A novel fragment of the corticotropin-beta-lipotropin precursor.
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Adrenocorticotropic Hormone↗
Biomedical subjects
F Sundler
Publications and source records attributed to F Sundler.
Vasoactive intestinal polypeptide nerves in the human female genital tract.
VIP, a recently recognized neuropeptide, has been demonstrated by immunohistochemistry in nerves of the human female genital organs. Such nerves were most numerous in the isthmic part of the fallopian tube and in the cervix. They were found in smooth muscles, around blood vessels, and beneath the epithelium. Immunoreactive VIP nerve cell bodies were found in paracervical tissue, suggesting a local origin of genital VIP nerves. Besides the well-known adrenergic and cholinergic nerves, peptidergic nerves may constitute a new component in the autonomic nervous system.
Blood Vessels↗
Origin and distribution of VIP (vasoactive intestinal polypeptide)-nerves in the genito-urinary tract.
VIP (Vasoactive Intestinal Polypeptide)-immunoreactive nerves were found throughout the genito-urinary tract of the cat; they were less numerous in the guinea pig and in the rat. In the cat, VIP nerves were particularly numerous in the neck of the urinary bladder and proximal urethra, in the uterine cervix and in the prostate gland. The nerves were found in smooth muscle, around blood vessels and in the connective tissue immediately beneath the epithelium. Ganglia were found below the trigonum area of the bladder, in the wall of the proximal urethra, and in paracervical tissue. VIP-immunoreactive nerve cell bodies occurred in all these ganglionic formations. These ganglia probably represent the origin of the VIP nerves of the genital tract since their removal in the female cat greatly reduced the VIP nerve supply. Transection of the hypogastric nerves had no overt effect. Transection of the cervix eliminated the VIP nerves above the level of the lesion, except those in the ovaries, supporting the view that the VIP nerves of the uterus and the oviduct are derived from a paracervical source.
Animals↗
Evidence that lipolytic peptide B occurs in the ACTH/MSH-cells of the pituitary and in the brain. An immunocytochemical study of its distribution in correlation to the distribution of neurophysin.
Several lipid-mobilizing peptides occur in the pituitary, among them beta-lipotropin and "lipolytic peptide A and peptide B". The latter two peptides are distinct from beta-lipotropin and appear to be chemically related to the neurophysins. Immunohistochemistry has now revealed that the lipolytic peptide B of the pituitary is localized in the ACTH- and MSH-cells. In addition, immunoreactive peptide B was found in axons of the posterior lobe of the pituitary. Immunoreactive peptide B was found also in nerve fibers and nerve cell bodies in the hypothalamus, particularly in the hypothalamo-hypophyseal tract and in the magnocellular neuronal system. Immunoreactive nerve fibers were numerous also in the periventricular nucleus of the thalamus. The antiserum against peptide B cross-reacts with neurophysin I, and hence, it cannot be excluded that at least part of the immunostaining in the brain reflects the presence of the latter component. However, the regional distribution of immunoreactive peptide B and neurophysin was not identical. Therefore, it is possible that authentic peptide B occurs not only in the pituitary but also in the brain.
Adrenocorticotropic Hormone↗
Ontogeny and ultrastructure of somatostatin and calcitonin cells in the thyroid gland of the rat.
Calcitonin cells are relatively numerous in the thyroid gland of the rat. In contrast, somatostatin cells are very scarce except at the time of birth and a few days thereafter, when they are conspicuously numerous. Somatostatin cells of the thyroid gland, which are ultrastructurally similar to somatostatin cells in gut and pancreas, also contain immunoreactive calcitonin. It is not clear whether somatostatin cells in the rat thyroid gland produce calcitonin or accumulate calcitonin from the environment.
Animals↗
VIP (vasoactive intestinal polypeptide)-containing nerves of intracranial arteries in mammals.
