Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P
The present study explores whether a peptide, such as substance P (SP), has some role subserving the atropine-resistant component of electrically-evoked contractions,in isolated rat urinary bladders. The electric field stimulation (EFS) employed herein,consisted in square wave pulses of 5 Hz, 50 ms...
Guardado en:
Publicado: |
1985
|
---|---|
Materias: | |
Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00316989_v17_n12_p1109_Dveksler http://hdl.handle.net/20.500.12110/paper_00316989_v17_n12_p1109_Dveksler |
Aporte de: |
id |
paper:paper_00316989_v17_n12_p1109_Dveksler |
---|---|
record_format |
dspace |
spelling |
paper:paper_00316989_v17_n12_p1109_Dveksler2023-06-08T14:57:10Z Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P acetylcholine atropine capsaicin substance p tetrodotoxin animal cell bladder drug administration drug comparison drug efficacy drug mechanism electrostimulation methodology muscle nonhuman preliminary communication priority journal rat smooth muscle contractility Acetylcholine Animal Atropine Bladder Capsaicin Dose-Response Relationship, Drug Electric Stimulation In Vitro Male Muscle Contraction Rats Rats, Inbred Strains Substance P Support, Non-U.S. Gov't Tetrodotoxin The present study explores whether a peptide, such as substance P (SP), has some role subserving the atropine-resistant component of electrically-evoked contractions,in isolated rat urinary bladders. The electric field stimulation (EFS) employed herein,consisted in square wave pulses of 5 Hz, 50 ms duration and supramaximal voltage (40 V), applied for 10 sec, every 3 min and conducted to the tissue via a pair of platinum ring electrodes, surounding the isolated preparations. In order to assess whether electric stimuli, induced urinary bladder inotropism through the activation of nerve structures, degeneration of intramural nerve elements was attempted by cooling the tissue (48 h at 4-5°C). After such procedure, 80-90% inhibition of responses to EFS, was detected. Moreover, tetrodotoxin, at 10-6 M, evoked similar effects than cooling. Atropine, at 10-6 M, failed to produce a significant decrement of contractile responses, whereas at 10-5 M, the electrically-induced inotropism declined around 40% in comparison with controls. In another set od experiments, atropinized urinary bladders (atropine at 10t̄5 M) were exposed to capsaicin (5 × 10-6 M) and this coincided with decreased (-43%) responses to EFS. Next, SP, at 10-9 M, was added to the medium containing capsaicin and complete restoration of full contractile responses to EFS, was observed. In as much as it has been proposed that capsaicin releases SP from sensory nerve fibers and since our experiments show that SP restored the inotropism elicited by electric stimuli on capsaicin-exposed preparations, it is suggested that SP could be involved, at least in part, in the non-cholinergic, EFS-evoked, contractile responses of isolated rat urinary bladders. © 1985. 1985 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00316989_v17_n12_p1109_Dveksler http://hdl.handle.net/20.500.12110/paper_00316989_v17_n12_p1109_Dveksler |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
acetylcholine atropine capsaicin substance p tetrodotoxin animal cell bladder drug administration drug comparison drug efficacy drug mechanism electrostimulation methodology muscle nonhuman preliminary communication priority journal rat smooth muscle contractility Acetylcholine Animal Atropine Bladder Capsaicin Dose-Response Relationship, Drug Electric Stimulation In Vitro Male Muscle Contraction Rats Rats, Inbred Strains Substance P Support, Non-U.S. Gov't Tetrodotoxin |
spellingShingle |
acetylcholine atropine capsaicin substance p tetrodotoxin animal cell bladder drug administration drug comparison drug efficacy drug mechanism electrostimulation methodology muscle nonhuman preliminary communication priority journal rat smooth muscle contractility Acetylcholine Animal Atropine Bladder Capsaicin Dose-Response Relationship, Drug Electric Stimulation In Vitro Male Muscle Contraction Rats Rats, Inbred Strains Substance P Support, Non-U.S. Gov't Tetrodotoxin Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P |
topic_facet |
acetylcholine atropine capsaicin substance p tetrodotoxin animal cell bladder drug administration drug comparison drug efficacy drug mechanism electrostimulation methodology muscle nonhuman preliminary communication priority journal rat smooth muscle contractility Acetylcholine Animal Atropine Bladder Capsaicin Dose-Response Relationship, Drug Electric Stimulation In Vitro Male Muscle Contraction Rats Rats, Inbred Strains Substance P Support, Non-U.S. Gov't Tetrodotoxin |
description |
The present study explores whether a peptide, such as substance P (SP), has some role subserving the atropine-resistant component of electrically-evoked contractions,in isolated rat urinary bladders. The electric field stimulation (EFS) employed herein,consisted in square wave pulses of 5 Hz, 50 ms duration and supramaximal voltage (40 V), applied for 10 sec, every 3 min and conducted to the tissue via a pair of platinum ring electrodes, surounding the isolated preparations. In order to assess whether electric stimuli, induced urinary bladder inotropism through the activation of nerve structures, degeneration of intramural nerve elements was attempted by cooling the tissue (48 h at 4-5°C). After such procedure, 80-90% inhibition of responses to EFS, was detected. Moreover, tetrodotoxin, at 10-6 M, evoked similar effects than cooling. Atropine, at 10-6 M, failed to produce a significant decrement of contractile responses, whereas at 10-5 M, the electrically-induced inotropism declined around 40% in comparison with controls. In another set od experiments, atropinized urinary bladders (atropine at 10t̄5 M) were exposed to capsaicin (5 × 10-6 M) and this coincided with decreased (-43%) responses to EFS. Next, SP, at 10-9 M, was added to the medium containing capsaicin and complete restoration of full contractile responses to EFS, was observed. In as much as it has been proposed that capsaicin releases SP from sensory nerve fibers and since our experiments show that SP restored the inotropism elicited by electric stimuli on capsaicin-exposed preparations, it is suggested that SP could be involved, at least in part, in the non-cholinergic, EFS-evoked, contractile responses of isolated rat urinary bladders. © 1985. |
title |
Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P |
title_short |
Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P |
title_full |
Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P |
title_fullStr |
Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P |
title_full_unstemmed |
Non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. Possible participation of substance P |
title_sort |
non-cholinergic inotropic responses evoked by electric field stimulation in the isolated rat urinary bladder. possible participation of substance p |
publishDate |
1985 |
url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00316989_v17_n12_p1109_Dveksler http://hdl.handle.net/20.500.12110/paper_00316989_v17_n12_p1109_Dveksler |
_version_ |
1768543790061060096 |