Absence of effects of dibutyryl cyclic guanosine 3′,5′-monophosphate on release of α-amylase,45Ca efflux,and protein synthesis in rat pancreas in vitro

Summary Dibutyryl cyclic GMP did not affect basal, or carbachol stimulated secretion of α-amylase from rat pancreas. The nucleotide did not have a significant effect on⁴⁵Ca release from the pancreas nor did it alter the response to carbachol. The dibutyryl analogue of cyclic GMP did not duplicate or alter the inhibitory effect of carbachol on³H-leucine incorporation into pancreatic trichloroacetic acid-precipitable protein.

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Résumé L'effet du dibutyryl GMPc sur la sécrétion d'α-amylase, l'efflux du⁴⁵Ca et la synthèse de nouvelles protéines dans le pancréas du rat, ont été étudiés. Le dibutyryl GMPc n'affecte ni la sécrétion d'enzyme basale ni celle stimulée par le carbachol. Le nucléotide n'a pas un effet significatif sur le relàchement du⁴⁵Ca du pancréas et n'altère pas la réponse du carbachol. L'analogue ne mime pas et ne change pas l'effet du carbachol sur l'incorporation du³H-leucine dans les protéines précipitées par l'acide trichloroacétique.

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Supported by a grant from the Medical Research Council of Canada. The authors acknowledge the secretarial aide of MissC. Picard.     

Effects of morphine administration on cerebellar guanosine 3',5'-monophosphate.

An increase in mouse cerebellar C-GMP levels during acute morphine treatment was observed, which was possibly related to the decrease in C-GMP phosphodiesterase levels also observed in acute treatment. Chronic treatment lowered C-GMP levels as did abrupt withdrawal without naloxone.     

Fetal calf serum alters cyclic adenosine 3',5'-monophosphate's effect on heme synthesis in vitro.

An investigation of the effect of cAMP on heme synthesis of rat bone marrow cells revealed that at 10(-2) M this cyclic nucleotide inhibits heme synthesis and that optimum stimulation occurs at 10(-4) M. Some unidentified constituent of fetal calf serum in the culture medium modifies the direction and degree of cAMP's effect.     

Free and sulfoconjugated dehydroepiandrosterone, cyclic adenosime-3',5'-monophosphate, and free estriol in maternal and cord blood.

When free DHEA, its sulfatide, and sulfate were assayed in maternal plasma as well as in umbilical cord arterial and venous plasma, rather high concentrations were found in either fraction from cord arterial plasma, reflecting the fetal contribution not only of free DHEA and DHEA sulfate, but also of the lipophile steroid sulfatide. Since high DHEA levels were associated with elevated c-AMP concentrations, a certain interrelationship of both parameters is indicated. In the course of delivery, a rapid decrease of free estriol in maternal plasma was observed. Higher concentration of free estriol in umbilical venous plasma pointed at its placental biosynthesis from fetal precursors.     

The effect of cyclic cytidine 3',5'-monophosphate (cCMP) on the in vitro development, hatching and attachment of the mouse blastocyst

The in vitro development and attachment of hatched mouse blastocysts on the untreated substratum was enhanced by 10 microM dibutyryl cCMP (dbcCMP). The result suggests that cCMP has an effect on embryonic development and on the blastocyst attachment process.     

Effects of starvation and Ca++ on glucose-induced accumulation of cyclic 3',5'-AMP in pancreatic islets.

Exposure to glucose in the presence of 3-isobutyl-1-methylxanthine leads to accumulation of cAMP in islets microdissected from ob/ob mice. This process is dependent on extracellular Ca++ but differs markedly from the glucose action on insulin release in the same in vitro system in disappearing after 18 h of starvation.     

The response of cyclic 3',5'-AMP and cyclic 3',5'-GMP phosphodiesterases to experimental diabetes

Alloxan diabetes caused a decrease in cyclic AMP phosphodiesterase in all affected rat tissues. Cyclic GMP phosphodiesterase activity was, however, decreased in adipose and liver, but increased increased in heart and uterus.     

Plasma cyclic 3',5'-guanosine monophosphate and cyclic 3',5'-adenosine monophosphate response to methacholine in man

Cholinergic agents are known to induce increases in tissue and plasma levels of cyclic GMP in experimental animals. We observed that i.m. injection of methacholine, a cholinergic agent, caused significant increases in plasma cyclic GMP and cyclic AMP in man.     

Interaction between dehydroepiandrosterone, glucose-6-phosphate dehydrogenase, and cyclic adenosine-3',5'-monophosphate in neoplastic and normal human mammary tissue.

When total DHEA, G-6-PDH activity, and c-AMP were determined in human neoplastic mammary tissue and corresponding normal tissue the G-6-PDH activity in the former tissue greatly exceeded that found in normal tissue. On the other hand, a remarkable decrease of total DHEA and c-AMP could be detected in cancer tissue, hinting at the participation of DHEA in the intracellular regulation of G-6-PDH and c-AMP levels.     

Adenosine promoted accumulation of adenosine 3',5'-monophosphate in rabbit vagus nerve.

Desheathed rabbit vagus nerve has been found to form cyclic AMP when incubated with adenosine. This accumulation of cyclic AMP is inhibited by theophylline but not by antiadrenergic agents, anticholinergic agents or local anaesthetics. Depolarizing media are not able to promote cyclic AMP accumulation in this preparation.