Stimulation of GTP hydrolysis in guinea pig bronchial membranes by mastoparan

Lung ◽  
1994 ◽  
Vol 172 (6) ◽  
Author(s):  
K.J. Rhoden ◽  
J.S. Douglas
Keyword(s):  
Guinea Pig ◽  
Gtp Hydrolysis ◽  
Stimulation Of

scholarly journals Adenosine-receptor-mediated stimulation of low-Km GTPase in guinea-pig cerebral cortex

1985 ◽  
Vol 232 (2) ◽  
pp. 501-504 ◽  
Author(s):  
V Hausleithner ◽  
M Freissmuth ◽  
W Schütz
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Radioligand Binding ◽  
Rank Order ◽  
Binding Studies ◽  
Gtp Hydrolysis ◽  
Sequence Of Events ◽  
Competition Binding ◽  
Cortical Membranes ◽  
Stimulation Of

Inhibition of receptor-coupled adenylate cyclase by hormones is proposed to be associated with GTP hydrolysis. Since adenosine inhibits cerebral-cortical adenylate cyclase via A1 adenosine receptors, the present study attempts to verify this mechanism for A1-selective adenosine derivatives. In guinea-pig cortical membranes N6-(phenylisopropyl)adenosine (PIA) increased the Vmax. of the low-Km GTPase, with an EC50 (concentration causing 50% of maximal stimulation) of about 0.1 microM, and the stimulatory effect was competitively antagonized by 5 microM-8-phenyltheophylline. The rank order of potency of the stereoisomers of PIA and of 5-(N-ethylcarboxamido)adenosine (NECA) to stimulate GTPase correlated with their ability to inhibit adenylate cyclase activity (R-PIA greater than NECA greater than S-PIA). Competition binding studies with (-)-N6- ([125I]iodo-4-hydroxyphenylisopropyl)adenosine suggest that adenylyl imidodiphosphate (p[NH]ppA), an essential component of the GTPase assay system, is a more potent A1-receptor agonist than ATP, with an IC50 (concentration giving half-maximal displacement of radioligand binding) of 7.9 microM. On the basis of the p[NH]ppA concentration used in the GTPase assay (1.25 mM), enzyme stimulation by adenosine seems to be highly underestimated. Nevertheless, adenosine-induced GTP hydrolysis reflects an increased turnover of guanine nucleotides at the Ni regulatory site and appears to be a crucial step in the sequence of events processing the inhibitory signal to adenylate cyclase.

Cell loss from human, canine and guinea-pig gastric mucosa measured by DNA radioimmunoassay

1984 ◽  
Vol 66 (6) ◽  
pp. 701-708 ◽  
Author(s):  
B. C. Hurst ◽  
W. D. W. Rees ◽  
A. Garner
Keyword(s):  
Guinea Pig ◽  
Animal Species ◽  
Colorimetric Assay ◽  
Cell Loss ◽  
Mucosal Cell ◽  
Normal Human ◽  
Dna Loss ◽  
Guinea Pig Stomach ◽  
Pavlov Pouch ◽  
Stimulation Of

1. A DNA radioimmunoassay, sensitive in the range 25–1000 ng, has been developed to measure gastric mucosal cell loss. Validity of the assay was based on antibody specificity, absence of interference from gastric contents, parallel tracer displacement by dilutions of gastric and standard DNA, and crossover with colorimetric assay. 2. With this assay, gastric DNA shedding was examined in two animal species and man. In the guinea-pig stomach, DNA loss was 20–100 pg/h and in the canine Pavlov pouch, 260–580pg/h. In the canine Pavlov pouch stimulation of acid secretion by histamine and exposure to exogenous acid increased DNA output. In the normal human stomach DNA loss was 544 k 175 pg/h and in duodenal ulcer patients, 649 k 225 pg/li. 3. DNA radioimmunoassay provides a sensitive and reproducible measure of cell exfoliation from the stomach and may be a useful tool for studying aspects of gastric mucosal defence.

