623 Which signal transduction pathway is involved in contraction of the female pig urethra upon stimulation of α1 adrenoceptors?

2004 ◽  
Vol 3 (2) ◽  
pp. 158
Author(s):  
R. Scott ◽  
R. Chess-Williams ◽  
C. Chapple
Keyword(s):  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Stimulation Of

Stimulation of proximal convoluted tubule phosphate transport by epidermal growth factor: signal transduction

1995 ◽  
Vol 269 (3) ◽  
pp. F339-F344 ◽  
Author(s):  
R. Quigley ◽  
D. A. Kennerly ◽  
J. N. Sheu ◽  
M. Baum
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Signal Transduction Pathway ◽  
Phosphate Transport ◽  
Transduction Pathway ◽  
Kinase C ◽  
Epidermal Growth ◽  
Stimulation Of

The present study investigated the signal-transduction pathway responsible for the epidermal growth factor (EGF) stimulation of phosphate transport (JPhos) in the rabbit proximal convoluted tubule (PCT). Genistein, 10(-4) M, bath and lumen, an inhibitor of EGF receptor tyrosine kinase activity, blocked the EGF effect on JPhos, consistent with a role for tyrosine kinase in the signal-transduction pathway. Both staurosporine (5 x 10(-8) M) and calphostin C (10(-8) M), inhibitors of protein kinase C, blocked the EGF stimulation of JPhos, indicating that protein kinase C is involved in EGF signaling. Intracellular calcium (Ca2+i) concentrations were measured in perfused tubules using fura PE3 to determine whether changes in Ca2+i were also part of the signaling pathway. After addition of 3 nM EGF, there was no change in Ca2+i, suggesting that stimulation of protein kinase C is not from phosphatidylinositol hydrolysis by phospholipase C-gamma. To determine whether phospholipase A2 (PLA2) is involved, the inhibitor mepacrine was used. Mepacrine (5 x 10(-5) M) had no direct effect on PCT transport but blocked the stimulatory effect of EGF on JPhos. PLA2 activity, assessed as free arachidonic acid release from proximal tubules in suspension, increased by 18.8% with 3 nM EGF. Thus the stimulation of JPhos by EGF is mediated via a signal-transduction pathway involving tyrosine kinase, protein kinase C, and PLA2.

Beta-adrenergic regulation of H+ secretion by cultured outer medullary collecting duct cells

1992 ◽  
Vol 263 (6) ◽  
pp. F1011-F1019 ◽  
Author(s):  
T. M. Manger ◽  
C. A. Pappas ◽  
B. M. Koeppen
Keyword(s):  
Signal Transduction ◽  
Collecting Duct ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists ◽  
Whole Cell Patch Clamp ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
Stimulation Of

The effects of the beta-adrenergic agonist isoproterenol (Iso) on cells of the inner stripe portion of the rabbit outer medullary collecting duct (OMCDi) grown in primary culture were examined using whole cell patch-clamp techniques and measurements of intracellular pH (pHi) and Ca2+. Iso (10(-6) M) increased the cellular Cl- conductance, and this effect was mimicked by treatment of the cells with dibutyryladenosine 3',5'-cyclic monophosphate (cAMP, 10(-5) M) or protein kinase A (PKA, 0.4 U/ml). Iso did not alter the baseline pHi, but it did increase the activity of both the Cl-/HCO3- antiporter and the H(+)-adenosinetriphosphatase (H(+)-ATPase). The increase in Cl-/HCO3- antiporter rate was mimicked by dibutyryl-cAMP plus 3-isobutyl-1-methylxanthine (cAMP + IBMX, 10(-4) M + 10(-5) M). However, the Iso-induced stimulation of the H(+)-ATPase activity was not mimicked by cAMP + IBMX. Measurements of intracellular Ca2+ showed that Iso also increased intracellular Ca2+ levels. This response was not dependent on extracellular Ca2+, nor did cAMP + IBMX appreciably alter intracellular Ca2+. Consequently, we postulate that beta-adrenergic agonists are potential stimulators of OMCDi H+ secretion. These agonists stimulate cellular HCO3- efflux through a signal transduction pathway involving cAMP and PKA. However, a different signal transduction pathway appears to mediate the stimulation of cellular H+ efflux. This second pathway may involve an elevation of intracellular Ca2+.

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