Possible Involvement of Cyclic Nucleotides in the Stimulation of Pituitary Function Elicited by Reserpine

2015 ◽  
pp. 259-266 ◽  
Author(s):  
A. Guidotti ◽  
B. Zivkovic ◽  
E. Costa
Keyword(s):  
Cyclic Nucleotides ◽  
Pituitary Function ◽  
Stimulation Of

scholarly journals Proceedings: Chlorpromazine stimulation of prolactin secretion: a test of pituitary function

1974 ◽  
Vol 29 (1) ◽  
pp. 97-97 ◽  
Author(s):  
R G Wilson ◽  
B N Cole ◽  
A R Boyns ◽  
A P Forrest
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Function ◽  
Stimulation Of

Cyclic nucleotides, calcium, bicarbonate, and protein secretion in canine pancreatic juice in response to cholecystokinin–pancreozymin

1979 ◽  
Vol 57 (6) ◽  
pp. 541-546 ◽  
Author(s):  
H. L. Cailla ◽  
H. Sarles ◽  
M. V. Singer
Keyword(s):  
Cyclic Amp ◽  
Pancreatic Juice ◽  
Cyclic Gmp ◽  
Cyclic Nucleotides ◽  
Parallel Increase ◽  
Calcium Bicarbonate ◽  
Strong Linear Correlation ◽  
Protein Output ◽  
Dose Dependent ◽  
Stimulation Of

The secretion of cyclic AMP, cyclic GMP, protein, calcium, and bicarbonate in the pancreatic juice of three nonanesthetized dogs with chronic gastric and duodenal Thomas cannulae has been studied. Intravenous infusions of increasing doses of cholecystokinin–pancreozymin (CCK) (1.5, 3, 6, 12, 24 Crick Harper-Raper (CHR) U kg−1 h−1) were administered together with a continuous submaximal dose of secretin (1 clinical unit (CU) kg−1 h−1). Doubling CCK doses every 45 min induced a parallel increase in the output of both cyclic nucleotides. Cyclic AMP output peaked at between 15 and 30 min for 3 and 6 U kg−1 h−1 of CCK and later for 12 and 24 U kg−1 h−1 of CCK whereas cyclic GMP output increased more constantly. Calcium output followed a pattern similar to that of cyclic GMP secretion. Flow rate and protein output attained their peaks at between 30 and 45 min. A strong linear correlation was found between the quantities of cyclic AMP, cyclic GMP, and the quantities of protein secreted in response to each CCK dose. This study demonstrates the presence of cyclic GMP in the canine pancreatic juice and the dose-dependent stimulation of the secretion of cyclic GMP and cyclic AMP by CCK in the presence of secretin.

Inhibition of IP3 and IP3-dependent Ca2+ mobilization by cyclic nucleotides in isolated gastric muscle cells

1993 ◽  
Vol 264 (5) ◽  
pp. G967-G974 ◽  
Author(s):  
K. S. Murthy ◽  
C. Severi ◽  
J. R. Grider ◽  
G. M. Makhlouf
Keyword(s):  
Cyclic Nucleotides ◽  
Muscle Cells ◽  
Dibutyryl Camp ◽  
Main Determinant ◽  
Inositol 1,4,5 Trisphosphate ◽  
Gastric Muscle ◽  
Intact Muscle ◽  
Camp And Cgmp ◽  
Permeabilized Muscle ◽  
Stimulation Of

