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PubMed1993

Effect of exposure to an alcohol diet for 10 days on the ability of interleukin-1 beta to release ACTH and corticosterone in the adult ovariectomized female rat.

Adult ovariectomized female rats were fed an alcohol diet for 10 days. Animals fed ad libitum, or fed an isocaloric diet (pair-fed), were also included in all experiments. The intravenous injection of interleukin-1 beta caused dose-related increases in plasma adrenocorticotropic hormone (ACTH) levels in all three groups of rats. However, alcohol-fed animals showed a significant blunting of their ACTH, but not corticosterone response, in comparison with rats fed ad libitum or pair-fed. In contrast, corticotropin-releasing factor (CRF) injection caused overall statistically comparable ACTH secretory rates in all animals, although small differences were observed in some cases. Exposure to mild electroshocks for 30 min significantly increased ACTH values in all animals, but alcohol-fed rats again showed blunted release. In this paradigm, pair-fed animals exhibited a response that was intermediate between that of the ad libitum and alcohol-fed groups. We conclude that chronic alcohol consumption decreases the response of the hypothalamic-pituitary axis to cytokines and mild footshocks. This suggests that the activity of both CRF nerve terminals in the median eminence, and of CRF perikarya in the hypothalamus, is inhibited by this treatment, although pituitary responsiveness to CRF appears unchanged.

Adrenocorticotropic Hormone↗
PubMed1990

Cholic acid and chenodeoxycholic acid transport in the hepatic acinus in rats. Effect of necrosis of zone 3 induced by bromobenzene.

The transport of cholic acid (CA) and chenodeoxycholic acid (CDC) and their influence on bile formation was investigated in rats treated with bromobenzene (BZ), a toxicant which selectively destroys zone 3 of the hepatic acinus. The necrosis equals 27-31% of the acinus cells. The absence of zone 3 in rats reduced the secretory rate maximum of CA and CDC by 18% (NS) and 25% (p less than 0.05), respectively. The maximum bile flow was not different from control during CA infusion but was lower during CDC infusion in BZ-treated animals. Although the bile acid concentration was lower in BZ-treated rats, only values obtained during the basal period and the beginning of the infusion reached the level of statistically significant difference. The bile salt-independent flow (BSIF) was not affected by the absence of zone 3. Our data suggest that zones 1 and 2 of the hepatic acinus can compensate for the secretion of CA and elaboration of BSIF when zone 3 is destroyed. However, necrosis of zone 3 reduces CDC secretion. Thus, the capacity for bile acid transport of the hepatocytes of different zones in the hepatic acinus may differ according to the circulating bile acid.

Animals↗
PubMed1999

Oral and ocular sicca symptoms and findings are prevalent in systemic lupus erythematosus.

The aims of this study were 1) to examine the frequency of oral and ocular sicca symptoms in patients with systemic lupus erythematosus (SLE); 2) to compare saliva and tear volume, salivary proteins, and features of the oral microflora and mucosa to a matched healthy control group; and 3) to relate the findings to disease parameters. Median disease duration was 5.5 (0.5-28) years, disease activity 5 (2-20), damage score 1 (0-7), and Schirmer I test 7.5 (0-30 mm). Seventeen and twelve patients complained of oral and ocular dryness, respectively. Unstimulated whole saliva and proline-rich proteins in submandibular saliva were significantly reduced in SLE. Oral microbial counts were generally higher in the patients than controls, and the number of oral mucosal changes was increased. The results show that sicca symptoms, although frequent, were not correlated to secretory rates of saliva or tears, but to oral microbial counts. There was no obvious correlation to patient's age, disease activity or duration.

Adolescent↗
PubMed1990

Fluctuation of blood melatonin concentrations with age: result of changes in pineal melatonin secretion, body growth, and aging.

