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PubMed1980

Prolongation of the effects of gonadotrophins and prostaglandin E2 on ovarian cyclic AMP formation by inhibitors of protein synthesis.

The effects of LH, FSH and PGE2 on the accumulation of cyclic AMP by isolated whole ovaries from 23-24 day-old rats were studied in time-course experiments in presence and absence of two inhibitors of protein synthesis, puromycin and cycloheximide. In absence of these inhibitors ovarian cyclic AMP levels reached peak levels within 30 min for all three stimulators and returned towards pre-stimulation levels within 2-4 h. When puromycin (500 microgram/ml) or cycloheximide (5 microgram/ml) was present together with LH, FSH or PGE2, respectively, ovarian cyclic AMP levels did not decrease after the initial peak but remained high for the entire incubation period (4-5 h). The release of cyclic AMP to the incubation medium was also much higher when puromycin or cycloheximide was present, illustrating that the effect of puromycin and cycloheximide was not caused by an inhibition of the cyclic AMP release. The effects of puromycin and cycloheximide were, in principle, the same when a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, was present. The results indicate either that there are, in the ovary, proteins with very rapid turn-over, necessary for the mechanism leading to refractoriness of the cyclic AMP system, or that the gonadotrophins and PGE2 as an early effect stimulate the production of a specific protein necessary for the development of refractoriness.

1-Methyl-3-isobutylxanthine↗
PubMed1979

[Effects of orciprenaline on the responses to Ca, K, acetylcholine and Ba in the isolated seminal vesicles of guinea pigs, especially in relation to cyclic AMP (author's transl)].

By using the isolated seminal vesicles of guinea pigs, the effects of dibutyryl cyclic AMP and beta-stimulant, orciprenaline, on the responses to Ca, K, acetylcholine and Ba were investigated, especially in relation to cyclic AMP. The following results were obtained. 1. Orciprenaline inhibited the contraction produced by Ca, K, acetylcholine and Ba in a dose-dependent manner, and the inhibition became larger in the order of Ca, K, acetylcholine and Ba. 2. Dibutyryl cyclic AMP showed the same results as those of orciprenaline. That is, dibutyryl cyclic AMP inhibited the contractions produced by acetylcholine and Ba. 3. Orciprenaline showed the increased level of cyclic AMP in a dose-dependent manner. But the increase was not remarkable in the concentration in which the contractions produced by the tested contractile agents were inhibited by about 50%. From these results, the following suggestions were obtained; (1) there exists beta-receptor in guinea pig seminal vesicles and (2) a part of actions of orciprenaline is due to a mechanism unrelated to cyclic AMP.

Acetylcholine↗
PubMed1985

Changes in cyclic AMP and cyclic GMP levels in the contraction-relaxation cycle of isolated smooth muscle cells from guinea-pig taenia caeci.

The present study was undertaken to investigate the role of cyclic AMP and cyclic GMP in the regulation of the contraction-relaxation cycle in isolated smooth muscle cells from guinea pig taenia caeci. The contraction of isolated smooth muscle cells induced by both caffeine (4 X 10(-3) M) and carbachol (10(-4) M) consisted of an initial activation phase and a following spontaneous relaxation phase. Isoproterenol (10(-4) M) inhibited the carbachol-induced contraction and raised intracellular cyclic AMP level of isolated smooth muscle cells. Both the inhibition of the carbachol-induced contraction and the rise in cyclic AMP level elicited by isoproterenol were blocked by propranolol (10(-4) M). Caffeine increased intracellular cyclic AMP level significantly and contracted isolated smooth muscle cells. Caffeine and carbachol contracted isolated smooth muscle cells and increased intracellular cyclic GMP level. Cyclic GMP was significantly increased in spontaneous relaxation phase. The data suggest that beta-adrenergic inhibitory effect on cholinergic excitation in the mammalian isolated smooth muscle cells is mediated by the change in intracellular cyclic AMP level and that cyclic GMP related to the relaxation in these single cells. Thus, it appears that caffeine-induced contraction might be due to the stimulation of Ca2+-induced Ca2+ release by cyclic AMP.

Animals↗
PubMed1977

Feto-maternal amino acid patterns and cyclic AMP in the human placenta with abnormal pregnancies, particularly with SFD.