Immunohistochemical and radioimmunochemical investigations have shown, in various species, the occurrence of numerous nerve fibres containing vasoactive intestinal polypeptide (VIP) in connection with blood vessels of the central nervous system. Pial arteries from pig, cat, and rat have the richest supply of VIP nerve fibres; those of cow, dog guinea pig and hamster have an intermediary number of nerves, while only few are found in pial arteries from the monkey, rabbit, gerbil, and mouse. The regional variation in VIP-nerve density follows the order: cerebral arteries greater than basilar greater than vertebral greater than spinal cord arteries. Unilateral extirpation of either the pterygopalatine or the superior cervical ganglia does not affect the amount or distribution of VIP fibres in the wall of brain vessels of the ipsilateral side. Measurement of the VIP content by radioimmunoassay shows mean concentrations in the pial arteries varying between 19 and 82 pmol/g tissue wet weight. Regional and species variations in measured VIP levels are similar to the variations in distribution of immunoreactive nerve fibres.
Animals↗
Immunohistochemical localization and vascular effects of vasoactive intestinal polypeptide in skeletal muscle of the cat.
Scattered vasoactive intestinal polypeptide (VIP)-immunoreactive nerves were found in the striated muscle of the hind limb of the cat, where they usually were associated with small blood vessels. VIP-immunoreactive nerves were also demonstrated in the sciatic nerve; after ligation an abundance of intensely immunoreactive VIP fibres were seen proximal to the ligation. Intraarterial infusion of VIP into isolated hind limb of the cat had dramatic effects on different sections of the vascular bed. Thus, VIP dilated the resistance vessels leading to a marked increment in muscle blood flow. VIP also relaxed the capacitance vessels causing regional pooling of blood; it increased the capillary surface area available for fluid exchange. Infusions of VIP at a dose of 8 microgram/min significantly inhibited the vasoconstriction, induced by electrical stimulation of the regional sympathetic nerves. It is suggested that local nervous release of VIP may act as a modulator of vascular tone in skeletal muscle.
Animals↗
Quinacrine accumulates in certain peptide hormone-producing cells.
Quinacrine is a fluorescent anti-malarial acridine derivative which binds selectively to a population of nerves, presumably peptidergic, and to certain peptide hormone-producing cells. Among these cells are glycopeptide hormone-producing cells in the adenohypophysis, the calcitonin cells in the thyroid, the insulin, glucagon and PP cells in the pancreatic islets, and the gastrin cells in the pyloric antrum. Available evidence suggests that the fluorophore accumulates in the secretory granules. The half-life of the fluorescence varies from one cell type to another, from 6 h in the gastrin cells to 40 h in the insulin cells. It cannot be excluded that the half-life of the fluorescence reflects the turn-over rate of the secretory granules and that the disappearance rate of the fluorescence is dependent upon the secretory activity of the cell.
Adrenal Medulla↗
Gastrin/CCK-like immunoreactivity in the nervous system of coelenterates.
Using immunocytochemistry, gastrin/CCK-like immunoreactivity is found in sensory nerve cells in the ectoderm of the mouth region of hydra and in nerve cells in the endoderm of all body regions of the sea anemone tealia. These results are corroborated by radioimmunoassay: One hydra contains at least 5 fmole and one tealia at least 2 nmole gastrin/CCK-like immunoreactivity. Reactivities towards gastrin and CCK antisera with different specificities suggest that the coelenterate gastrin/CCK-like peptide contains the C-terminal amino-acid sequence common to mammalian gastrin and CCK. In addition the radioimmunochemical data indicate that the coelenterate peptide also contains an amino-acid sequence that resembles the sequence 20-30 of porcine CCK-33, but that no other sequences of gastrin are present. Thus, it is probably more CCK-like than gastrin-like.
Animals↗
Peptidergic nerves persist after jejunal autotransplantation: an experimental study in the piglet.
The gut has been shown to contain four types of peptidergic nerves besides the adrenergic and cholinergic ones. They store substance P, enkephalin, somatostatin and VIP (vasoactive intestinal peptide) respectively. It is not previously known which of the neurons are intrinsic or extrinsic to the gut wall. Jejunal autotransplantation was performed in 10 piglets. This procedure implies degeneration of the extrinsic neurons (extrinsic denervation). The transplants were examined 1 to 4 mo postoperatively with histochemical techniques for demonstration of the intramural adrenergic and the different peptidergic nerves. The distribution of the peptidergic nerves was not changed indicating that they all originate within the gut. Following extrinsic denervation adrenergic nerves on the contrary were completely missing.
