Rise In Cyclic AMP Research Articles

Cyclic AMP levels in various tissues of the domestic fowl ( Gallus domesticus) as affected by glucagon, epinephrine and insulin

1. 1. The effects of glucagon, epinephrine and insulin on the in vivo time course changes in blood glucose and in blood, muscle and liver cyclic AMP levels of the domestic fowl have been studied. 2. 2. Intravenous injections of glucagon and epinephrine produced a rapid increase in blood cyclic AMP (10- and 6-fold, respectively) followed by a more gradual increase in blood glucose. The patterns of response, however, in blood, muscle and liver, following either glucagon or epinephrine administration were different. Glucagon markedly elevated hepatic tissue levels while it had only a minimal effect on muscle. Epinephrine, in contrast, elevated cyclic AMP levels to a similar extent in both tissues. The decrease in peak cyclic AMP levels following epinephrine treatment was biphasic for both muscle and liver. 3. 3. The time course patterns for the rise and fall of cyclic AMP in liver, muscle and blood were nearly the same suggesting a rapid transfer of tissue cyclic AMP to blood. Maximal cyclic AMP levels occurred 5–10 min and 10–20 min after intravenous injections of epinephrine and glucagon, respectively. 4. 4. Insulin depressed blood glucose levels but elevated blood, muscle and liver cyclic AMP levels. The cyclic AMP pattern following insulin injection is different than that observed in mammals.

Cyclic AMP formation and thyroid secretion by incubated mouse thyroid lobes.

The effects of TSH on the concentration of cyclic AMP, the number of intracellular colloid droplets and the release of hormonal radioiodine was studied in incubated mouse thyroid lobes. TSH increased all 3 parameters with a similar time course but cyclic AMP accumulation preceded colloid droplet formation and iodine release. The increase in thyroidal cyclic AMP was induced by TSH in a concentration range of 0.3-30 mU/ ml in contrast to the other measures of secretion which were elicited by a ten—fold lower concentration of TSH. Theophylline increased the response to TSH only for concentrations of TSH which by themselves increased cyclic AMP. The TSH stimulated increase in cyclic AMP was blocked by chlorpromazine but was unaffected by colchicine, vinblastine or cytochalasin B. Ouabain, removal of Na+ from the medium, or elevation of the medium concentration of Ca++ partially reduced the TSH stimulated rise in cyclic AMP whereas removal of Ca++ from the medium or addition of Li+ was without effect. (Endocri...

Insulin Action in Isolated Rat Thymocytes: II. INDEPENDENCE OF INSULIN AND CYCLIC ADENOSINE MONOPHOSPHATE

Abstract Dibutyryl cyclic adenosine 3',5'-monophosphate(dibutyryl cyclic AMP), cyclic adenosine 3',5'-monophosphate (cyclic AMP), and prostaglandin E1 (PGE1) stimulated α-aminoisobutyric acid (AIB) influx in thymocytes from suckling rats. Dibutyryl cyclic AMP increased influx at concentrations as low as 30 µm; a maximal effect was seen at 1 mm. Cyclic AMP had 1% of the activity of its dibutyryl derivative. PGE1 increased AIB influx at concentrations as low as 30 nm. Dibutyryl cyclic AMP increased AIB influx by increasing the maximal influx capacity (Jmax) without affecting the Km. This is in contrast to the effect of insulin which, in addition to raising the Jmax, also lowers the Km. When insulin was added with either PGE1 or dibutyryl cyclic AMP, the effects were additive. PGE1 elevated thymocyte cyclic AMP levels, whereas insulin neither lowered basal cyclic AMP levels nor blocked the rise in cyclic AMP produced by PGE1. We concluded that (a) insulin increased AIB influx by a mechanism not involving changes in cyclic AMP levels, and (b) cyclic AMP and prostaglandin E1 increased AIB influx by a different mechanism than insulin.

Adenylcyclase-phosphodiesterase system in arterial smooth muscle

Isoproterenol, epinephrine, and norepinephrine increase cyclic AMP formation in rat aorta through their stimulatory effect on adenyl cyclase. Isoproterenol, and epinephrine and norepinephrine in the presence of phentolamine, have a relaxing effect on the rat aortic strip. Propranolol prevents the rise in cyclic AMP with the three catecholamines and modifies the epinephrine-induced contraction. Inhibition of phosphodiesterase is also accompanied by relaxation of arterial smooth muscle.

Effects of angiotensin II on cyclic 3′ 5′ AMP in rat uterus

Angiotensin II induces dose-dependent contractions in rat uterus without any detectable variation in adenyl cyclase activity or in tissue cyclic AMP level. Angiotensin II, incubated at the concentration of 10 −5M together with 10 −6M of the relaxing agent adrenaline, decreases but does not suppress the activation of adenyl cyclase induced by 10 −6M adrenaline alone; despite the persistent rise in cyclic AMP brought about by adrenaline, angiotensin induced a contractor response. These results suggest that the angiotensin-elicited contraction in rat uterus is not mediated by the adenyl cyclase-cyclic AMP system.

Immobilization stress induced changes in adrenocortical and medullary cyclic AMP content in the rat.

The levels of adrenal cyclic AMP in adrenal cortex and medulla have been examined during immobilization stress under varying conditions. After 30 min of immobilization, there was a highly significant rise in whole adrenal cyclic AMP, returning to base line levels after 150 min. Theophylline pretreatment shifted the maximal cyclic AMP increase after immobilization to 10 min, with return to almost base line values at 30 min. Hypophysectomy blocked the rise in adrenal cyclic AMP and, in fact, there was a small but significant decrease after 10 or 30 min of immobilization. Denervation of the adrenal gland did not alter the level of cyclic AMP in unstressed animals but reduced the elevation of cyclic AMP to about 50% of the response observed in the intact adrenals of stressed animals. There was no increase in cyclic AMP in the adrenal medulla after stress although the medullary component of cyclic AMP was 50% of the total. There was a highly significant cortical increase in cyclic AMP after immobilization. Finally, a significant increase was observed in adrenocortical cyclic AMP in denervated adrenals of stressed animals but not in the medulla. Thus, either the splanchnic nerve or the adrenal medulla via the nerve may be releasing a factor which takes part in the regulation of adrenocortical cyclic AMP. (Endocrinology88: 338, 1971)

Hormonal regulation of myocardial adenosine 3′,5′-monophosphate

A simple, sensitive, and specific method for measuring changes in adenosine 3′,5′-monophosphate (cyclic AMP) has been applied to the investigation of hormonal control of myocardial cyclic AMP in the rat ventricular slice. Catecholamines have been demonstrated to produce a 100% increase in cyclic AMP levels. Insulin had no effect on cyclic AMP levels and did not alter the catecholamine-induced rise. The presence of Ca 2+ in the extracellular fluid was not essential for the production of cyclic AMP, nor was it required for the catecholamine-induced rise in cyclic AMP. Neither glucagon, triiodothyronine or ouabain had any significant effect on cyclic AMP levels in the rat-heart slice.