The mechanisms by which cAMP and cGMP and agents that stimulate one (isoproterenol and nitroprusside) or both cyclic nucleotides (VIP) decrease cytosolic free Ca2+ ([Ca2+]i) and inhibit contraction were examined in dispersed, intact, and saponin-permeabilized gastric muscle cells. In these cells, the [Ca2+]i transient responsible for initial contraction is mediated by inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ release (K. N. Bitar, P. G. Bradford, J. W. Putney, Jr., and G. M. Makhlouf, Science Wash. DC 232: 1143-1145, 1986, and J. Biol. Chem. 261: 16591-16596, 1986). In intact muscle cells, dibutyryl cAMP and all three relaxant agents inhibited contraction, [Ca2+]i, and net Ca2+ efflux (i.e., Ca2+ release) in a concentration-dependent fashion. In permeabilized muscle cells, cAMP, cGMP, and all three relaxant agents 1) inhibited cholecystokinin (CCK)-induced IP3 production (maximal 38-48%), 2) inhibited CCK- and IP3-induced Ca2+ efflux (maximal 55-59%) and contraction (maximal 59-66%), and 3) stimulated Ca2+ uptake (maximal 25-30%), in a concentration-dependent fashion. cAMP and cGMP were equipotent inhibitors of IP3 production and of CCK- and IP3-induced Ca2+ efflux and contraction, whereas cGMP was distinctly more potent as a stimulant of Ca2+ uptake. For all functions, maximal effects induced by cAMP and cGMP were similar to those induced by the three relaxant agents. Inhibition of Ca2+ release was the main determinant of inhibition of contraction; stimulation of Ca2+ uptake was relatively minor (< 5% of Ca2+ efflux). Decrease in IP3 production did not contribute to inhibition of Ca2+ efflux and contraction since inhibition of IP3-induced Ca2+ efflux was similar to inhibition of CCK-induced IP3-dependent Ca2+ efflux.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of extracellular calcium on amylase release from dispersed pancreatic acini.

1979 ◽  
Vol 236 (6) ◽  
pp. E754
Author(s):  
J D Gardner ◽  
C L Costenbader ◽  
E R Uhlemann
Keyword(s):  
Guinea Pig ◽  
Vasoactive Intestinal Peptide ◽  
Cyclic Nucleotides ◽  
Extracellular Calcium ◽  
Enzyme Release ◽  
Amylase Release ◽  
Pancreatic Acini ◽  
Basal Rate ◽  
Derivatives Of ◽  
Stimulation Of

In dispersed acini prepared from guinea pig pancreas, removing extracellular calcium did not alter the basal rate of amylase release but reduced the stimulation of enzyme release caused by cholecystokinin, carbachol, secretin, and vasoactive intestinal peptide as well as that caused by derivatives of cyclic nucleotides. In acini incubated in a calcium-free, EGTA-containing medium the increase in amylase release caused by each secretagogue tested did not change during the initial 10 min of incubation, decreased by approximately 65% during the subsequent 40 min, and remained constant thereafter. Removing extracellular calcium did not alter the maximally effective concentrations of cholecystokinin or vasoactive intestinal peptide but abolished the decrease in stimulated enzyme secretion seen with supramaximal concentrations of cholecystokinin. Incubating pancreatic acini with cholecystokinin or carbachol plus secretin or vasoactive intestinal peptide caused potentiation of amylase release, and removing extracellular calcium reduced the stimulation of enzyme release caused by the two secretagogues in combination but did not alter their potentiating interactions.

Effects of PTH, ADH, and cyclic AMP on distal tubular Ca and Na reabsorption

1980 ◽  
Vol 239 (5) ◽  
pp. F478-F485 ◽  
Author(s):  
L. S. Costanzo ◽  
E. E. Windhager
Keyword(s):  
Parathyroid Hormone ◽  
Cyclic Amp ◽  
Antidiuretic Hormone ◽  
Cyclic Nucleotides ◽  
Adenosine Monophosphate ◽  
Water Reabsorption ◽  
Ca Transport ◽  
Distal Tubules ◽  
Stimulation Of

Tubular microperfusion experiments were performed in rats to examine the effects of thyroparathyroidectomy (TPTX), parathyroid hormone (PTH), antidiuretic hormone (ADH), and cyclic AMP (cAMP) on distal tubular Ca, Na, and water reabsorption. TPTX caused a significant decrease in the Ca reabsorptive rate as compared to intact animals. PTH (5 U/kg; 2 U x kg-1 x h-1) replacement in TPTX animals restored Ca transport to control levels. Application of either cAMP (10(-3) M) or 8-(p-chlorophenylthio)-cyclic 3',5'-adenosine monophosphate (10(-5) M) to the surface of the kidney caused a stimulation of Ca reabsorption similar to that produced by PTH. Neither TPTX nor PTH changed Na or water reabsorption significantly, whereas the cyclic nucleotides increased both of these parameters. These later actions of cAMP duplicated effects of ADH observed in these distal tubules.

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