To clarify the causes of SFD from the view-point of placental function, investigations were made on feto-maternal amino acid circumstances and on how cyclic AMP behaves in the placenta, particularly in relation to the transport of amino acid across the placenta. Amino acids were measured by gas liquid chromatography (hydrogen-flame ion detector), c-AMP by the binding protein method, adenyl cyclase activity by Krishna's method, and proteins by Lowry's method. Results show: (1) The levels of maternal amino acids were indistinctive between the SFD group and the normal pregnancy group. (2) The feto-maternal ratio of amino acid concentrations (f/m ratio) was lower in the SFD group than in the normal control. (3) The level of c-AMP in the placenta was lower in the SFD group than in the control. (4) The lower level of placenta c-AMP in the SFD placenta seems partly attributable to the decreased adenyl cyclase activity. (5) There was a positive correlation (gamma=0.61) between the content of c-AMP in the placenta and the f/m ratio of amino acid concentrations. These findings suggest a decline in placental active transport of acids in SFD; adenyl cyclase and c-AMP in the placenta presumably play a key role in such course.

Adenylyl Cyclases↗
PubMed1975

Concentrations of cyclic AMP in rabbit ovarian tissue during the preovulatory period and pseudopregnancy after induction of ovulation by administration of human chorionic gonadotrophin.

Concentrations of cyclic AMP were measured in rabbit ovaries at various times after injection of an ovulatory dose of human chorionic gonadotrophin (HCG). A biphasic increase in cyclic AMP concentration occurred during the preovulatory period, with peaks 30 min and 3-4 h after HCG injection. Concentrations of cyclic AMP had returned to those observed in ovaries of control oestrous animals before the onset of ovulation 10-12 h after administration of HCG, and remained low throughout the period of pseudopregnancy. Concentrations of cyclic AMP in the newly formed and developing corpora lutea were similar to the concentrations observed in the remainder of the tissue during this period. No significant increase in cyclic AMP concentration was observed 7-9 days after initiation of ovulation. Concentrations of ATP were also investigated during the preovulatory period. The dose-response relationship of HCG to cyclic AMP production in oestrous rabbit ovaries was investigated.

Adenosine Triphosphate↗
PubMed1981

Culture sensitization and inhibition of luteinizing hormone responsive production of cyclic AMP in luteal cells by luteinizing hormone, prostaglandin F2 alpha and [D-Trp6]-luteinizing hormone releasing hormone.

Many cells are able to regulate their sensitivity to hormones. In order to investigate the mechanism(s) by which rat luteal cells regulate their sensitivity to LH, we have developed and characterized a cell culture model. Cultures of dispersed rat luteal cells were exposed to graded doses of bovine LH, an analogue of LH releasing hormone (LH-RH) ([D-Trp6]-LH-RH), and prostaglandin F2 alpha (PGF2 alpha) for 3 h. The media containing these hormones were then replaced with fresh hormone-free medium and the cells cultured for 24 h. In order to test the sensitivity of these cultures after 24 h, the medium was discarded and replaced by medium alone, or medium containing a standard dose of bovine LH for 1 h. The amount of cyclic AMP accumulated during this hour was used as an index of the sensitivity of the cells to LH. Control cultures became 'supersensitive' to LH with augmented production of cyclic AMP during culture but LH-receptor binding activity was not increased. During the first 2 h of culture, LH (100 ng/ml) increased accumulation of cyclic AMP by fourfold, but after 5 h of culture, stimulation of cyclic AMP accumulation by the same dose of LH was increased 32-fold, 299-fold at 13 h and 359-fold at 21 h of culture. The increase in LH-responsive accumulation of cyclic AMP with cultured was severely impaired by early exposure of cells to LH, LH-RH analogue or PGF2 alpha during the first 2 h of culture. Also, both LH-RH analogue and PGF2 alpha acutely inhibited LH-stimulated accumulation of cyclic AMP. Inhibition of culture-induced sensitization of LH responsiveness was not altered by the addition of 3-isobutyl-1-methylxanthine. Scatchard analysis of LH binding sites indicated that pretreatment of luteal cells with LH (or human chorionic gonadotrophin at an equivalent dose) reduced the number of free LH receptors when measured after 24 h of culture, but total receptor binding activity was not changed. However, a similar effect was not seen with cells treated with PGF2 alpha or LH-RH analogue. It is suggested that 'culture-induced' supersensitivity may represent either recovery of pre-isolation sensitivity or result from the loss of an endogenous factor(s) which retards the coupling of the LH receptor and adenylate cyclase. Although PGF2 alpha and LH-RH analogue have been shown to directly prevent the occupied LH receptor from activation of adenylate cyclase, the present observations have indicated that this inhibitory process was continued even when these agents were removed from the culture medium.

