Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the effects of prostaglandin E1 (PGE1) used in hypotensive anesthesia on the adrenal endocrine function, aldosterone, corticosterone (Comp B) and cAMP production were measured in isolated glomerulosa (G-c) and fasciculata cells (F-c) of the rats. Rat glomerulosa and fasciculata cells were obtained by enzymatic digestion of the adrenals of male wistar rats. The cell pellet was suspended in Hank's balanced salt solution containing 0.1% BSA and distributed in 900 microliters aliquots to polyethylene tubes. The samples were preincubated for 90 min in a 37 degrees C water bath aerated with 5% CO2/95% O2. PGE1 or ACTH 50 microliters was added and incubated for 4 hr. Total volume of the incubation medium is 1.0 ml. Aldosterone and cAMP were measured by radioimmunoassay and Comp B was determined by fluorimetric method. PGE1 increased significantly the basal secretion of aldosterone and Comp B in G-c and F-c, respectively. The steroidogenic effect of PGE1 was dose dependent in aldosterone production. This aldosterone production was also accompanied with cAMP production. On the other hand, significant increase of cAMP was not observed in comp B production. These results suggest that cAMP may be the second messenger in PGE1-induced aldosterone production in G-c. But PGE1 receptors in F-c seem not to be coupled to the adenylate cyclase system. The addition of ACTH and PGE1 resulted in inhibition of aldosterone secretion when compared with that obtained by ACTH alone. Several researchers have shown that low doses of PGE1 depressed the basal aldosterone secretion. These findings may be contributing to Na-uresis effect during PGE1-induced hypotension.
 ...
PMID:[Role of prostaglandin E1 in steroidogenesis by isolated rat adrenal cells]. 166 72

Perfusing preswollen deepithelialized rabbit cornea in vitro on its endothelial side with balanced salt solution containing physiological glucose concentration and 10(-6)M adenosine, we can obtain "temperature reversal" from 500-520 microns to less than 400 microns, during 7 hours. Low concentrations of adenosine improve the fluid pump supposedly by inhibiting adenylate cyclase, since c-AMP inhibits the pump.
 ...
PMID:The effect of cyclic AMP on the rabbit corneal endothelial fluid pump. 630 89

Schwann cells play an important role in both the development and regeneration of peripheral nerves. Proliferation and differentiation of Schwann cells are critically dependent on changes in the levels of cAMP. ATP is a fast excitatory transmitter in the peripheral nervous system, inducing depolarization of the vagus nerve through occupancy of P2-purinergic receptors. In the present study we demonstrate that extracellular ATP stimulates phospholipase C and inhibits adenylate cyclase activities in cultured Schwann cells. Addition of ATP inhibited, in a concentration-dependent manner, forskolin- or isoprenaline-stimulated adenylate cyclase activity. The rank order of potency corresponding to different purinergic receptor agonists was 2-methylthio-ATP > ATP = ADP > or = adenosine 5'-[gamma-thio]triphosphate (ATP[S]) > UTP, consistent with the involvement of a P2y subtype. Adenosine and adenosine 5'-[alpha,beta-methylene]-triphosphate (pp[CH2pA) were ineffective. Preincubation with pertussis toxin completely blocked this inhibitory effect. When Schwann cells were pre-labelled with myo-[3H]inositol and incubated in Hanks' balanced salt solution containing Ca2+ and Mg2+, addition of ATP[S] resulted in a concentration-dependent increase in the release of InsP with a concomitant increase in intracellular free [Ca2+] ([Ca2+]i). Under these conditions, the effects of both ATP and UTP were of lower magnitude. Removal of Ca2+ and Mg2+ from the assay medium resulted in a significant increase in the effects of ATP[S], ATP and UTP. The decreased response observed in the presence of both bivalent cations (1.2 mM Ca2+ and 1 mM Mg2+) could not be explained either by increased degradation of ATP by Ca2+/Mg2+-dependent nucleotidases or by cation influx. The rank order of potency for the effects of agonists on phospholipase C activity was ATP[S] = adenosine 5'[gamma-imido]triphosphate > ATP -UTP > ADP, indicating the involvement of a P(2U) receptor subtype in this response. Adenosine, AMP and pp[CH2]pA were ineffective. These results demonstrate that immortalized Schwann cells express P(2U) and P(2Y) purinoceptors, which are coupled to stimulation of phospholipase C and inhibition of adenylate cyclase, respectively. Our observations unveil signal-transduction pathways that may be used by ATP to regulate proliferation and differentiation of Schwann cells, and ultimately to influence nerve homeostasis.
 ...
PMID:P2-purigenic receptors regulate phospholipase C and adenylate cyclase activities in immortalized Schwann cells. 867 70

