Pharmacology of neuroendocrine peptides

Daniel, E. E.; Collins, Stephen M.; Fox, J. E. T.; Huizinga, Jan D.

doi:10.1002/cphy.cp060120

Cited by 10 publications

(7 citation statements)

References 455 publications

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“…Moreover, although ATP caused the relaxation of smooth muscle in many regions of the gastrointestinal tract, it does not mimic transmission everywhere, for instance in guinea-pig taenia caecum (Tomita & Watanabe, 1973). VIP in some organs of the gut is claimed to be the inhibitory transmitter, but this is not supported by electrophysiological evidence since VIP does not produce membrane potential changes that mimic the response to NANC nerve stimulation (Hoyle & Burnstock, 1989;Daniel, Collins, Fox & Huizinga, 1989).…”

Section: Introductionmentioning

confidence: 99%

Non‐adrenergic, non‐cholinergic inhibitory responses to nerve stimulation in rat colonic circular muscle

Serio¹,

Mulè²,

Postorino³

1992

Experimental Physiology

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SUMMARYThe nerve-mediated response to electrical field stimulation (EFS) in rat colonic circular muscle was investigated using the single sucrose-gap technique. EFS with a single pulse (04 ms, supramaximal voltage) elicited transient TTX-sensitive hyperpolarization (IJP) often followed by an 'off' depolarization associated with muscular contraction. No relaxation associated with the IJP could be seen unless tone was pharmacologically induced by carbachol (10-6 M). IJPs were due to non-adrenergic, non-cholinergic (NANC) nerve activation since they were not affected by atropine (10-' M) or guanethidine (10-6 M) superfusion. The mechanism underlying the IJP was presumably an increase in K+ conductance, and the NANC neurotransmitter might open largely apamin-sensitive, Ca2l-dependent K+ channels. Purines or vasoactive intestinal polypeptide (VIP) did not mimic the effects of NANC nerve stimulation. Therefore, the NANC inhibitory system. producing IJPs, in rat colonic circular muscle is not purinergic or VIPergic in nature.

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Section: Introductionmentioning

confidence: 99%

Non‐adrenergic, non‐cholinergic inhibitory responses to nerve stimulation in rat colonic circular muscle

Serio¹,

Mulè²,

Postorino³

1992

Experimental Physiology

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“…The majority of gastrointestinal endocrine cells containing PYY (mainly L cells) are located in the mucosa of the distal intestine, especially the colon (10,11), where they are considered the main source of PYY. Sjolund et al (33) reported an increase in the number of PYY-positive cells in the mucosa of the transverse colon of 10 patients with colonic inertia.…”

Section: Discussionmentioning

confidence: 99%

“…In the gastrointestinal system, PYY is located in endocrine cells in the ileal and colonic mucosa, NPY in the enteric nerves, and PP mainly in the islet endocrine cells in the pancreas (10,11). Extrapancreatic PP has also been detected in the colon and rectum by radioimmunoassay (RIA) (12).…”

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confidence: 99%

Abnormality of Peptide YY and Pancreatic Polypeptide Immunoreactive Cells in Colonic Mucosa of Patients with Colonic Inertia