Animals↗
Immunocytochemical demonstration of enkephalin and beta-endorphin in endocrine tumors of the rectum. A survey of 27 colo-rectal carcinoids.
In a histopathological and immunocytochemical study of biopsy and/or operation specimens from 27 patients with endocrine tumors of the colon and rectum ("hind-gut carcinoids") enkephalin-immunoreactive tumor cells were observed in two cases. Both patients were obese women, about 50 years of age, with a history of constipation. The tumors were situated near the anus in the dorsal wall of the rectum. One tumor had metastasized to a lymph node, and the other showed vascular invasion. The tumor cells were non-argentaffin; some were argyrophil. One tumor contained only few enkephalin-immunoreactive cells but had numerous beta-endorphin-immunoreactive cells, which were distinct from the former. The other contained large numbers of enkephalin-immunoreactive cells but no beta-endorphin cells. Both tumors also harboured glucagon-immunoreactive cells; in one there were also cells containing immunoreactive pancreatic polypeptide. These cells were distinct from the enkephalin-storing ones. No 5-hydroxytryptamine could be detected in the two tumors.
Colonic Neoplasms↗
Neuronal VIP in salivary glands: distribution and release.
Nerves containing vasoactive intestinal peptide (VIP) were observed in salivary glands of rat, cat and man. VIP nerves were numerous in the cat while they were moderate in number in rat and man. The measured concentrations of immunoassayable VIP were in agreement with the immunohistochemical findings. Electrical stimulation of the feline chorda lingual nerve, which stimulates salivary secretion and local blood flow, resulted in a marked elevation of VIP in the venous effluent from the submandibular gland. VIP was not measurable in saliva. Gel permeation chromatography of extracts from cat submandibular gland and from venous plasma collected before and during nervous stimulation revealed one immunoreactive peak with an elution position identical to that of highly purified porcine VIP. The finding of neuronal VIP in salivary glands, its release upon nerve stimulation and its known effect on local blood flow support the view that VIP is a neurotransmitter in the salivary glands.
Animals↗
Gastrin cell proliferation after chronic stimulation: effect of vagal denervation or gastric surgery in the rat.
Chronic stimulation of the antral gastrin cells by elevated antral pH was achieved by fundectomy, antrum exclusion, fundectomy plus antrum exclusion, antrocolic transposition, and vagal denervation plus pyloroplasty. For comparison we studied also the effects of pyloroplasty alone and of portacaval shunting. All operations that elevated the antral pH resulted in high gastrin concentrations in serum. Particularly high concentrations were observed in fundectomized rats. Vagal denervation of fundectomized or antrum excluded rats reduced the serum gastrin concentration slightly compared with the corresponding innervated animals. Portacaval shunting reduced the gastrin concentration in serum. The antral gastrin concentration was raised or unchanged following fundectomy and vagal denervation, and reduced following antrum exclusion, antrum exclusion plus vagotomy, fundectomy plus antrum exclusion, fundectomy plus vagotomy, antrocolic transposition and portacaval shunt. The gastrin cell density in the antral mucosa was raised following fundectomy, vagotomy, and fundectomy plus vagotomy, unchanged following fundectomy plus antrum exclusion and antrocolic transposition, and reduced following antrum exclusion and portacaval shunting. Ultrastructurally the gastrin (G) cells in the excluded antrum and in the antrum of fundectomized rats showed signs of secretory activity in that the granule volume density or the number of granules per unit cytoplasm was lowered. In the fundectomized rats moreover, the endoplasmic reticulum of the G cells was increased, the Golgi area enlarged and the proportion and volume density of electron dense granules greatly increased. The granule profile diameter was not affected by either antrum exclusion or fundectomy. The results on the excluded antrum indicate that elevated antral pH per se is not sufficient to produce gastrin cell proliferation. In the fundectomized rats, where the hyperlasia of antral gastrin cells was considerable, there is the added stimulus of ingested food. In fundectomized plus antrum excluded rats this stimulus is eliminated and no proliferation ensues. The passage of intestinal material, as in the rats subjected to antrocolic transposition, did not elicit gastrin cell proliferation which seems to suggest that the character of the luminal material is important. We propose therefore that gastrin cell proliferation is due to the combined stimulation of high antral pH and passage of food. Vagal innervation is not required.