The inflammatory exudate at the post-anaphylaxis phase of allergic inflammation in rats has an ability to enhance histamine production by bone marrow cells. To analyze the mechanism of the inflammatory exudate-induced histamine production pharmacologically, the effects of several drugs were examined in cultures of bone marrow cells. Incubation of the bone marrow cells in the presence of the inflammatory exudate that had been centrifuged and dialyzed against Hanks' balanced salt solution increased histidine decarboxylase activity in the cells and histamine concentration in the conditioned medium. The induction of histamine production by the inflammatory exudate was inhibited by actinomycin D (0.01-1 microM), an inhibitor of RNA synthesis, and cycloheximide (0.1-10 microM), a protein synthesis inhibitor. The protein kinase C inhibitors staurosporine (2-20 nM), K-252a (6-200 nM), and H-7 (10.3-103 microM) also inhibited the inflammatory exudate-induced histamine production in a concentration-dependent manner. The tyrosine kinase inhibitor genistein (3.7-37 microM) also inhibited the inflammatory exudate-induced histamine production, but the protein kinase A inhibitor H-89 (0.2 microM), and the adenylate cyclase activator forskolin (0.1 microM) showed no effect. These findings suggest that histamine production induced by the inflammatory exudate is mediated by the de novo synthesis of histidine decarboxylase and by the activation of protein kinase C and tyrosine kinase.
 ...
PMID:Pharmacological analysis of the inflammatory exudate-induced histamine production in bone marrow cells. 913

To determine the potential value of measuring adenylylcyclase activity as a pre-transplant functional marker of pancreatic islet cell quality, a production rate of adenosine 3':5'-monophosphate was measured with a fluorometric assay in rat islet cells before transplantation. Islets were stored for different periods of time (0 to 96 hours) and in different preservation solutions. The adenylylcyclase activities of islets stored in University of Wisconsin (UW) solution for 3 hours after isolation were significantly higher than those stored in Hanks' balanced salt solution. Similarly, the adenylylcyclase activities of islets stored for more than 24 hours in UW solution decreased significantly with prolonged storage time. Preoperative adenylylcyclase activity was compared with post-transplant islet function in a rat model of diabetes. Transplant success was evaluated by measuring blood glucose level and body weight. Although all transplants were ultimately successful in this study, the rate at which they achieved euglycemia varied, and this is the property that correlated with pre-transplant basal or forskolin-stimulated adenylylcyclase activity. Additional studies showed that it was feasible to measure adenylylcyclase activity in human islet cells. We conclude that preoperative measurement of basal and stimulated adenylylcyclase activity may provide a useful clinical marker for assessing islet cell quality and differences in preservation media and may predict transplant success. Based on these data, additional studies evaluating the feasibility of using adenylylcyclase activity as a research and clinical marker of islet cell viability are warranted.
 ...
PMID:Preoperative assessment of adenylylcyclase activity as a functional marker of islet cell quality after transplantation in rats. 1021 70

Dictyostelium discoideum amoeba are found in soil, feeding on bacteria. When food sources become scarce, they secrete factors to initiate a multicellular development program, during which single cells chemotax towards aggregation centers(1-4). This process is dependent on the release of cyclic adenosine monophosphate (cAMP)(5). cAMP is produced in waves through the concerted action of adenylate cyclase and phosphodiesterases, and binds to G protein-coupled cAMP receptors(6,7). A widely used assay to analyze the mechanisms involved in the developmental cycle of the lower eukaryote Dictyostelium discoideum is based on the observation of cell aggregation in submerged conditions(8,9). This protocol describes the analysis of the role of coronin A in the developmental cycle by starvation in tissue-culture plates submerged in balanced salt solution (BSS)(10). Coronin A is a member of the widely conserved protein family of coronins that have been implicated in a wide variety of activities(11,12). Dictyostelium cells lacking coronin A are unable to form multicellular aggregates, and this defect can be rescued by supplying pulses of cAMP, suggesting that coronin A acts upstream of the cAMP cascade(10). The techniques described in these studies provide robust tools to investigate functions of proteins during the initial stages of the developmental cycle of Dictyostelium discoideum upstream of the cAMP cascade. Therefore, utilizing this aggregation assay may allow the further study of coronin A function and advance our understanding of coronin biology.
 ...
PMID:Investigating the Function of Coronin A in the Early Starvation Response of Dictyostelium discoideum by Aggregation Assays. 2740 5