Animals↗
PubMed1985

Calmodulin regulation of cellular cyclic AMP production in response to arginine vasopressin, prostaglandin E2 and forskolin in rat renal papillary collecting tubule cells in culture.

The effect of calmodulin on the stimulation of cyclic AMP production by arginine vasopressin (AVP), prostaglandin E2 (PGE2) and forskolin was examined in cultured renal papillary collecting tubule cells of the rat. In the presence of the phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine submaximal concentrations of AVP (1 nmol/l), PGE2 (20 nmol/l) and forskolin (240 nmol/l) significantly increased cellular cyclic AMP accumulation by 2.3-, 6.0- and 8.4-fold respectively. Two chemically dissimilar inhibitors of calmodulin, namely trifluoperazine and N-(6-amino-hexyl)-5-chloro-1-naphthalenesulphonamide (W-7), attenuated the AVP-, PGE2- and forskolin-stimulated cellular production of cyclic AMP in a dose-related manner. Cellular production of cyclic AMP was inhibited by 50% (ID50) by doses ranging from 16 to 28 mumol trifluoperazine/l and 35 to 44 mumol W-7/1. Basal accumulation of cellular cyclic AMP was also decreased by treatment with either trifluoperazine or W-7, but the effective dose was higher than that which inhibited cellular cyclic AMP production stimulated by AVP, PGE2 and forskolin. Since forskolin directly activates adenylate cyclase at a site of the catalytic unit and the cellular action of AVP to activate adenylate cyclase is mediated through receptor-guanine nucleotide regulatory-catalytic units, the present study indicates calmodulin regulation of basal, AVP-, PGE2- and forskolin-activated adenylate cyclase in the papillary collecting tubule cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Synergism between calcium-mediated and cyclic AMP-mediated activation of chloride secretion in isolated guinea pig distal colon.

Synergistic effects of Ca2+-mediated secretagogues and cyclic AMP-mediated secretagogues on Cl- secretion by guinea pig distal colon were studied in vitro using Ussing chambers. Short-circuit current (Isc) and bidirectional fluxes of 22Na+ and 36Cl- were measured. Bethanechol (10(-4) M, a Ca2+-mediated secretagogue) caused an increase in Isc, which was enhanced 4-20 fold when the tissue was pretreated with prostaglandin E2 (10(-7)-10(-6) M), vasoactive intestinal polypeptide (5 x 10(-9)-10(-8) M) (cyclic AMP-mediated secretagogues), or 8-bromocyclic AMP (5 x 10(-4)-2 x 10(-3) M). Measurement of 36Cl flux showed that the increase in Isc in the presence of both 8-bromocyclic AMP and bethanechol resulted principally from increased Cl- secretion. On the other hand, the net absorptive flux of 22Na was not influenced under these conditions. Potentiation of the increase in Isc was also elicited by the combination of A23187 (5 x 10(-6) M) and 8-bromocyclic AMP (10(-3) M). The results are consistent with the notion that simultaneous activation of the cyclic AMP-mediated and Ca2+-mediated systems produces a synergistic increase in colonic Cl- secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1975

Decreased cyclic AMP and insulin response to glucose in isolated islets of neonatal rats.

The (3H) cyclic AMP accumulation was measured in incubations of pancreatic islets from one-day, six-day, and thirty-five-day-old rats exposed to a low (0.6 mg./ml.) or a high (3.0 mg./ml.) glucose concentration with or without the addition of 0.1 mM. of the phosphodiesterase inhibitor 3-isobutyl- 1 -methylxanthine (IBMX). In the thirty-five-day-old rats, (3H) cyclic AMP accumulation was significantly enhanced after sixty minutes' incubation in a high glucose concentration and further increased by IBMX. These changes were paralleled by a stimulated insulin release, measured simultaneously. By contrast, in the one-day-old rats, no effect of glucose with or without IBMX was seen on (3H) cyclic AMP, while the minor insulin release due to high glucose alone was markedly potentiated by IBMX. Even in the presence of this agent the insulin response to glucose was, however, clearly inferior to that seen in the thirty-five-day-old animals. The stimulatory patterns of glucose-induced insulin release in the six-day-old animals was intermediate between the other two age groups. At this age, stimulation of (3H) cyclic AMP due to glucose was observed only in the presence of IBMX. Measurement of (3H) cyclic AMP after three minutes' incubation confirmed these different stimulatory patterns of glucose in the age groups studied. It is suggested that the inefficiency of glucose to stimulate the adenyl cyclase-cyclic AMP system of the beta cell from fetal and neonatal animals may be one important factor determining the insensitivity to the insulin-releasing action of glucose that exists at this stage of development.

