Effects of L-DOPA and 6-hydroxydopamine on the intracellular cAMP content in rat kidney with neurotrophic dysfunction of the organ

1993 ◽  
Vol 115 (6) ◽  
pp. 631-633
Author(s):  
L. K. Egorova
Keyword(s):  
Rat Kidney ◽  
Intracellular Camp ◽  
Camp Content ◽  
6 Hydroxydopamine ◽  
Intracellular Camp Content

Effects of PGI2 and Its More Stable Forms on the Aggregation and on the Camp Content of Human Platelets

1979 ◽  
Author(s):  
E. Nemesánszky ◽  
I. Blaskó ◽  
I. Stadler ◽  
G. Sas ◽  
L. A. Pálos
Keyword(s):  
Ethyl Ester ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Intracellular Camp ◽  
Camp Content ◽  
Prolonged Duration ◽  
Potent Inhibitory Effect ◽  
Stable Forms ◽  
Derivatives Of ◽  
Intracellular Camp Content

The authors investigated the anti-aggregating properties of some relatively stable derivatives of PGI2 concurrently determining the intracellular cAMP content of platelets. The ethyl-ester derivative of PGI2 and the complexes of PGI2-ethyl ester with β-cyclodextrine proved to be more stable than PGI2-sodium salt. Their stimulating effect on adenyl-cyclase correlated with the potent inhibitory effect on platelet aggregation as well. The enhancing effect of these compounds for the intracellular cAMP content have a prolonged duration time -lasting 300 minutes- compared with the only a few minutes’ effect of PGE1.These stable forms of PGI2 might be clinically useful as highly effective antiaggregating compounds.

Effects of PGI2 and its more Stable forms on the Aggregation and on the Camp Content of Human Platelets

1979 ◽  
Author(s):  
E. Nemesánszky ◽  
Gy. Blaskó ◽  
I. Stadler ◽  
G. Sas ◽  
L.A. Pálos
Keyword(s):  
Ethyl Ester ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Adenyl Cyclase ◽  
Intracellular Camp ◽  
Camp Content ◽  
Potent Inhibitory Effect ◽  
Stable Forms ◽  
Derivatives Of ◽  
Intracellular Camp Content

The authors investigated the anti-aggregating properties of some relatively stable derivatives of PGI2 concurrently determining the intracellular cAMP content of platelets. The ethyl-ester derivative of PGI2 and the complexes of PGI2-ethyl ester with β-cyclodextrine proved to be mora stable than PGI2-sodium salt. Their stimulating effect on adenyl-cyclase correlated with the potent inhibitory effect on platelet aggregation as well. The enhancing effect of these compounds for the intracellular cAMP conten t have a prolonged dura tion time -las ting 300 minutes - compared with the only a few minutes’ effect of PGE1.These stable forms of PGI2 might be clinically useful as highly effective anti-aggregating compounds.

Effects of calcium antagonist TMB-8 on active Na and Cl transport in rabbit ileum

1986 ◽  
Vol 250 (5) ◽  
pp. G691-G697 ◽  
Author(s):  
M. Donowitz ◽  
S. Cusolito ◽  
G. W. Sharp
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Intracellular Camp ◽  
Bathing Solution ◽  
Rabbit Ileum ◽  
Camp Content ◽  
Cl Transport ◽  
Transport Effects ◽  
Intracellular Camp Content

The effects of 3,4,5-trimethoxybenzoate 8-(N,N-diethylamino)octyl ester (TMB-8), an agent that traps calcium within intracellular stores, were studied on active electrolyte transport in rabbit ileum under basal conditions and after altering transport by increasing the intracellular cAMP content or by exposure to two agonists that act by altering intracellular Ca2+ (carbachol and serotonin). TMB-8 decreased the ileal short-circuit current and increased active Na and Cl absorption by increasing the mucosal-to-serosal Na and Cl fluxes. These effects were reversed by increasing the bathing solution Ca2+ to 4 mM, a concentration that itself did not alter basal ileal transport. The maximum glucose- and amino acid (alanine)-induced increase in Na absorption in the ileum was not affected by TMB-8. The effects on basal transport of TMB-8 were not associated with a change in 45Ca2+ entry across the ileal serosal surface. TMB-8 did not alter cAMP-induced secretion, as judged by its lack of effect on the increase in short-circuit current caused by 8-bromo-cAMP (10(-4) M). TMB-8 totally prevented the transport effects of carbachol but did not inhibit the effects of serotonin. These data suggest a role for intracellular Ca2+ in regulation of basal ileal Na and Cl transport but not in cAMP-induced secretion. There appear to be several pools of intracellular Ca2+ involved in neurohumoral effects on active electrolyte transport.

