Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paracervical ganglia of the female rat were studied to elucidate the variety of neural elements in the ganglia. Light and electron microscopy, histochemistry, and immunohistochemistry were employed to reveal subtypes of neurons; small, intensely fluorescent (SIF) cells; and nerve terminals and to examine the relationships between these elements. On the basis of their histochemical markers, four subtypes of principal neurons were identified: acetylcholinesterase (ACHE)-positive, noradrenergic, neuropeptide tyrosine-immunoreactive (NPY-I), and vasoactive intestinal polypeptide-immunoreactive (VIP-I). The NPY-I neurons appeared to be the most numerous and the noradrenergic the least common type of neuron. Four subtypes of chemically coded SIF cells were revealed: catecholamine-containing, NPY-I, and those immunoreactive for calcitonin-gene-related peptide (CGRP-I) and cholecystokinin-octapeptide (CCK-8-I). The SIF cells were present as single cells among and adjacent to principal neurons and as large clusters near the edges of the ganglia or in nearby nerve trunks. Synaptic contacts on SIF cells, or between SIF-cell processes and neurons, were not observed. Seven subtypes of nerve terminals were stained: ACHE-positive, CGRP-I, CCK-8-I, VIP-I, substance P-I, enkephalin-I, and atrial natriuretic factor-I. Nerve terminals enwrapped the neurons as perineuronal plexuses in synaptic-like relationships. These results demonstrate that the paracervical ganglia of the female rat are a complex system of neural elements. For example, several classes of chemically coded neurons, SIF cells, and terminals exist in the ganglia. Each of these components contains a number of substances, some of which are putative neurotransmitters, which could influence activity in the ganglia or in the effector organs innervated by the ganglia.
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PMID:Paracervical ganglia of the female rat: histochemistry and immunohistochemistry of neurons, SIF cells, and nerve terminals. 288 3

Smooth muscle cells were isolated from the fundus of the canine gallbladder and examined for the presence of opioid receptors. The cells contracted in a concentration-dependent manner in response to three opioid peptides (Met-enkephalin, dynorphin1-13 and Leu-enkephalin), which are known derivatives of opioid precursors present in myenteric neurons of the gut. The order of potency was Met-enkephalin greater than dynorphin1-13 greater than Leu-enkephalin. The contractile response to opioid agonists was selectively inhibited by opioid antagonists (naloxone and Mr2266) but not by muscarinic, CCK/gastrin or tachykinin antagonists. Equivalent responses to the three opioid peptides exhibited differential sensitivity to preferential antagonists of mu (naloxone) and kappa (Mr2266) opioid receptors consistent with the presence of the three main types of opioid receptors (mu, delta and kappa) on canine gallbladder muscle cells.
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PMID:Characterization of opioid receptors on isolated canine gallbladder smooth muscle cells. 289 8

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88

Functional and specific receptors for vasoactive intestinal peptide (VIP) (determined by their capacity to bind 125I-VIP and activate adenylate cyclase) and cyclic AMP-dependent phosphodiesterase activities were characterized in enterocytes of human fetal small intestine between 18 and 23 weeks of gestation. Half-maximal stimulation of the cyclase and inhibition of 125I-VIP binding in membrane preparations were respectively observed at 1.4 and 5 X 10(-10) M VIP. The peptides structurally related to VIP activated the cyclic AMP generating system at pharmacological doses (10(-7) M and above) in the following order of potency: VIP greater than PHI greater than GRF greater than secretin. Other peptides or test substances, including GIP, pancreatic glucagon, somatostatin-14, gastrin, CCK, neurotensin, pancreatic polypeptide, PYY, substance P, histamine and isoproterenol are inactive in this system, while the ubiquitous adenylate cyclase activators NaF, forskolin and prostaglandins were effective. These results, combined with the appearance of intestinal VIP in nerve fibers at 8 weeks and with the morphological and enzymatic maturation at 9-12 weeks of the intestinal mucosa, indicate that this neuropeptide may regulate either the differentiation or function of enterocytes during the early development of human intestinal mucosa.
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PMID:Vasoactive intestinal peptide receptor activity in human fetal enterocytes. 298 18