Adenylyl Cyclases↗
PubMed1986

Association of changes in intracellular cyclic AMP with changes in phagocytosis in cultured rat pigment epithelium.

Papavarine, cholera toxin, and isoproterenol each elevated cyclic AMP in cultured rat retinal pigment epithelium and reduced the phagocytosis of isolated rod outer segments (38-66% of controls) during a 4 hour incubation. In addition, cultured pigment epithelium was preincubated with 25 mM exogenous cyclic AMP for two days and then incubated with outer segments for 4 hours either in the continued presence of exogenous cyclic AMP (condition A) or in the absence of exogenous cyclic AMP (condition B). Under condition B phagocytosis was 38% higher than under condition A. Intracellular cyclic AMP decreased under condition B but remained constant under condition A. These observations provide evidence that short term decreases in intracellular cyclic AMP are associated with increases in phagocytosis of outer segments by cultured rat pigment epithelium.

Animals↗
PubMed1990

Neuropeptide Y and somatostatin inhibit stimulated cyclic AMP production in rabbit ciliary processes.

The interaction of adrenergic and peptide receptors linked to adenylate cyclase and the inhibition by bioactive peptides of stimulated cyclic AMP production has been investigated in intact, excised rabbit ciliary processes. Cyclic AMP production stimulated by isoproterenol, vasoactive intestinal peptide, or forskolin was inhibited by the biologically active peptides neuropeptide Y, somatostatin, and the synthetic somatostatin analogue SMS 201-995. IC50s determined from dose-response curves of inhibition are consistent with the known abilities of these ligands to modulate cyclic AMP and physiological responses in other tissues. Inhibition by neuropeptide Y or SMS 201-995 was unaffected by the specific alpha 2-adrenergic antagonist yohimbine, which shows that peptide inhibition is not occurring via peptide binding to the inhibitory alpha 2-adrenergic receptor. These results suggest that endogenous peptides may participate in modulation of cyclic AMP production and subsequent physiological events influenced by cyclic AMP levels in rabbit ciliary processes by inhibiting stimulated cyclic AMP synthesis.

Animals↗
PubMed1977

Is cyclic AMP the regulator of hepatic ornithine decarboxylase activity?

The role of cyclic AMP in the regulation of hepatic ornithine decarboxylase (ODC) activity in the rat was studied in the whole animal and in the perfused organ. Dibutyryl cyclic AMP or butyrate given to intact rats increased ODC activity; this increase was abolished by hypophysectomy 1 h prior to administering ether compound. Administration of 1 mg 1-methyl-3-isobutylxanthine (MIX) to intact rats increased ODC activity within 4 hours whereas hypophysectomy 1 h before treatment prevented this increase. No change in hepatic cyclic AMP content was seen in either intact or hypophysectomized rats following MIX. Perfusion with 0.5 mM dibutyryl cyclic AMP decreased ODC activity in isolated livers whereas perfusion with 0.5 mM 8-bromocyclic GMP produced a small increase in ODC activity. These data suggest that the effect of dibutyryl cyclic AMP in intact animals may be a property of the butyrate and that this action as well as the action of MIX may be mediated through the permissive effect of pituitary and/or adrenal hormones. The normal hepatocyte does not increase its ornithine decarboxylase activity after direct exposure to dibutyryl cyclic AMP.

Animals↗
PubMedDate not supplied

alpha2-adrenergic agonist-induced inhibition of cyclic AMP formation in transfected cell lines using a microtiter-based scintillation proximity assay.

Human embryonic kidney cells (HEK-7) were transfected with the gene for the human alpha2C receptor (alpha2C4). Cells were grown in 96-well microtiter plates and cyclic AMP levels were measured by scintillation proximity assay, a modified radioimmunoassay technique. Radioactivity was quantified using a TopCount Scintillation detector. Cyclic AMP was increased in a dose-dependent manner by the addition of exogenous forskolin. The forskolin-induced enhancement of cyclic AMP was inhibited dose-dependently by the addition of alpha2-adrenergic agonists, and this inhibition was blocked by the addition of adrenergic antagonists. The extent of the inhibitory response caused by alpha2-adrenoceptor agonists was related to the receptor density in clonal cell lines derived from the transfected parental HEK-7 cells. By using cells grown in microtiter format, and employing the technological advantages of scintillation proximity assay and TopCount detection, it was possible to simultaneously evaluate the effects of multiple experimental permutations on cellular production of cyclic AMP with minimal disturbance of the cells and minimal and/or automated manipulation of the cyclic AMP formed. This combination of techniques should allow rapid testing of the actions of adrenergic agonists and antagonists on cells transfected with receptors linked to cyclic AMP formation.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1975

Cyclic-AMP and pancreatic bicarbonate secretion in response to secretin in dogs.