Melatonin in the systemic circulation of rats fluctuates with age, and the causes for such changes were investigated. Male rats (aged 7 days, 16 days, 18 days, 20 days, 30 days, 48 days, 60 days, and greater than 17 months) were adapted under a lighting regime of 12L:12D for at least 7 days. Pineals and blood samples from the trunk or confluens sinuum were collected in the dark period. Melatonin in tissues was extracted, identified, and determined by gas chromatography-mass spectrometry (GC-MS) and/or radioimmunoassay. Tissue melatonin levels obtained by radioimmunoassay correlated closely with those quantified by GC-MS. Thus, the melatonin radioimmunoassay used is a reliable assay method for melatonin in the plasma and pineal of the rat. Plasma melatonin in the confluens sinuum of rats exhibited episodic release superimposed on a basal release pattern. It was suggested that there are two pools of melatonin in the pineal gland, a readily releasable pool and a bound pool. The mean plasma levels of melatonin in the confluens sinuum of rats increased with age with the highest level recorded at 60 days old and declined to a lower level at greater than 17 months old. The above age-related changes, being similar to the alterations in pineal melatonin levels with growth and aging, suggest that, under our experimental conditions, levels of pineal melatonin increase or decrease with its secretory rate. In developing rats, the age-related increase in the rate of secretion of pineal melatonin as reflected by increases in melatonin levels in the confluens sinuum or pineal melatonin content before adulthood is different from the changes in melatonin levels in the systemic circulation which showed an early developmental rise, followed by an active period and then a prepubertal decline. However, when the body weight was taken into consideration, changes in the levels of pineal melatonin content per 100 gm body weight or the calculated blood melatonin levels (plasma melatonin in the confluens sinuum/body:head ratio) correlated well with the fluctuation of serum melatonin in the systemic circulation. Thus, the developmental changes in the concentrations of melatonin in the general circulation are the result of 1) changes in the rate of pineal melatonin secretion and 2) increase in the dilution factor because of increase in body size. In old rats, levels of plasma melatonin in the confluens sinuum and pineal melatonin content decreased indicating a decline in the rate of pineal melatonin secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1985

Insulin potentiates cholecystokinin (CCK)-induced secretion of pancreatic kallikrein.

The effects of insulin on pancreatic kallikrein secretion were studied in streptozotocin diabetic rats and after acute administration of insulin to normal rats. Studies on total protein and amylase secretion were included for comparison. In diabetic rats, the concentration of amylase in pancreatic tissue as well as basal and CCK-stimulated amylase exocrine secretion were significantly reduced. Insulin treatment restored pancreatic tissue concentration and exocrine release of amylase to normal. Insulin deficiency did not induce any change in the concentration of kallikrein or trypsin-like activity in pancreatic tissue. However, basal kallikrein secretion was higher in diabetic rats than in controls. Insulin treatment of diabetics rats did not alter basal kallikrein secretion but potentiated CCK-stimulation of kallikrein release. In normal rats, CCK induced an increase of pancreatic protein, amylase, and kallikrein secretion but not pancreatic juice flow. Additional administration of insulin potentiated the CCK-induced secretory rate of pancreatic juice, protein, and kallikrein but not amylase. A 1.6 times higher concentration of kallikrein was found in the portal vein than in arterial blood, indicating an endocrine release of pancreatic kallikrein. No difference in the concentration of circulating kallikrein was observed between the control and the insulin-treated group.

Amylases↗
PubMed1990

Exocrine and endocrine release of kallikrein after reflex-induced salivary secretion.

Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and beta-adrenergic stimulation but greatly increased after alpha-adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex-induced salivary gland response. Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P less than 0.005). Only heat stress increased circulating glandular kallikrein (12.7 +/- 0.8 ng ml-1 before heat exposure and 53.3 +/- 14.1 ng ml-1 40 min afterwards, P less than 0.005). There were no indications that the endocrine release of kallikrein was due to non-specific leakage. Atropine abolished heat-induced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P less than 0.05). However, phentolamine did not, which may indicate as an yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P less than 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.

Animals↗
PubMed1982

Degeneration secretion of amylase from the parotid gland of the rat.

In anaesthetized rats the parotid saliva secreted during degeneration of the auriculo-temporal nerve contains amylase in fairly constant concentration, the amylase output varying with the secretory rate. The amount of amylase was not reduced by adrenoceptor blocking agents; it was increased by sympathectomy carried out one week in advance. A sympathetic degeneration secretion of amylase could also be demonstrated while the post-ganglionic sympathetic nerves were degenerating; a simultaneous parasympathetic degeneration secretion provided the salivary flow needed for the transport of the amylase.

