TY - JOUR
T1 - Regulation of VIP release from rat enteric nerve terminals
T2 - Evidence for a stimulatory effect of NO
AU - Allescher, H. D.
AU - Kurjak, M.
AU - Huber, A.
AU - Trudrung, P.
AU - Schusdziarra, V.
PY - 1996/10
Y1 - 1996/10
N2 - The basal release of vasoactive intestinal polypeptide (VIP) from freshly prepared enriched synaptosomes was 159.1 ± 17.3 fmol/mg protein (100%), which constituted 2.5% of the total VIP content. Basal VIP release was reduced by 65% by removal of external Ca2+. Release of VIP was stimulated by depolarization with KCl (65 mM, 143%) and in the presence of veratridine (10-6 M, 184%), monensin (10-5 M, 131%), and the Ca2+ ionophore A-23187 (10-6 M, 160%). Stimulation of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent mechanisms using isoproterenol (10-6-10-4 M) and forskolin (10-6 and 10-5 M) had no stimulatory influence on VIP release. In contrast, sodium nitroprusside (10-4 M, 198%), the nitric oxide (NO) donor 3-(morpholino)sydnonimine (10-4 M, 155%), and the guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo-cGMP (10-4 M, 196%) caused a significant release of VIP. L-Arginine (10-3 M, 246%) also caused a significant increase of VIP release that was antagonized by the NO synthase inhibitor N(ω)-nitro-L-arginine methyl ester (5 x 10-4 M, 131%), which had no effect when given alone. The results demonstrate that VIP can be released from enriched synaptosomes by Ca2+-dependent mechanisms by NO agonists or NO-dependent mechanisms. It is speculated that this VIP release is induced by a presynaptic stimulatory mechanism of NO and this effect could enhance or contribute to the action of NO.
AB - The basal release of vasoactive intestinal polypeptide (VIP) from freshly prepared enriched synaptosomes was 159.1 ± 17.3 fmol/mg protein (100%), which constituted 2.5% of the total VIP content. Basal VIP release was reduced by 65% by removal of external Ca2+. Release of VIP was stimulated by depolarization with KCl (65 mM, 143%) and in the presence of veratridine (10-6 M, 184%), monensin (10-5 M, 131%), and the Ca2+ ionophore A-23187 (10-6 M, 160%). Stimulation of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent mechanisms using isoproterenol (10-6-10-4 M) and forskolin (10-6 and 10-5 M) had no stimulatory influence on VIP release. In contrast, sodium nitroprusside (10-4 M, 198%), the nitric oxide (NO) donor 3-(morpholino)sydnonimine (10-4 M, 155%), and the guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo-cGMP (10-4 M, 196%) caused a significant release of VIP. L-Arginine (10-3 M, 246%) also caused a significant increase of VIP release that was antagonized by the NO synthase inhibitor N(ω)-nitro-L-arginine methyl ester (5 x 10-4 M, 131%), which had no effect when given alone. The results demonstrate that VIP can be released from enriched synaptosomes by Ca2+-dependent mechanisms by NO agonists or NO-dependent mechanisms. It is speculated that this VIP release is induced by a presynaptic stimulatory mechanism of NO and this effect could enhance or contribute to the action of NO.
KW - calcium
KW - guanosine 3',5'-cyclic monophosphate
KW - nitric oxide
KW - reduced nicotinamide adenine dinucleotide phosphate diaphorase
KW - vasoactive intestinal polypeptide
UR - http://www.scopus.com/inward/record.url?scp=0029861586&partnerID=8YFLogxK
U2 - 10.1152/ajpgi.1996.271.4.g568
DO - 10.1152/ajpgi.1996.271.4.g568
M3 - Article
C2 - 8897874
AN - SCOPUS:0029861586
SN - 0193-1857
VL - 271
SP - G568-G574
JO - American Journal of Physiology - Gastrointestinal and Liver Physiology
JF - American Journal of Physiology - Gastrointestinal and Liver Physiology
IS - 4 34-4
ER -