CCK-octapeptide (CCK-8) (EC50 = 0.5 nM), in the presence of Li+, increased 3H-inositol phosphate (IP) accumulation in guinea pig gastric glands prelabeled with 3H-inositol. CCK-8 desulfate, human gastrin I and pentagastrin were much less potent than CCK-8. Antagonists of CCK receptors such as proglumide, dibutyryl-c-GMP and CBZ-Tyr (SO3H)-Met-Gly-Trp-Met-AspNH2 shifted the CCK dose response curve to the right. However, histamine (H1 and H2), cholinergic, substance P and alpha- and beta-adrenergic receptor antagonists had no effect on 3H-IP accumulation induced by CCK. The results suggest that CCK receptor activation in gastric glands leads to an enhanced breakdown of inositol phospholipids which may relate to calcium mobilization and pepsinogen secretion.
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PMID:Cholecystokinin receptor mediated hydrolysis of inositol phospholipids in guinea pig gastric glands. 298 60

Single-label and double-label immunohistochemical techniques were used to demonstrate the coexistence of substance P-like immunoreactivity (SPLI) and cholecystokinin-8-like immunoreactivity (CCK-8-LI) in an extensive fiber system within the telencephalic cortex of turtle. All SPLI-containing fibers and terminals of this system contain CCK-8-LI and vice versa. The fibers of this system course from more medial cortical regions to more lateral ones, originating either from neurons in the more medial cortices or from extracortical neurons, the axons of which ascend the medial wall of the cortex. The precise location of the neurons that give rise to this cortical projection system is uncertain, but a hypothalamic location seems most likely at present. The fibers and terminals of this system are found throughout the entire mediolateral and rostrocaudal extent of the telencephalic cortex of turtle and are largely confined to the cell body layer of the cortex. Fewer SPLI/CCK-8-LI-containing fibers are found in pyriform (olfactory) cortex than in the other cortices. Ultrastructural studies indicate that SPLI/CCK-8-LI-containing terminals make asymmetric synapses on cell bodies or their proximal dendrites. Both SPLI and CCK-8-LI are found in large dense core vesicles in these labeled terminals. Labeled terminals also contained numerous small, round, unlabeled vesicles clustered near synaptic release sites and a number of unlabeled large dense core vesicles. Quantification of the percentage of the large dense core vesicles that were labeled in SP-labeled terminals, in CCK-8-labeled terminals, and in terminals labeled for both SP and CCK-8 provided suggestive evidence that SPLI and CCK-8-LI must be contained within the same large dense core vesicles. Radioimmunoassay indicated that the SP/CCK-8-containing system of turtle cortex contains 0.93 +/- 0.090 pg of SP/microgram of cortical tissue protein and 0.31 +/- 0.11 pg of CCK-8/micrograms of cortical tissue protein. The CCK-8-like material in turtle cortex coelutes with CCK-8-sulfate, using gradient elution high pressure liquid chromatography (HPLC). The SP-like material, although immunologically highly similar to undecapeptide SP (Reiner, A., J. E. Krause, K. T. Keyser, W. D. Eldred, and J. F. McKelvy (1984) J. Comp. Neurol. 226: 50-75), does not coelute with undecapeptide SP using gradient elution HPLC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The co-occurrence of a substance P-like peptide and cholecystokinin-8 in a fiber system of turtle cortex. 298 51

This is a survey of the results of recent investigations on gastrointestinal (GI) peptide hormones. In addition to the classical GI hormones (secretin, gastrin, and cholecystokinin-pancreozymin (CCK-PZ], there are at least nine other peptides whose structures and GI effects are known. These include vasoactive intestinal polypeptide (VIP), gastric inhibitory polypeptide (GIP), motilin, pancreatic polypeptide (PP), substance P, neurotensin, somatostatin, enkephalins, and a bombesin-like gastrin-releasing peptide. It is now obvious that the traditional distinctions between hormones, neurotransmitters, and paracrines are rapidly becoming obsolete, as the actions and interactions of these substances within the complex motor system of the GI tract are gradually revealed. The study of perturbed states and toxic effects on the motor function of the small intestine is complicated by the integration of the activity of the small intestine with the activities of the body as a whole. A contemporary approach for evaluating intestinal contractile activity is described that uses computer assistance to measure the intercontractile interval (ICI). This technique may prove useful in assessing the effects of toxicological agents on spontaneous intestinal motor activity in vitro when the agents are delivered to the target sites by physiological mechanisms, in contrast to adding them to the tissue bath.
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PMID:Gastrointestinal hormones and the quantitation of spontaneous duodenal motor activity. 305 20