In anesthetized dogs given secretin intravenously in doses doubling every 60 min and ranging from 0.5 to 8 units per kg body weight per hr, cyclic-AMP levels in pancreatic tissue rose continuously, whereas DNA concentrations were slightly decreased. Bicarbonate concentrations and bicarbonate outputs, cyclic-AMP tissue concentrations and bicarbonate outputs, as well as cyclic-AMP tissue concentrations and juice outputs, were significantly correlated. In conscious pancreatic fistula dogs, there was also a significant correlation between cyclic-AMP and bicarbonate concentrations and outputs in the pancreatic juice after stimulation by exogenous secretin. Accordingly, enhanced release of endogenous secretin achieved by intraduodenal acidification led to a dose-dependent increase in bicarbonate and cyclic-AMP outputs in both conscious and anesthetized dogs. Phosphodiesterase inhibitors (aminophylline, caffeine, and papaverine) given alone to the conscious dogs did not initiate pancreatic bicarbonate secretion, but they potentiated bicarbonate responses to exogenous secretin. These data suggest that cyclic-AMP plays a part in secretin-stimulated pancreatic secretion.

Aminophylline↗
PubMed1992

Activation of protein kinase A is necessary but not sufficient for ethanol-induced desensitization of cyclic AMP production.

Acute addition of EtOH to PC 12 pheochromocytoma cells increases cyclic AMP production, whereas chronic exposure to EtOH results in a decrease in the stimulation of cyclic AMP production in response to 2-chloroadenosine and forskolin. This EtOH-induced desensitization was not observed after chronic EtOH treatment of A126-1B2-1 cells which are a protein kinase A-deficient mutant cell line derived from PC 12 cells. Furthermore, in the parental PC 12 cell line the cell-permeable protein kinase A inhibitor, Rp-isomer of adenosine 3',5'-monophosphorothioate, blocked the development of EtOH-induced desensitization. Thus, activation of protein kinase A is apparently necessary for EtOH-induced desensitization of cyclic AMP production. Chronic treatment of PC 12 cells with forskolin qualitatively mimicked the desensitization observed with chronic EtOH exposure. However, the degree of desensitization induced by forskolin was significantly less than that caused by EtOH even though the acute addition of forskolin caused a greater increase in cyclic AMP production. Furthermore, the acute addition of EtOH inhibited forskolin-stimulated cyclic AMP production, yet inclusion of EtOH during the chronic forskolin treatment of PC 12 cells resulted in a greater degree of desensitization. These findings indicate an obligatory role of protein kinase A in EtOH-induced desensitization of cyclic AMP production in PC 12 cells. However, because protein kinase A activation alone is not sufficient to account for the degree of desensitization, EtOH probably also acts through a mechanism in addition to activation of protein kinase A.

2-Chloroadenosine↗
PubMedDate not supplied

Histamine-induced cyclic AMP formation in the chick hypothalamus: interaction with vasoactive intestinal peptide.

Effects of histamine (HA) on cyclic AMP production and its action upon the effects evoked by vasoactive intestinal peptide (VIP) were studied in the chick hypothalamus. HA (0.1-1000 microM) potently stimulated cyclic AMP formation in the hypothalamic slices, reaching maximal effect (2.5-3.5-fold increase) at a 100 microM concentration, and displaying an EC50 value of approximately 6.5 microM/ The stimulatory action of HA was mimicked by agonists of HA receptors, with the following rank order of potency: HA>4-methylHA (H2)>or=Nalpha,Nalpha-dimethylHA (H3>>H1=H2)>or=2-methylHA (H1)>>amthamine (H2)>>dimaprit (H2) approximately tele-methylHA. The HA (100 microM)-evoked increase in cyclic AMP production was concentration-dependently antagonized by selective H2-HA receptor blockers (aminopotentidine>>cimetidine>or=ranitidine>>zolantadine) and was not affected by mepyramine and thioperamide, a selective H1- and H3-HA receptor antagonist, respectively. The pharmacological profile of HA receptors linked to the cyclic AMP-generating system in the chick hypothalamus indicates that they represent either an avian-specific H2-like HA receptor or a novel subtype of HA receptors. Chicken VIP (cVIP; 0.1-3 microM) potently stimulated cyclic AMP synthesis in the chick hypothalamus in a concentration-dependent manner. A combination of cVIP with HA produced cyclic AMP response more than additive, and such a synergistic interaction was antagonized by ranitidine. It is suggested that in the avian brain HA and VIP may play in concert to regulate neuroendocrine processes.