Effects of Electrical Stimulation of the Superior Cervical Ganglion on Cochlear Blood Flow in Guinea Pig

1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Superior Cervical Ganglion ◽  
Cochlear Blood Flow ◽  
Cervical Ganglion ◽  
Stimulation Of

scholarly journals Turnover of protein-bound serine phosphate in respiring slices of guinea-pig cerebral cortex. Effects of putative transmitters, tetrodotoxin and other agents

1973 ◽  
Vol 132 (3) ◽  
pp. 475-482 ◽  
Author(s):  
Martin Reddington ◽  
Richard Rodnight ◽  
Michael Williams
Keyword(s):  
Cerebral Cortex ◽  
Cyclic Amp ◽  
Guinea Pig ◽  
Electrical Pulses ◽  
Phosphorus Turnover ◽  
Serine Phosphate ◽  
Stimulation Of

1. The effect of various agents on the turnover of protein-bound phosphorus in respiring slices of cerebral cortex was studied. 2. Confirming previous work turnover was increased by the application of electrical pulses for 10s to the tissue. 3. Turnover was also increased by exposure of the slices for 10min to noradrenaline (0.5mm), 5-hydroxytryptamine (1μm) and histamine (0.1mm). 4. When slices were stimulated by electrical pulses in the presence of histamine the increase in turnover was the sum of the responses given by each agent above, suggesting that different phosphorylating systems were involved. 5. Tetrodotoxin (0.5μm) blocked the increased turnover due to electrical pulses, but not that due to histamine. Tetrodotoxin also prevented the increase in tissue cyclic AMP content caused by the application of electrical pulses. 6. Phosphoprotein turnover was not affected by adenosine, despite the increase in tissue cyclic AMP content given by this agent. 7. Adenosine blocked the phosphoprotein response to histamine, but did not affect the response to electrical pulses. 8. The results are discussed in relation to the hypothesis that the stimulation of protein phosphorus turnover by electrical pulses is secondary to the release of cyclic AMP in the tissue.

scholarly journals Termination of aquired and natural immunological tolerance with specific complexes.

1975 ◽  
Vol 142 (2) ◽  
pp. 312-320 ◽  
Author(s):  
G S Habicht ◽  
J M Chiller ◽  
W O Weigle
Keyword(s):  
T Cells ◽  
B Cells ◽  
Bovine Serum Albumin ◽  
Guinea Pig ◽  
Serum Albumin ◽  
Gamma Globulin ◽  
Immunological Tolerance ◽  
Detailed Mechanism ◽  
Thyroid Lesions ◽  
Stimulation Of

It was possible to terminate the induced unresponsive state to bovine serum albumin (BSA) and the natural unresponsive state to autologous thyroglobulin in rabbits (RTg) by immunization with complexes composed of heterologous cross-reacting antibody and the tolerated antigens. The unresponsive state was terminated in rabbits made unresponsive by neonatal injections of BSA and then 3 mo later injected with complexes composed of BSA and guinea pig antihuman serum albumin. This termination was manifested by the presence of anti-BSA plaque-forming cells. Similarly, the natural unresponsive state was terminated in adult rabbits injected with complexes between RTg and guinea pig antibovine thyroglobulin (BTg) in that thyroid lesions and circulating anti-RTg were produced. The results can be best explained by the presence of unresponsive T cells and competent B cells, where the guinea pig gamma globulin (antibody) activates T cells specific for the guinea pig gamma globulin portion of the complexes and thus permits stimulation of B cells competent to the exposed determinants of the tolerated (BSA or RTg) portion of the complexes. The detailed mechanism for the activation of B cells in tolerant animals is discussed.

The effect of diazepam on adenosine uptake and adenosine-stimuiated adenylate cyclase in guinea-pig brain

1982 ◽  
Vol 60 (3) ◽  
pp. 302-307 ◽  
Author(s):  
M. J. York ◽  
L. P. Davies
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Adenosine Deaminase ◽  
Small Component ◽  
Extracellular Adenosine ◽  
Pig Brain ◽  
Adenosine Uptake ◽  
Adenosine Antagonist ◽  
Guinea Pig Brain ◽  
Stimulation Of

We have used the adenosine-stimulated adenylate cyclase of guinea-pig brain to examine the potency of diazepam as an adenosine uptake inhibitor. Diazepam at concentrations in the range 10–500 μM stimulates the production of cAMP in incubated slices of guinea-pig cerebral cortex, with maximal fivefold stimulations over basal levels by 200 μM diazepam. The increases can be largely (but not completely) blocked by the adenosine antagonist theophylline or by addition of excess adenosine deaminase to the system. It appears that the stimulation of cAMP production is due to a blockade of adenosine uptake which results in an increase in extracellular adenosine and concomitant activation of the adenosine receptor coupled to adenylate cyclase. Since the cAMP response to standard adenosine uptake blockers (dipyridamole, dilazep) can be completely blocked by theophylline or adenosine deaminase, a small component of the diazepam response cannot be explained by an adenosine effect. The concentration of diazepam at which the first significant cAMP increase occurs is 10 μM or slightly lower. This is significantly higher than the concentration of diazepam needed to saturate the pharmacologically characterized central nervous system receptors for benzodiazepines.

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