In cultured rat hepatocytes, the effects of gut hormones on bile acid uptake and release were studied. It was found that cultured hepatocytes continued to secrete bile acids into the culture medium and incorporated them effectively as a function of incubation time. Gut hormones such as secretin, glucagon, vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI), gastric inhibitory polypeptide (GIP), tetragastrin, cholecystokinin-octapeptide (CCK-8), pancreatic polypeptide (PP), neurotensin substance P, beta-endorphin (beta-End), methionine-enkephalin (Met-enk), motilin, bombesin and somatostatin (SS) had no effect on bile acid uptake by cultured hepatocytes. In bile acid release studies, only secretin caused a dose-dependent stimulation of bile acid release, while other gut hormones had no effect on bile acid release into medium. These results indicate that secretin acts directly on cultured rat hepatocytes and/or bile canaliculi, besides its effect on the bile duct, and influences bile acid metabolism.
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PMID:Effects of gut hormones on bile acid uptake and release in cultured rat hepatocytes. 359 53

Immunohistochemistry and radioimmunoassay (RIA) revealed that corticotropin releasing factor (CRF)-like immunoreactivity was found to be colocalized with substance P (SP)-, somatostatin (SST)- and leu-enkephalin (LENK)-like immunoreactivity in the dorsal root- and trigeminal ganglia, the dorsal horn of the spinal cord (laminae I and II), the substantia gelatinosa, and at the lateral border of the spinal nucleus and in the tractus spinalis of the trigeminal nerve. These peptides were also located in fast blue labeled cells of the trigeminal ganglion following injection of the dye into the spinal trigeminal area. This indicates that there are possible sensory projections of these peptides into the spinal trigeminal area. Capsaicin treatment of neonatal rats resulted in a marked decrease in the density of CRF-, SP-, VIP- and CCK-containing neurons in the above mentioned hindbrain areas, whereas SST- and LENK-immunoreactivity were not changed. RIA revealed that, compared to controls, CRF, SP and VIP concentrations in these areas were decreased in rats pretreated with capsaicin, while SST levels were increased; CCK and LENK levels were unchanged. It is concluded that the primary afferent neurons of the nucleus and tractus spinalis of the trigeminal nerve are richly endowed with a number of peptides some of which are sensitive to capsaicin action. The close anatomical proximity of these peptide containing neurons suggests the possibility of a coexistance of one or more of these substances.
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PMID:Corticotropin releasing factor-like immunoreactivity in sensory ganglia and capsaicin sensitive neurons of the rat central nervous system: colocalization with other neuropeptides. 387 38

Intestinal adaptation has been studied in rats with pancreatic atrophy induced by feeding a copper-deficient diet and penicillamine and in rats with carbohydrate maldigestion induced by feeding of an alpha-glucosidase inhibitor (acarbose). Pancreatic atrophy led to a significant increase of weight, protein, and DNA content as well as specific activities and total amounts of the enzymes sucrase and maltase in the distal but not in the proximal part of the small intestine. Plasma levels of CCK and GIP were significantly higher in rats with pancreatic atrophy, whereas plasma levels of gastrin and insulin were lower. Tissue concentrations of gastrin in the antrum and GIP in duodenum and jejunum were unchanged. Duodenal CCK and jejunal substance P, somatostatin, and VIP and ileal substance P and somatostatin were significantly decreased in rats with acinar atrophy. Glucosidase inhibition by acarbose feeding led to weight increase of the small intestine and cecum. This was more marked when acarbose was fed together with a fiber-free diet. Under these conditions the protein and DNA content also increased significantly in both gut segments and maltase and sucrase content predominantly in the distal part. Insulin plasma concentration decreased significantly in the acarbose-fed groups, whereas GIP, gastrin, and CCK plasma concentrations remained unchanged. After fiber-rich diet tissue concentrations of gastrin in the antrum and insulin in the pancreas were significantly higher and GIP concentrations in the duodenum and jejunum significantly lower than after fiber-free diet. Acarbose increased the pancreatic insulin concentration only in the fiber-free group and did not influence gastrin and GIP concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptation of the small intestine to induced maldigestion in rats. Experimental pancreatic atrophy and acarbose feeding. 389 54


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