Serosal application of Ba2+ induces oscillatory chloride secretion via activation of submucosal cholinergic neurones in guinea-pig distal colon

2002 ◽  
Vol 174 (3) ◽  
pp. 257-264 ◽  
Author(s):  
M. NISHIKITANI ◽  
A. KOKUBO ◽  
H. TAKEMURA ◽  
K. SAIGENJI ◽  
K. KAWAHARA
Keyword(s):  
Guinea Pig ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Cholinergic Neurones

5-HT activates nitric oxide-generating neurons to stimulate chloride secretion in guinea pig distal colon

1998 ◽  
Vol 275 (4) ◽  
pp. G829-G834 ◽  
Author(s):  
Atsukazu Kuwahara ◽  
Hirofumi Kuramoto ◽  
Makoto Kadowaki
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Evoked Response ◽  
Evoked Responses ◽  
No Donor ◽  
Simultaneous Application

The participation of nitric oxide (NO) in serotonin (5-hydroxytryptamine; 5-HT)-evoked chloride secretion in guinea pig distal colon was examined. Submucosal/mucosal segments were mounted in Ussing flux chambers, and an increase in short-circuit current ( I sc) was used as an index of secretion. Addition of 5-HT to the serosal side produced a concentration-dependent (10−7–10−5M) increase in I sc caused by chloride secretion. N G-nitro-l-arginine (l-NNA) significantly reduced the 5-HT-evoked early (P-1) and late (P-2) responses to 61.1 and 70.6% of control, respectively. Neurally evoked response was also inhibited by l-NNA. The NO donor sodium nitroprusside (SNP, 10−4 M) increased basal I sc mainly because of chloride secretion. The SNP-evoked response was significantly reduced by tetrodotoxin but was unchanged by atropine or indomethacin. These results suggest that the 5-HT-evoked increase in I sc is associated with an NO-generating mechanism. Atropine significantly reduced the 5-HT (10−5 M)-evoked P-1 and P-2 responses to 71.8 and 19.7% of control, respectively. Simultaneous application of atropine andl-NNA further decreased the 5-HT-evoked responses more than either drug alone; application ofl-NNA and atropine decreased the 5-HT-evoked P-1 and P-2 responses to 68.5 and 39.2% of atropine-treated tissues, respectively. These results suggest that noncholinergic components of P-1 and P-2 responses are 71.8 and 19.7% of control, respectively, and that NO components of P-1 and P-2 responses are 32 and 61%, respectively, of the noncholinergic component of the 5-HT-evoked responses. The results provide evidence that NO may participate as a noncholinergic mediator of 5-HT-evoked chloride secretion in guinea pig distal colon.

Mechanical stimulation releases nucleotides that activate P2Y1 receptors to trigger neural reflex chloride secretion in guinea pig distal colon

2003 ◽  
Vol 469 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Helen J. Cooke ◽  
Jianjing Xue ◽  
Jun Ge Yu ◽  
Jacqueline Wunderlich ◽  
Y.-Z. Wang ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Mechanical Stimulation ◽  
Distal Colon ◽  
Chloride Secretion

H2 receptors mediate cyclical chloride secretion in guinea pig distal colon

1990 ◽  
Vol 258 (6) ◽  
pp. G887-G893 ◽  
Author(s):  
Y. Z. Wang ◽  
H. J. Cooke
Keyword(s):  
Guinea Pig ◽  
Chloride Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Chloride Ions ◽  
H2 Antagonist ◽  
H2 Receptors ◽  
Peak Increase

We tested the hypothesis that histamine mediates ion secretion in the guinea pig distal colon by stimulating H2 receptors on submucosal neurons. Serosal addition of histamine evoked a transient increase in short-circuit current (Isc) followed by recurrent cyclical increases in Isc. The transient phase of the response was examined previously and was not investigated in these studies. Histamine (1.5-2.5 x 10(-5) M) evoked a peak increase in Isc of 177 +/- 25 microA/cm2 at intervals of 5 min for 1-2 h. The duration of each recurrent cycle averaged 2.1 +/- 0.3 min. The H2 agonist dimaprit evoked recurrent cycles that had larger amplitudes than those caused by histamine. In the presence of histamine or dimaprit, the amplitude of the first cycle of the response was always less than subsequent cycles, regardless of the initial concentration. The cyclical responses to histamine, 2-methylhistamine, or dimaprit were unaltered by the H1 blocker pyrilamine, were reduced by the H2 antagonist cimetidine, and were abolished by the neuronal blocker tetrodotoxin. Blockade of prostaglandin formation with piroxicam did not prevent the recurrent cycles. The recurrent cycles were inhibited by the chloride transport blocker bumetanide and by removal of chloride ions. Our results demonstrate that histamine mediates prolonged cyclical chloride secretion in the guinea pig distal colon by activating H2 receptors on submucosal neurons involved in regulation of epithelial chloride transport.