Animals↗
PubMed1975

Regulation of the in vitro early anamnestic antibody response by exogenous cholera enterotoxin and cyclic AMP.

Keyhole limpet hemocyanin was injected into the hind foot pads of rabbits. Six days later cell suspensions were prepared from the popliteal lymph nodes. Various amounts of hemocyanin (1 ng to 100 mug) were added to 1 times 10-7 cells to induce an anamnestic antibody response. Various amounts of cholera enterotoxin, which stimulates the enzyme adenylate cyclase, or dibutyryl cyclic adenosine 3'5'-monophosphate (AMP), were added to the cultures with or without hemocyanin. De novo synthesis of antibody, protein, deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) from radioactive precursors was assayed. The addition of cholera toxin or dibutyryl cyclic AMP for the first 24 hr with optimal (1 mug) or supraoptimal (100 mug) amounts of hemocyanin enhanced antibody synthesis by at least 100 to 200%. Addition of the toxin or dibutyryl cyclic AMP for the same period to cells minus hemocyanin or with suboptimal amounts (1 to 100 ng) of antigen failed to enhance antibody synthesis. Addition of these agents for 72 to 120 hr to hemocyanin-induced cultures consistently inhibited antibody synthesis. These agents slightly inhibited DNA and RNA synthesis. The increase in protein synthesis caused by the toxin or dibutyryl cyclic AMP was almost totally accounted for by the increase in antibody synthesis. Neither toxin nor cyclic nucleotide promoted the antibody response in the presence of antibody to rabbit thymus-derived lymphocytes; these lymphocytes as well as bursa-equivalent lymphocytes were required for potentiation of the response. Macrophages were not required either for induction of the anamnestic response or for enhancement of this synthesis by cyclic nucleotide or cholera toxin. Both IgM and IgG antibody synthesis were regulated by exogenous cholera toxin and dibutyryl cyclic AMP. A number of possible cellular mechanisms of regulation of the antibody response through the cyclic AMP pathway were discussed. These included the effects of modifications of this pathway on the activities of T lymphocytes early (0 to 24 hr) and B lymphocytes late (72 to 120 hr) in the response and on the apparent reversal of high zone tolerance.

Animals↗
PubMed1991

Cyclic AMP-receptor proteins in heart muscle of rats flown on Cosmos 1887.

A frequent cellular response to organismal stress is the increase in ligand binding by beta-adrenergic receptors. The extracellular signal is amplified by intracellular increases in cyclic AMP and the ensuing activation of cyclic AMP-dependent protein kinase (cAPK). The molecular mechanisms involve the binding of cyclic AMP to regulatory (R) subunits of cAPK, thus freeing the catalytic subunit for protein phosphorylation. This study was carried out to determine the cellular compartmentalization of the cyclic AMP-receptor proteins in heart ventricular tissue obtained from rats flown on the Cosmos 1887 mission. Photoaffinity labeling of soluble and particulate cell fractions with an [32P]-8-azido analog of cyclic AMP was followed by electrophoretic separation of the proteins and by autoradiographic identification of the labeled isoforms of cAPK R subunits. The results showed that RII in the particulate subcellular fraction was significantly decreased in heart cells from rats in the flight group when compared to controls. Protein banding patterns in both the cytoplasmic fraction and in a fraction enriched in chromatin-bound proteins showed some variability in tissues of individual animals, but exhibited no changes that could be directly attributed to flight conditions. No significant change was apparent in the distribution of RI or RII cyclic AMP binding in the soluble fractions. These findings indicate that the cardiac cell integrity or its protein content is not compromised under flight conditions. There is, however, what appears to be an adaptive molecular response which can be detected using microanalytical methods, indicating that a major hormone regulated mechanism may be affected during some phase of travel in space.

Animals↗