Xanthine derivatives without PDE effect stimulate voltage-activated chloride conductance of toad skin

2003 ◽  
Vol 284 (2) ◽  
pp. C521-C527 ◽  
Author(s):  
Wolfram Nagel ◽  
Uri Katz
Keyword(s):  
Intracellular Camp ◽  
Voltage Sensitivity ◽  
Inhibitory Effects ◽  
Amphibian Skin ◽  
Toad Skin ◽  
Camp Content ◽  
Xanthine Derivatives ◽  
X 32 ◽  
Intracellular Camp Content ◽  
Stimulation Of

The effect of xanthine derivatives on the voltage-activated Cl− conductance ( G Cl) of amphibian skin was analyzed. 3-Isobutyl-1-methylxanthine (IBMX) and the recently synthesized xanthine derivatives 3,7-dimethyl-1-propyl xanthine (X-32) and 3,7-dimethyl-1-isobutyl xanthine (X-33), which lack inhibitory effects on phosphodiesterases in CHO and Calu-3 cells, increased voltage-activated G Cl without effect on baseline conductance at inactivating voltage. Half-maximal stimulation of G Cl occurred at 108 ± 9 μM for X-32 and X-33 after apical or basolateral application. The stimulation of G Cl, which occurs only in the presence of Cl− in the mucosal solution, is caused by a shift of the voltage sensitivity to lower clamp potentials and an increase of the maximally activated level. Furosemide reversed both the shift of sensitivity and the increase in magnitude. These patterns are fundamentally different from those seen after application of membrane-permeant, nonmetabolized analogs of cAMP, and they indicate that the xanthines stimulate G Cl directly. This notion is strengthened by the lack of influence on intracellular cAMP content, which is consistent with the observations in CHO and Calu-3 cells. We propose that the xanthine derivatives increase the voltage sensitivity of a regulative component in the conductive Cl− pathway across amphibian skin.

scholarly journals Mechanism of bile salt-induced mucin secretion by cultured dog gallbladder epithelial cells

1996 ◽  
Vol 316 (3) ◽  
pp. 873-877 ◽  
Author(s):  
J. Henriëtte KLINKSPOOR ◽  
Guido N. J. TYTGAT ◽  
Sum P. LEE ◽  
Albert K. GROEN
Keyword(s):  
Epithelial Cells ◽  
Bile Salt ◽  
Bile Salts ◽  
Cholesterol Gallstone ◽  
Direct Interaction ◽  
Gallstone Formation ◽  
Intracellular Camp ◽  
Mucin Secretion ◽  
Camp Content ◽  
Intracellular Camp Content

1. Hypersecretion of gallbladder mucin has been proposed to be a pathogenic factor in cholesterol gallstone formation. Using cultured gallbladder epithelial cells, we demonstrated that bile salts regulate mucin secretion by the gallbladder epithelium. In the present study we have investigated whether established second messenger pathways are involved in bile salt-induced mucin secretion. 2. The effect of activators and inhibitors on mucin secretion was studied by measuring the secretion of [3H]N-acetyl-D-glucosamine-labelled glycoproteins. Intracellular cAMP content of the cells was measured using a radioimmunoassay. 3. Incubation of the cells with 10 mM taurocholate did not increase the intracellular cAMP content (25.7 versus control 22.8 pmol of cAMP/mg of protein). No stimulation of mucin secretion was observed after incubation with 1–100 μM concentrations of the calcium ionophores ionomycin and A23187. The stimulatory effect of 10 mM tauroursodeoxycholate (TUDC) on mucin secretion could not be inhibited by the addition of EDTA. Activation of protein kinase C (PKC) by 1 μg/ml phorbol 12-myristate 13-acetate (PMA) caused an increase in mucin secretion (342% versus control 100%), comparable with the effect of 40 mM TUDC. The effect of 10 ng/ml PMA could partially be inhibited by a concentration of 2 μM of the PKC inhibitor staurosporin. Staurosporin had no inhibitory effect on mucin secretion induced by TUDC. 4. In gallbladder epithelial cells bile salts do not stimulate mucin secretion via one of the classical signal transduction pathways. We hypothesize that bile salts act on mucin secretion via a direct interaction with the apical membrane.