PACAP evokes chloride secretion in guinea-pig distal colon: Comparison with VIP

1992 ◽  
Vol 40 (2) ◽  
pp. 189
Author(s):  
A Kuwahara ◽  
Y Kuwahara ◽  
I Tsutsui ◽  
T Mochizuki ◽  
N Yanaihara
Keyword(s):  
Guinea Pig ◽  
Distal Colon ◽  
Chloride Secretion

Action of pituitary adenylate cyclase-activating polypeptide on ion transport in guinea pig distal colon

1993 ◽  
Vol 264 (3) ◽  
pp. G433-G441 ◽  
Author(s):  
A. Kuwahara ◽  
Y. Kuwahara ◽  
T. Mochizuki ◽  
N. Yanaihara
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Ion Transport ◽  
Short Circuit ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Dependent Manner ◽  
Evoked Responses ◽  
Concentration Dependent Manner ◽  
Pituitary Adenylate Cyclase

The aim of the present study was to investigate the action of pituitary adenylate cyclase-activating polypeptide (PACAP) on ion transport in the guinea pig distal colon. Submucosal/mucosal segments from distal colon were mounted in Ussing flux chambers, and increases in short-circuit current (Isc) were used as an index of secretion. Serosal addition of PACAP-38 and PACAP-27 produced concentration-dependent (10(-10)-10(-6) M) increases in Isc. Furosemide and chloride-free solutions significantly reduced the PACAP-evoked responses. Tetrodotoxin (TTX) completely blocked PACAP-evoked responses. Atropine significantly reduced the PACAP-evoked responses but did not abolish the responses. The results suggest that PACAP evokes chloride secretion through cholinergic and noncholinergic neural mechanism. Vasoactive intestinal polypeptide (VIP), peptide histidine-isoleucine amide, and helodermin evoked Isc in a concentration-dependent manner. Atropine reduced but did not abolish the VIP- and related peptides-evoked responses. TTX also significantly decreased the responses to higher concentrations of VIP and related peptides but did not abolish the responses. The results suggest that VIP and related peptides act on both submucosal neurons and the epithelial cell itself. VIP tachyphylaxis significantly decreased PACAP-38- and PACAP-27-evoked responses. These results provide evidence that PACAP recognizes, in some part, VIP receptors in the submucosal neurons to evoke chloride secretion.

Acetylcholine release from colonic submucous neurons associated with chloride secretion in the guinea pig

1992 ◽  
Vol 262 (1) ◽  
pp. G131-G136 ◽  
Author(s):  
N. H. Javed ◽  
H. J. Cooke
Keyword(s):  
Guinea Pig ◽  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Electrical Field Stimulation ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Ach Release ◽  
Response Characteristics ◽  
Flux Chambers

Electrical field stimulation of submucous neurons in the guinea pig distal colon evokes an increase in chloride secretion sensitive to cholinergic blockade. This study was undertaken in the guinea pig to determine the feasibility of measuring acetylcholine (ACh) release simultaneously with ion transport in sheets of colonic submucosa/mucosa set up in flux chambers modified for perfusion of the submucosal surface. Release of [3H]ACh was determined in the absence of cholinesterase inhibitors as the stimulus-evoked outflow of 3H from preparations preloaded with [3H]choline. [3H]ACh released in response to electrical stimulation correlated with short-circuit current at frequencies from 0.5 to 10 Hz. At 5 and 10 Hz, the stimulus-evoked release of [3H]ACh decreased during subsequent stimulation periods. The stimulus-evoked increase in [3H]ACh was attenuated by tetrodotoxin. [3H]ACh release evoked at stimulus frequencies of 0.5-10 Hz was not altered by atropine despite a reduction in short-circuit current. This study illustrates the feasibility of measuring ACh release simultaneously with ion transport in flux chambers. The results provide new information on the response characteristics of colonic submucous neurons and provide direct evidence for regulation of chloride secretion by ACh.

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