Animals↗
Importance of the kidneys for gastrin elimination and gastric function.
1. The gastrin concentrations in serum were elevated after nephrectomy in rats and mice indicating the importance of the kidney for elimination of gastrin in these species. In guinea-pigs and rabbits nephrectomy did not cause increased serum gastrin concentrations. In rats there was a gradual rise in the serum gastrin level up to 48 hr after bilateral nephrectomy and also after ureteral ligation. After the latter operation the concentrations of gastrin in serum were lower than after nephrectomy. Significant elevation of the gastrin level 48 hr after ureteral ligation indicates that gastrin is eliminated at least partly through glomerular filtration. The gastric histidine decarboxylase activity after nephrectomy or ureteral ligation generally reflected the concentration of circulating gastrin.2. After bilateral ureteral ligation gastric acid secretion in conscious fistula rats was uniformly inhibited with no response to pentagastrin or histamine 24 or 48 hr after the operation. After nephrectomy basal acid secretion was reduced and there was no response to pentagastrin. The response to histamine was still present, although reduced at all dose levels. Linear transformation of the dose-response curve indicated mixed inhibition. The incidence of gastric ulcer was 75% 48 hr after nephrectomy and 30% after ureteral ligation. Since basal and pentagastrin-stimulated acid secretion were unaffected by nephrectomy in rats with the upper two-thirds of the intestine removed, the intestine appears to produce factors which are responsible for the inhibition of gastric secretion.2. On the whole, the gastrin concentration in serum and gastric histidine decarboxylase activity were not increased after five-sixths nephrectomy. Gastric ulcers were seen in the rats with the highest serum urea levels; one in addition had high serum gastrin concentration and gastric histidine decarboxylase activity. Basal, pentagastrin- and histamine-stimulated acid secretion were not affected by subtotal nephrectomy. It appears that in the rat about one sixth of the renal mass is the minimum required for handling gastrin degradation and excretion.
Animals↗
Mechanisms of gastric acid secretion after pylorus and oesophagus ligation in the rat.
1. The effect of vagotomy on gastric acid secretion was studied in chronic gastric fistula rats at various times after denervation. In these rats basal and pentagastrin-induced acid output was permanently reduced. Thus, the magnitude of the acid response to pentagastrin in the conscious fistula rat is dependent upon an intact vagus. 2. The acid response to pylorus ligation in vagally intact rats was unaffected by drainage of the stomach and therefore not caused by distension. Bilateral vagotomy, performed simultaneously with the ligation, completely abolished acid secretion, while unilateral vagotomy reduced the acid output by half. Hence, in innervated rats, an intact vagal impulse flow appears to be essential for the acid response to pylorus ligation. When the pylorus ligation was performed 2-8 weeks after truncal vagotomy, the acid output showed a progressive return towards pre-denervation values. In the denervated rats the acid response to pylorus ligation was blocked by drainage of the stomach and therefore probably caused by distension, a mechanism which is independent of the vagal impulse flow. 3. The response to pylorus ligation in innervated rats was blocked by atropine and chlorisondamine but not by metiamide. In the denervated rats, the response to pylorus ligation was blocked by all three drugs. 4. Following ligation of both the pylorus and the oesophagus the acid response was poor. With drainage of the oesophagus the acid response was much enhanced, suggesting that oesophageal distension inhibits acid secretion. In the vagotomized rat the poor acid response to oesophageal + pyloric ligation could not be overcome by drainage of the oesophagus. In the innervated rat gastric distension could overcome the inhibition induced by oesophageal ligation. Also in chronically, but not in acutely vagotomized rats, gastric distension brought about a good acid response. Conceivably, gastric reflex mechanisms can activate acid secretion through vagal and/or intramural pathways. Both in innervated and denervated rats the response to gastric distension was inhibited by atropine, chlorisondamine and metiamide. 5. The results suggest that in the innervated rat vago-vagal reflexes are important for the gastric hypersecretion following ligation of the pylorus, and for the acid response to gastric distension following ligation of the pylorus and oesophagus. In the chronically vagotomized rat local intramural reflexes elicited by gastric distension are responsible for the acid response.