Differentiation of African trypanosomes is controlled by a density sensing mechanism which signals cell cycle arrest via the cAMP pathway

1997 ◽  
Vol 110 (21) ◽  
pp. 2661-2671 ◽  
Author(s):  
E. Vassella ◽  
B. Reuner ◽  
B. Yutzy ◽  
M. Boshart
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Mammalian Host ◽  
Intracellular Camp ◽  
Quiescent State ◽  
Camp Content ◽  
African Trypanosomes ◽  
Sensing Mechanism ◽  
Camp Signalling ◽  
Cycle Arrest

Differentiation of African trypanosomes from replicating slender bloodstream forms to nondividing stumpy forms limits the parasite population size, allowing survival of the mammalian host and establishment of a stable host-parasite relationship. Using a novel in vitro culture system we have shown that slender to stumpy differentiation is induced by parasite density alone and thus is independent of host cues. Here we investigate the density sensing mechanism and show that trypanosomes release a soluble activity of low relative molecular mass, termed stumpy induction factor (SIF), which accumulates in conditioned medium. SIF activity triggers cell cycle arrest in G1/G0 phase and induces differentiation with high efficiency and rapid kinetics. Membrane-permeable derivates of cAMP or the phosphodiesterase inhibitor etazolate perfectly mimic SIF activity. Furthermore, SIF activity elicits an immediate two- to threefold elevation of intracellular cAMP content upon addition to slender forms. We conclude that SIF and hence density sensing operate through the cAMP signalling pathway. Temporal correlation of markers indicates that cell cycle arrest invariably precedes differentiation. Thus, our results indicate that the cell cycle regulation of bloodstream forms is under dominant control of cAMP signalling. Irreversible commitment to the quiescent state is elicited by a cAMP agonist within a period shorter than one complete cell cycle.

scholarly journals Urinary Reabsorption in the Rat Kidney by Anticholinergics

2021 ◽  
Author(s):  
Hideki Oe ◽  
Hatsumi Yoshiki ◽  
Xinmin Zha ◽  
Hisato Kobayashi ◽  
Yoshitaka Aoki ◽  
...  
Keyword(s):  
Absorption Rate ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Intracellular Camp ◽  
Dependent Manner ◽  
Bladder Epithelium ◽  
Duct Cells ◽  
Urine Production ◽  
Saline Administration ◽  
Collecting Duct Cells

Abstract Anticholinergics, therapeutic agents for overactive bladder, are clinically suggested to reduce urine output. We investigated whether this effect is due to bladder or kidney urine reabsorption. Various solutions were injected into the bladder of urethane-anesthetized SD rats. The absorption rate for 2 hr was examined following the intravenous administration of the anticholinergics imidafenacin (IM), atropine(AT), and tolterodine(TO). The bilateral ureter was then canulated and saline was administered to obtain a diuretic state. Anticholinergics or 1-deamino-[8-D-arginine]-vasopressin (dDAVP) were intravenously administered. After the IM and dDAVP administrations, the rat kidneys were immunostained with AQP2 antibody, and intracellular cAMP was measured. The absorption rate was ~10% of the saline injected into the bladder and constant even when anticholinergics were administered. The renal urine among peaked 2 hr after the saline administration. Each of the anticholinergics significantly suppressed the urine production in a dose-dependent manner, as did dDAVP. IM and dDAVP increased the intracellular cAMP levels and caused the AQP2 molecule to localize to the collecting duct cells' luminal side. The urinary reabsorption mechanism through the bladder epithelium was not activated by anticholinergic administration. Thus, anticholinergics suppress urine production via an increase in urine reabsorption in the kidneys' collecting duct cells via AQP2.

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