Evidence for immunoreactive neurotensin in dog intestinal mucosa

Orci, Lelio; Baetens, O.; Rufener, C.; Brown, Marvin R.; Vale, Wylie; Guillemin, Roger

doi:10.1016/0024-3205(76)90236-8

Cited by 137 publications

(33 citation statements)

References 9 publications

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“…The distribution of NT-positive cells in the ileum agreed with that in the reports issued by Orci et al (1976) …”

Section: Discussionsupporting

confidence: 79%

“…It was recently reported that somatostatin and neurotensin, originally isolated from the mammalian hypothalamus (Brazeau et al 1973; Carraway and Leeman 1973), exist not only in several parts of the brain (Hokfelt et al 1975; Carraway and Leeman 1976b) but also in the gastrointestinal tract (Polak et al 1975; Orci et al 1976). Somatostatin plays an important role in the inhibition of the release of several peptides such as HGH (Siler et al 1973) TSH (Siler et al 1974), insulin (Alberti et al 1973), glucagon (Koerker et al 1974) and gastrin (Bloom et al 1974) and of the secretion of hydrochloric acid and pepsinogen (Gomez-Pan et al 1975;Barros D'Sa et al 1975).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Neurotensin-positive and somatostatin-positive cells in the canine gut.

Ito

Yamada

Hayashi

et al. 1979

Tohoku J. Exp. Med.

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“…The distribution of NT-positive cells in the ileum agreed with that in the reports issued by Orci et al (1976) …”

Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Neurotensin-positive and somatostatin-positive cells in the canine gut.

Ito

Yamada

Hayashi

et al. 1979

Tohoku J. Exp. Med.

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“…However, its physiological role remains un- Uhl, Kuhar & Snyder, 1977;Kobayashi, Brown & known. The recent demonstration of the presence of Vale, 1977) and in some regions of the digestive tract NT-like immunoreactivity in the blood of man (Carraway & Leeman, 1976;Orci, Baetens, Rufner, (Blackburn, Bloom & Polack, 1978) as well as of its Brown, Vale & Guillemin, 1976;Polack, Sullivan, elevated blood concentration following the ingestion Bloom, Buchan, Facer, Brown & Pearse, 1977). The of food (Mashford, Nilsson, Rokaeus & Rosell, 1978; peptide exhibits a large spectrum of biological activiBesterman, Bloom, Sarson, Blackburn, Johnston, Patel, Stewart, Modigliani, Guerin & Mallinson, 1978) raised the possibility that NT behaves as a circulating hormone.…”

Section: Introductionmentioning

confidence: 99%

The Stimulatory Effects of Neurotensin and Related Peptides in Rat Stomach Strips and Guinea‐pig Atria

Quirion

Regoli

Rioux

et al. 1980

British J Pharmacology

107

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The stimulatory effects of neurotensin (NT) and several NT fragments were evaluated in two pharmacological preparations: rat stomach strips and isolated spontaneously beating atria of guinea‐pigs. In rat stomach strips, NT elicited a dose‐dependent contractile effect in concentrations varying between 1.3 × 10−9 and 5.4 × 10−7 M. The contractile effect of NT (1.3 and 5.4 × 10−8 m) in this tissue was not modified by atropine (3.4 × 10−7 m), methysergide (2.0 × 10−6 m), a mixture of cimetidine (8.0 × 10−6 m) and diphenhydramine (7.8 × 10−6 m), indomethacin (1.4 × 10−5 m), 8‐Leu‐angiotensin II (1.0 × 10−6 m), glucagon (2.0 × 10−6 m) or somatostatin (3.0 × 10−7 m). Rat stomach strips desensitized by bradykinin (6.1 × 10−6 m) or substance P (7.4 × 10−6 m) maintained their sensitivities to NT (1.3 and 5.4 × 10−8 m). In guinea‐pig atria, NT produced a dose‐dependent positive inotropic action in concentrations varying between 5.4 × 10−10 and 2.7 × 10−7 m. The inotropic effect of NT (2.7 × 10−9 m) was not influenced by methysergide (2.8 × 10−6 m), atropine (3.4 × 10−7 m), practolol (1.5 × 10−5 m), 8‐Leu‐angiotensin II (1.0 × 10−6 m), or indomethacin (1.4 × 10−5 m), but it was reduced by 37% by cimetidine (4.0 × 10−5 and 2.0 × 10−4 m). A combination of cimetidine (4.0 × 10−5 m) and diphenhydramine (3.9 × 10−6 m) did not produce a greater inhibition of NT than cimetidine alone. Atria desensitized by bradykinin (6.1 × 10−6 m) or glucagon (2.0 × 10−6 m) maintained their sensitivities to NT (2.7 × 10−9 m). Substance P was inactive both as an agonist or antagonist of NT. These results suggest the existence of specific NT receptors in rat stomach strips and guinea‐pig atria. The data derived from our structure‐activity study suggest that the minimum structure required for the full stimulation of NT receptors in these two preparations is H‐Arg9‐Pro10‐Tyr11‐Ile12‐Leu13‐OH. The sequence PyroGlu1‐Leu2‐Tyr3‐Glu4‐Asn5‐Lys6‐Pro7‐Arg8‐ and the amino acids Ile12 and Leu13 appear to contribute mainly to the affinity or binding of NT to its receptor. The chemical groups responsible for the full activation (intrinsic activity) of NT receptors seem to be located in the sequence ‐Arg9‐Pro10‐Tyr11.

