽  
Author(s):  
S-B Hu ◽  
L A Tannahill ◽  
S L Lightman
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Mrna Expression ◽  
Protein Kinase A ◽  
Arginine Vasopressin ◽  
In Situ Hybridization Histochemistry ◽  
Kinase C ◽  
Kinase A

ABSTRACT Studies have been performed to investigate the regulation of arginine vasopressin (AVP) mRNA expression in fetal hypothalamic cultures. AVP mRNA-positive neurones were identified by in-situ hybridization histochemistry, and changes in mRNA expression were quantitated by nuclease protection assay. Both protein kinase C and protein kinase A activators increased the expression of AVP mRNA, in contrast to dexamethasone, which inhibited the responses to both protein kinase C and protein kinase A activation.

scholarly journals Bimodal role of conventional protein kinase C in insulin secretion from rat pancreatic β cells

2004 ◽  
Vol 561 (1) ◽  
pp. 133-147 ◽  
Author(s):  
Hui Zhang ◽  
Masahiro Nagasawa ◽  
Satoko Yamada ◽  
Hideo Mogami ◽  
Yuko Suzuki ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Kinase C

[Ca2+]i and protein kinase C in vasopressin-induced prostacyclin and ANP release in rat cardiomyocytes

1994 ◽  
Vol 266 (2) ◽  
pp. H597-H605 ◽  
Author(s):  
V. Van der Bent ◽  
D. J. Church ◽  
M. B. Vallotton ◽  
P. Meda ◽  
D. C. Kem ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Arginine Vasopressin ◽  
Cellular Responses ◽  
Rat Cardiomyocytes ◽  
Kinase C ◽  
Transient Rise ◽  
V2 Antagonist ◽  
Pkc Activation ◽  
Membranous Protein

Exposure of cultured, spontaneously beating rat cardiomyocytes to arginine vasopressin (AVP) led to marked increases in the release of prostacyclin (PGI2) and atrial natriuretic peptide (ANP). These responses were accompanied by a rapid, transient rise of cytosolic free Ca2+ concentration ([Ca2+]i) and of membranous protein kinase C (PKC) activity. Ca2+ influx and PKC activity appeared to play important but distinct roles in AVP-induced cellular responses, insofar as only AVP-induced ANP secretion was abolished by the Ca2+ channel antagonist nifedipine, whereas both AVP-induced PGI2 production and ANP release were abolished by the PKC inhibitors staurosporine and CGP-41251. The AVP-induced increase in [Ca2+]i could also be mimicked with the vasopressin (V1-subtype) agonist Octapressin, but not with the V2-agonist 1-desamino-8-D-arginine vasopressin, and was fully abolished by the V1-antagonist [d(CH2)5Tyr(Me)]AVP, but not by d(CH2)5-D-Leu-VAVP (V1-/V2-antagonist). These results indicate that V1-vasopressinergic receptors mediate AVP-induced PGI2 production and ANP secretion in rat cardiomyocytes and that, whereas both Ca2+ influx and PKC activation are required for AVP-induced ANP secretion, AVP-induced PGI2 formation is mainly regulated by PKC.

scholarly journals Protein kinase C pathway mediates the protective effects of glucagon-like peptide-1 on the apoptosis of islet β-cells

2015 ◽  
Vol 12 (5) ◽  
pp. 7589-7594 ◽  
Author(s):  
LIHAI ZHANG ◽  
YUESHENG WANG ◽  
JIAO WANG ◽  
YINGLAN LIU ◽  
YANBIN YIN
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protective Effects ◽  
Β Cells ◽  
Kinase C ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1
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