CAMP accumulation release

Ohno T, Kato N, Ishii C, Shimizu M, Ito Y, Tomono S and Kawazu S. 1993. Genistein augments cyclic adenosine 3 5 -monophosphate(cAMP) accumulation and insulin release in MIN6 cells. Endocr Res 19(4) 273-285. 

D-l Dopamine Receptor-Mediated Activation oi Adenylate Cyclase, cAMP Accumulation, and PTH Release in Dispersed Bovine Parathyroid Cells... 

Affinity of drugs for the dopamine receptor in bovine parathyroid cells determined in experiments measuring cAMP accumulation, adenylate cyclase, or PTH release. 

The dopamine-stimulated formation of cAMP may initiate the dopamine-induced release of IR-PTH. A linear relationship exists between the dopamine-induced release of IR-PTH and the logarithm of the dopamine-induced accumulation of cAMP (17). Similarly, other agents increasing cAMP accumulation and IR-PTH release (e.g. beta-adrenergic agonists, secretin and phosphodiesterase inhibitors, also display such a log-linear relationship. Additional support for the possibility that intracellular cAMP might initiate PTH secretion comes from the observations that cholera toxin (JJ.), phosphodiesterase inhibitors (17) and dibutyryl cAMP (18), agents known to increase intracellular cAMP or mimic the biochemical effects of cAMP, increase the release of IR-PTH. 

Figure 5. Comparison of the potency of isoproterenol in eliciting physiological and biochemical responses from the rat IL. Substantially lower concentrations of isoproterenol stimulate the release of IR-aMSH (aMSH) than are required to enhance cAMP accumulation by intact IL cells (cAMP), stimulate adenylate cyclase activity in cell-free homogenates of IL tissue (cyclase), or occupy the specific binding sites defined with IHYP (binding) (19).

For each response examined, inhibition of isoproterenol-stimulated cAMP accumulation by intact cells ( ) inhibition of basal release of IR-aMSH by intact cells ( J occupancy of specific [3H]-spiroperidol binding sites in a cell-free homogenate (Q) and inhibition of isoproterenol-stimulated adenylate cyclase activity in a cell-free homogenate (M), the effect achieved with the indicated concentration of apomorphine is expressed as a percentage of the maximal effect of apomorphine (33). 

Although earlier studies failed to find consistent effects of DA on cAMP levels or adenylate cyclase activity in anterior pituitary cells [13], intact pituitary gland [14,15] or homogenates [13,16], a functional connection between the two is now supported by many experimental approaches. DA and DA agonists inhibit cAMP levels in cultured rat pituitary cells at concentrations in the nanomolar range, comparable to those which inhibit PRL release [17-21], DA also inhibits cAMP accumulation stimulated by VIP or TRH [20]. Inhibition is also seen in human prolactinoma cells [22]. 

GH release [52], that dexamethasone, which increases the GH response to GRF, also increases the stimulation of cAMP accumulation by GRF but not basal levels [54] and that the ED,() of increasing GH (1.6 x 10 12 M) closely matches the ED5() of increasing cAMP levels (6 x 10 12 M). The increase of cAMP levels is caused by a stimulation of the adenylate cyclase in a GTP-dependent manner [55]. 

The GH release inhibitory action of SRIF at least in part involves inhibition of adenylate cyclase [55,56]. Most likely this occurs through coupling with the inhibitory regulatory G protein of the enzyme, since the effect is GTP-dependent and is blocked by pertussis toxin. However, in sheep cells SRIF inhibits GRF-stimulated GH release without any effect on cAMP levels whereas in rats GRF stimulation of GH is completely inhibited by SRIF but cAMP accumulation only in part [57], An additional site of action of SRIF appears to be at the level of GRF-stimulated Ca2+ mobilization (see below). 

Studies in rat alveolar type II cells have demonstrated that terbutaline stimulates sodium influx as well as potassium and chloride release via cAMP accumulation. 

Reisine T (1984) Somatostatin desensitization loss of the ability of somatostatin to inhibit cAMP accumulation and adrenocorticotropin release. J Pharmacol Exp Ther 229 14-20... 

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