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“…The presence of neurotensin in the small intestine has been shown (ORCI et al, 1976;HELMSTAEDTER et al, 1977;POLAK et al, 1977;SUNDLER et al, 1977; Japanese Journal of Physiology SCHULTZBERG et al, 1980). However, the possibility that neurotensin acts as a neurotransmitter on the intestinal smooth muscle or in the intestinal muscularis mucosa like VIP in the gastric muscularis mucosa (ANGEL et al, 1983) and the presence of synaptic neurotensin receptors on the non-adrenergic inhibitory nerve cell was not clear.…”

Section: Effects Of Neurotensin On the Is Ps In The Presence Of Atromentioning

confidence: 99%

“…It has been shown that neurotensin is present in cells of the mucosa of the small intestine (ORcI et al, 1976;HELMSTAEDTER et al, 1977;POLAK et al, 1977;SUNDLER et a1.,1977;BUCHAN et a!., 1979) and that some neurotensin immunoreactive fibers exist in the myenteric plexus of the duodenum and other regions of the gastrointestinal tract (SCHULTZBERG et a!.,1980). The possible role of the tridecapeptide neurotensin on the permeability of local capillaries has been discussed (CARRAWAY and LEEMAN, 1973) or on the regulation of the carbohydrate metabolism (RoSELL et al, 1976).…”

mentioning

confidence: 99%

Effects of neurotensin on the non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum.

Ohkawa

1985

Jpn.J.Physiol

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The effects of neurotensin on the non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum were investigated. The resting membrane potential of the duodenal smooth muscle cells was reduced by neurotensin at the concentration of 3 x 10-6 M or more. The amplitude of the non-adrenergic inhibitory potentials was decreased by neurotensin (1-3 x 10-6 M). In the Ca2+-free solution, the amplitude of the inhibitory potentials was also decreased. The increased amplitude of the non-adrenergic inhibitory potentials evoked in the high calcium solution (Ca2, +5 mM) was decreased by neurotensin (10-8 M). Neither atropine (1.4 x 10_6 M) nor propranolol (3.4 x 10_e M) blocked the inhibitory action of neurotensin (10-6 M) on the inhibitory potential. The frequency of the spontaneous action potentials of the duodenal smooth muscle cells was strongly increased with accompanying depolarization by neurotensin 8 x 10-8 M. The tonic contraction of the duodenal smooth muscles was produced by neurotensin (3-8 x 10-8 M). The results obtained suggest that neurotensin relates to the non-adrenergic inhibitory, pathway in the control mechanism on intestinal motility.

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Evidence for immunoreactive neurotensin in dog intestinal mucosa

Cited by 137 publications

References 9 publications

Neurotensin-positive and somatostatin-positive cells in the canine gut.

Neurotensin-positive and somatostatin-positive cells in the canine gut.

The Stimulatory Effects of Neurotensin and Related Peptides in Rat Stomach Strips and Guinea‐pig Atria

Effects of neurotensin on the non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum.

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