Nervous release of vasoactive intestinal polypeptide in the gastrointestinal tract of cats: possible physiological implications.

Fahrenkrug, J.; Haglund, Ulf; Jodal, Mats; Lundgren, Ove; Olbe, L; Muckadell, O. B. de

doi:10.1113/jphysiol.1978.sp012541

Cited by 304 publications

(100 citation statements)

References 29 publications

(18 reference statements)

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“…In a recent study it was shown that stimulation of the pelvic nerves to the colon produced a significant increase of vasoactive intestinal polypeptide (VIP) in the venous effluent from the large bowel (Fahrenkrug, Haglund, Jodal, Lundgren, Gibe & Schaffalitzky de Muckadell, 1978) supporting the idea that VIP is a neurotransmitter in the vasodilatation elicited by pelvic nerve stimulation. It has been demonstrated that subthreshold pelvic nerve stimulation as regards blood flow effect increases the capillary filtration coefficient indicating release of a substance which increases capillary permeability (Fasth & Hulten, 1973c).…”

Section: Discussionmentioning

confidence: 91%

“…Inhibitory neurones are present throughout the gut but seems to be KININ SYSTEM AND PELVIC NERVES centrally controlled only in the stomach (Martinsson, 1965) and in the rectum (Fasth et al 1980). In a recent report by Fahrenkrug et al (1978) it was suggested that direct vagal release of VIP is responsible for the gastric receptive relaxation. Whether this hormone might also be involved in the pelvically controlled non-adrenergic relaxation of the large intestine remains to be shown.…”

Section: Discussionmentioning

confidence: 99%

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Studies on the atropine‐resistant sacral parasympathetic vascular and motility responses in the cat colon.

Fasth¹,

Hultén²,

Nordgren³

et al. 1981

The Journal of Physiology

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SUMMARY1. Pelvic nerve stimulation in atropinized cats elicits a sustained contraction of the proximal colon and a relaxation of the rectum. Concomitantly there is an immediate but transient vasodilatation which is followed by recurrent increases and a slight post-stimulatory hyperaemia. Direct stimulation ofthe pelvic nerve produces secretion of colonic kallikrein and activation of the plasma kinin system. The present study examines whether Trasylol, which inhibits the kinin system, affects the atropine-resistant responses observed on pelvic nerve stimulation.2. After i.v. or close I.A. administration of Trasylol, the initial vasodilatation on pelvic nerve stimulation was markedly reduced and in a few experiments completely blocked. The recurrent blood flow increases and the post-stimulatory hyperaemia observed on prolonged stimulation were completely abolished. In contrast the proximal colonic contraction and the rectal relaxation appeared unchanged after Trasylol.3. The reactivity of the vascular bed after Trasylol injection was studied by recording the changes of vascular resistance following sympathetic vasoconstrictor fibre activation and infusion of bradykinin before and after Trasylol injection. The responses were quantitatively unchanged excluding an unspecific interference with nervous transmission or vascular smooth muscle reactivity.4. The results show that the atropine-resistant vasodilatation in the cat colon as elicited by pelvic nerve stimulation is partly abolished by a kallikrein inhibitor. This observation lends further support to the hypothesis that kinins might be involved in this response. The motor response, however, appears not be dependent on such a mechanism.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Studies on the atropine‐resistant sacral parasympathetic vascular and motility responses in the cat colon.

Fasth¹,

Hultén²,

Nordgren³

et al. 1981

The Journal of Physiology

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“…Several neurotransmitters have been proposed to mediate these mechanisms including adenosine triphosphate (ATP; Burnstock, 1972), vasoactive intestinal polypeptide (VIP; Fahrenkrug, Haglund, Jodal, Lundgren, Olbe & Schaffalitzky de Muckadell, 1978) and kinins (Fasth, 1973).…”

Section: Introductionmentioning

confidence: 99%

The effect of apamin on non‐adrenergic, non‐cholinergic vasodilator mechanisms in the intestines of the cat.

Jodal¹,

Lundgren²,

Sjöqvist³

1983

The Journal of Physiology

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SUMMARY1. The effects of apamin, a polypeptide isolated from bee venom, on different vasodilator mechanisms in the small and large intestines were studied in atropinized cats.2. In the large intestine vasodilatation in response to pelvic nerve stimulation was either abolished or markedly diminished by I.A. apamin. However, neither the contraction of colonic muscle which occurred under these conditions nor sympathetic vasoconstriction was significantly influenced by apamin, suggesting that the effect of the peptide was not a non-specific effect on nerves or vascular smooth muscle.3. In the small intestine it was observed that the nervous vasodilatation induced by transmural electrical field stimulation or mechanical mucosal stimulation was either diminished or abolished by apamin.4. Intestinal vasodilatation, caused by close I.A. infusions of 5-hydroxytryptamine (5-HT), was abolished by apamin. After giving apamin 5-HT infusions induced a vasoconstriction in five out of six experiments.5. Vasodilatation induced by vasoactive intestinal polypeptide (VIP) was not significantly affected by apamin.6. In a series of in vitro experiments on rat portal vein, dose--response curves of several putative intestinal neurotransmitters were determined in the presence and absence of apamin. The following substances were tested: VIP, substance P, bradykinin, 5-HT, ATP and adenosine. Apamin had no effect on the dose-response curves of any of these compounds.7. The results are discussed in relation to the possibility that apamin may act by blocking the release of a putative peptidergic transmitter from nerve terminals.

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“…It is very difficult to assess the VIP concentration in nerve endings, but 10-~ M VIP may be compatible concentration as a neurotransmitter, when we compared with that of venous concentration after nerve stimulation (Fahrenkrug et al 1978). The CCK secretion by VIP was atropine-resistant and similar results were observed with gastrinreleasing peptide (GRP) stimulation (Nakano et al 1988).…”

Section: Discussionmentioning

confidence: 99%

“…VIP is mainly located in nerve cells and considered to be one of the neurotransmitters of peptidergic nerves (Said and Rosenberg 1976;Fahrenkrug et al 1978). In an attempt to further elucidate the mechanisms of neural regulation of CCK release, we examined CCK secretion by VIP in an isolated perfused rat duodenum system.…”

mentioning

confidence: 99%

Vasoactive intestinal polypeptide stimulates cholecystokinin secretion in perfused rat duodenum.

Funakoshi

Nakano²,

Miyazaki³

1989

Tohoku J. Exp. Med.

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Nervous release of vasoactive intestinal polypeptide in the gastrointestinal tract of cats: possible physiological implications.

Cited by 304 publications

References 29 publications

Studies on the atropine‐resistant sacral parasympathetic vascular and motility responses in the cat colon.

Studies on the atropine‐resistant sacral parasympathetic vascular and motility responses in the cat colon.

The effect of apamin on non‐adrenergic, non‐cholinergic vasodilator mechanisms in the intestines of the cat.

Vasoactive intestinal polypeptide stimulates cholecystokinin secretion in perfused rat duodenum.

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