et al. 2004

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The etiopathology of colonic inertia remains unclear. Current studies show that pancreatic polypeptide-fold family members can serve as regulators of colonic motility and transit. Thus, the cells containing these peptides on colonic mucosa could be abnormal in patients with colonic inertia. We aimed to evaluate the immunocytochemical staining of peptide YY (PYY) and pancreatic polypeptide (PP) immunoreactive cells, and detect if alteration of these cells relates to an increase in enterochromaffin cells (EC) demonstrated by chromogranin A (CgA), in the colonic mucosa of patients with colonic inertia. Nineteen consecutive patients (18 female, 1 male; age, 43.7+/-11.5 years) who underwent subtotal colectomy for colonic inertia were assessed. The control group consisted of 15 patients (all female; age, 50.7+/-12.5 years) who underwent colonoscopic biopsies from the right and left colon for indications other than constipation, inflammatory bowel diseases, diarrhea, or neoplasm. Hollande's-fixed, paraffin-embedded tissues of both right and left colons were collected. Immunocytochemical staining of PYY, PP, or CgA was performed on 4-microm tissue sections with the respective primary rabbit antibody, the biotinylated secondary antibody, and enzyme-labeled streptavidin. The average number of positive cells per microscopic field (200x) was calculated. Positive cells were classified as strongly, moderately, and weakly staining. The proportion of the variously stained cells is expressed as the percentage of the entire positive cell population. On both sides of the colon, the percentages of strongly and moderately stained PYY positive cells were higher in the patient group compared to the controls (right side, 10.6 and 27.3 vs. 6.1 and 18.7%, respectively; left side, 9.4 and 23.9 vs. 6.2 and 23.1%, respectively) (P < 0.01). Furthermore, in the patients with colonic inertia, the percentages of strongly and moderately stained PYY-positive cells were higher in the right-side colon than in the left (P < 0.01). There was no difference in the number of PYY-positive cells between the patients and the controls. PP-positive cells were very rare in all specimens and were found in 7 of 19 cases (36.84%) in the right-side colon and 16 of 19 (84.21%) in the left-side colon in the patient group (P < 0.01, left vs. right). In contrast, the number of EC in the left colon of patients (16.8+/-10.2) was significantly higher than that in the right side (9.4+/-6.0) (P < 0.01) or that in the left side in the control group (10.4+/-6.0) (P < 0.05). We conclude that in the colonic mucosa of patients with colonic inertia, PYY-positive cells present with higher immunoreactivity, indicating that they may contain more hormones, especially on the right side of the colon. However, the PPY- and PP-positive cells did not relate to the increased EC. and It is therefore suggested that the altered PYY in the colonic mucosa may partially contribute to the etiopathology of colonic inertia.

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“…6,7 On the one hand, the metabolic pathway of sulfation can form pharmacologically active sulfate conjugates; these are the cases in which the sulfated conjugates trigger the biological effects of minoxidil and the neuroendocrine peptide cholecystokinin (CKK). 8,9 On the other hand, sulfation is an activation process of N-or O-hydroxy derivatives (such as aromatic amines and amides) that leads to chemical mutagens and carcinogens. 10 SULT1 and SULT2 are important enzyme families, which are mainly responsible for the sulfation of steroids and polyphenols.…”

Section: Introductionmentioning

confidence: 99%

Sulfotransferases and Breast Cancer Resistance Protein Determine the Disposition of Calycosin in Vitro and in Vivo

Zhu

Zheng

et al. 2017

Mol. Pharmaceutics

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Sulfation is a key process of drug disposition that generally regulates drug effectiveness and toxicity. Calycosin derived from the dry root extract of Radix Astragali exhibits a variety of biological effects that easily undergo extensive phase II metabolism. However, the sulfation pathway of calycosin lacks information. We investigated the disposition mechanisms of calycosin sulfate in vitro and in vivo. We characterized the sulfation metabolism and excretion of calycosin using bidirectional transport studies. We confirmed that sulfate conjugate is breast cancer resistance protein (BCRP) substrate using the intestinal perfusion model and pharmacokinetics studies in Bcrp1 mice. Results showed that calycosin is rapidly and extensively metabolized to calycosin-3'-sulfate (C-3'-S) in the intestine and liver. The overexpression of BCRP led to a substantial increase (approximately 14-fold, p < 0.01) of excreted C-3'-S in the BCRP overexpressed Madin-Darby canine kidney II (MDCK II/BCRP) cells. The chemical inhibition of BCRP caused reduction (about 2-fold, p < 0.01) in C-3'-S apical excretion. Furthermore, in intestinal perfusion studies, the deletion of Bcrp1 significantly decreased C-3'-S excretion in the small intestine (82.6-90.6%, p < 0.01) and colon (97.6-98.2%, p < 0.01). In contrast, plasma level of C-3'-S was increased to 40-fold (p < 0.01) in Bcrp1 mice. In conclusion, calycosin undergoes an extensive sulfation metabolism and BCRP is a critical determinant to the disposition of C-3'-S.

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Pharmacology of neuroendocrine peptides

Abstract: The sections in this article are: Gastrin and Cholecystokinin ( CCK ) Classification of Gastrin‐ CCK Receptors Locus of Receptors Modulation of Gastrin‐ CCK Receptors … Show more

Cited by 10 publications

References 455 publications

Non‐adrenergic, non‐cholinergic inhibitory responses to nerve stimulation in rat colonic circular muscle

Non‐adrenergic, non‐cholinergic inhibitory responses to nerve stimulation in rat colonic circular muscle

Abnormality of Peptide YY and Pancreatic Polypeptide Immunoreactive Cells in Colonic Mucosa of Patients with Colonic Inertia

Sulfotransferases and Breast Cancer Resistance Protein Determine the Disposition of Calycosin in Vitro and in Vivo

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