Animals↗
Effects of various gastrointestinal peptides on parietal cells and endocrine cells in the oxyntic mucosa of rat stomach.
1. The effects of secretin, glucagon, cholecystokinin-pancreozymin (CCK-PZ), gastric inhibitory peptide (GIP), vasoactive intestinal peptide (VIP), somatostatin, neurotensin and enkephalin on basal, pentagastrin- and histamine-stimulated gastric acid secretion were investigated in the conscious fistula rat. 2. Glucagon and GIP were ineffective inhibitors of basal and pentagastrin-stimulated secretion. CCK-PZ stimulated acid secretion at a low dose level but at higher doses it inhibited both pentagastrin- and histamine-induced secretions. VIP was ineffective at low doses and at high doses its action was complicated by reflux of stimulated pancreatic and intestinal secretions into the stomach. Met-enkephalin inhibited histamine- but not pentagastrin-stimulated secretion. Neurotensin inhibited the response to pentagastrin but had no effect on histamine-stimulated secretion. Secretin and somatostatin were potent inhibitors of basal and pentagastrin-stimulated acid secretion with little or no effect on the response to histamine. 3. At doses completely inhibitory to pentagastrin-stimulated secretion secretin and somatostatin did not block the mobilization of gastric mucosal histamine by pentagastrin, although somatostatin caused partial competitive inhibition at lower doses of pentagastrin. Thus secretin and somatostatin inhibited pentagastrin-induced secretion neither by blocking gastric mucosal histamine mobilization nor by abolishing the direct action of histamine on the parietal cell -- findings which are inconsistent with the proposed role of histamine as the mediator of the action of gastrin on the parietal cell.
Animals↗
Immunoreactive avian pancreatic polypeptide occurs in nerves of the mammalian nasal mucosa and eustachian tube.
Nerves staining with antibodies against avian pancreatic polypeptide were detected in the mucosa of the nasal cavity and around the Eustachian tube of rats, guinea pigs, rabbits and cats. The nerves were numerous in guinea pig and rabbit but few in rat and cat. They were predominantly located around large and medium-sized blood vessels. Occasionally, single nerve fibres were noted around the acini of seromucous glands. This localization suggests that nerves storing immunoreactive avian pancreatic polypeptide are involved primarily in the regulation of local blood flow.
Amino Acid Sequence↗
High content of tyrosine and arginine in peptides and proteins from the growth hormone producing cells of the adenohypophysis.
Fluorescence histochemistry has demonstrated an abundance of tyrosine and arginine residues in the growth hormone (GH) producing cells of the pituitary of several mammals. Granules from pig pituitaries were purified by passage through a succession of Millipore filters followed by centrifugation on a continuous sucrose gradient. One granular fraction, rich in GH, was found to contain proteins or peptides rich in tyrosine and arginine. Gel chromatography of the acid-soluble components from sedimented pituitary granules revealed that the arginine- and tyrosine-rich material was heterogeneous. The arginine-containing peptides and proteins could be separated into several peaks with molecular weights from 5000-10,000 and higher. The tyrosine-containing material comprised one peptide with a molecular weight of 5000-10,000 and another much smaller peptide. Since GH itself is not excessively rich in either tyrosine or arginine, the tyrosine- and arginine-containing proteins or peptides probably constitute as yet unidentified granular components, distinct from GH itself.
Animals↗