TY - JOUR

T1 - Modulatory mechanisms in the isolated internally perfused ventricle of the whelk Busycon canaliculatum.

AU - Huddart, H.

AU - Hill, R .B.

PY - 1996/7

Y1 - 1996/7

N2 - 1. 1. Isolated cannulated ventricles commenced spontaneous beating on application of perfusion pressure of 10 cm water. Complete hearts showed a fast patterned cyclical rhythm, whereas ventricles devoid of atrial material showed a continuous slow rhythm. 2. 2. Perfused ventricles were inhibited by ACh with a threshold at 10∞ mol 1−1 and arrested at 10−7 mol 1−1 and ventricles under stimulation by 5HT could be arrested by ACh at this concentration. 3. 3. Perfused ventricles were stimulated by 5HT, with threshold at 10−9 mol 1−1 and maximum at 10−5 mol 1−1. Metoclopramide was without affect on 5HT responses, but metitipine and methysergide did inhibit such responses suggesting that the 5HT receptor present possessed mixed properties of the vertebrate 5-HT1 and 5-HT2 receptor subtypes. 4. 4. Ventricles were very sensitive to the excitatory actions of FMRFamide in the 10-9 to 105 mol 1-1 range. Preparations were insensitive to GAPFLRFamide, but SCP-B was modestly excitatory (threshold 10−7 mol l−9. 5. 5. Preparations were not significantly affected by adenosine, ATP, and guanosine, but GTP was strongly excitatory at 10−7 mol 1−1 6. 6. 5HT and FMRFamide responses were additive. Preparations responded strongly to the adenylate cyclase activator forskolin and dibutyryl cAMP enhanced spontaneous contractions and 5HT responses, suggesting that the 5HT receptor may operate via a cAMP secondary mechanism. 7. 7. The IP3 inhibitor lithium (10 mmol l−1), caused slight inhibition of FMRFamide responses, suggesting that the receptor to this peptide may operate via IP3 as a second messenger. 8. 8. Neuromodulation in this preparation would appear to involve ACh as inhibitor, 5HT and FMRFamide as upregulators, with no clear roles for FMRFamide-related peptides and GTP.

AB - 1. 1. Isolated cannulated ventricles commenced spontaneous beating on application of perfusion pressure of 10 cm water. Complete hearts showed a fast patterned cyclical rhythm, whereas ventricles devoid of atrial material showed a continuous slow rhythm. 2. 2. Perfused ventricles were inhibited by ACh with a threshold at 10∞ mol 1−1 and arrested at 10−7 mol 1−1 and ventricles under stimulation by 5HT could be arrested by ACh at this concentration. 3. 3. Perfused ventricles were stimulated by 5HT, with threshold at 10−9 mol 1−1 and maximum at 10−5 mol 1−1. Metoclopramide was without affect on 5HT responses, but metitipine and methysergide did inhibit such responses suggesting that the 5HT receptor present possessed mixed properties of the vertebrate 5-HT1 and 5-HT2 receptor subtypes. 4. 4. Ventricles were very sensitive to the excitatory actions of FMRFamide in the 10-9 to 105 mol 1-1 range. Preparations were insensitive to GAPFLRFamide, but SCP-B was modestly excitatory (threshold 10−7 mol l−9. 5. 5. Preparations were not significantly affected by adenosine, ATP, and guanosine, but GTP was strongly excitatory at 10−7 mol 1−1 6. 6. 5HT and FMRFamide responses were additive. Preparations responded strongly to the adenylate cyclase activator forskolin and dibutyryl cAMP enhanced spontaneous contractions and 5HT responses, suggesting that the 5HT receptor may operate via a cAMP secondary mechanism. 7. 7. The IP3 inhibitor lithium (10 mmol l−1), caused slight inhibition of FMRFamide responses, suggesting that the receptor to this peptide may operate via IP3 as a second messenger. 8. 8. Neuromodulation in this preparation would appear to involve ACh as inhibitor, 5HT and FMRFamide as upregulators, with no clear roles for FMRFamide-related peptides and GTP.

KW - ACh

KW - Busycon canaliculatum

KW - caffeine

KW - cyclopiazonic acid

KW - dibutyryl cAMP FMRFamide

KW - forskolin

KW - GAPFLRFamide

KW - GTP

KW - 5-hydroxytryptamine

KW - lithium

KW - methysergide

KW - metitipine

KW - SCP-B

KW - ventricle

U2 - 10.1016/0306-3623(95)02111-6

DO - 10.1016/0306-3623(95)02111-6

M3 - Journal article

VL - 27

SP - 809

EP - 818

JO - General Pharmacology: The Vascular System

JF - General Pharmacology: The Vascular System

SN - 0306-3623

IS - 5

ER -