Amylases↗
PubMed1967

The relation between secretion of urate and p-aminohippurate in the rabbit kidney.

1. The renal excretion of urate in the rabbit was examined during infusion of other anions which are secreted by the kidney. A reduction of urate excretion occurred after administration of p-aminohippurate (PAH) and Diodrast which was proportional to the secretory rate of these compounds. On the other hand, urate was a less efficient inhibitor of PAH secretion.2. Stop-flow experiments showed that tubular secretion of urate at maximal values for secretion of PAH and Diodrast was almost completely suppressed.3. 2,4-Dinitrophenol, fumarate, succinate, salicylate, and probenecid depressed the excretion of urate and PAH, but the tubular secretion of urate was apparently more depressed than that of PAH by these inhibitors.4. It is concluded that a common transport system for urate and PAH is involved in the tubular secretion of urate and PAH in the rabbit. However, the affinity of urate for the transport system appears to be smaller than that of PAH.

Acids↗
PubMed1977

Secretion of fluid and amylase in the perfused rat pancreas.

1. The isolated rat pancreas was perfused with physiological salt solutions of varying composition. Flow of pancreatic juice and output of amylase during rest and after stimulation with pure secretin, pure cholecystokinin-pancreozymin (CCK-PZ), caerulein or acetylcholine (ACh) were measured. 2. Basal fluid secretion was abolished replacing perfusion fluid NA+ or Cl- by Tris+ or SO42- respectively. Readmission of Na+ or Cl- caused a transient increase above the normal control level of both fluid and amylase output. Exposure to K+-free solution severely reduced fluid output and K+ readmission resulted in a transient increase in secretory rate. 3. Maximal stimulation with ACh (10(-7) M), CCK-PZ (1-5 X 10(-10) M) or caerulein (10(-10) M) caused marked sustained fluid and amylase secretion. Maximal secretin stimulation (5-7 X 10(-9) M) caused marked sustained fluid but only a small sustained amylase secretion following an initial transient. 4. Under continuous secretin stimulation, replacement of the CO2/HCO3-buffered control fluid by a CO2/HCO3-free Tris buffered solution caused a sharp decrease in pancreatic juice flow. In the absence of extracellular CO2/HCO3-secretin did not evoke fluid or enzyme secretion. In contrast the effects of ACh, CCK-PZ or caerulein were independent on CO2/HCO3-. Monobutyryl cyclic AMP (10(-3) M) caused marked sustained fluid secretion and transient enzyme secretion. The effect was entirely dependent on the presence of CO2/HCO3-in the perfusion fluid. 5. Ouabain (10(-4)-10(-3) M) markedly inhibited both secretin- and caerulein-evoked fluid secretion while caerulein-evoked amylase secretion was hardly affected. Similar findings were made with K+-free solution. 6. The effect of maximal secretin stimulation on amylase secretion was greatly augmented in the presence of a maximally stimulating concentration of caerulein. The effects on fluid secretion of secretin and caerulein were simply additive. The effects of secretin on both amylase and fluid secretion, in the presence of caerulein, were entirely dependent on the presence of CO2/HCO3- in the perfusion fluid. 7. We conclude that two different fluid secretion processes occur in the rat exocrine pancreas. One stimulated by ACh and CCK-PZ, that is independent of extracellular CO2/HCO3- and another stimulated by secretin involving H+ or HCO3-transport. Only the effects of secretin seem to be mediated by intracellular cyclic AMP.

Acetylcholine↗
PubMed2006

Galactosamine prevents ethinylestradiol-induced cholestasis.

Ethinylestradiol (EE) induces intrahepatic cholestasis in experimental animals being its derivative, ethinylestradiol 17beta-glucuronide, a presumed mediator of this effect. To test whether glucuronidation is a relevant step in the pathogenesis of cholestasis induced by EE (5 mg/kg b.wt. s.c. for 5 consecutive days), the effect of simultaneous administration of galactosamine (200 mg/kg b.wt. i.p.) on biliary secretory function was studied. A single injection of this same dose of galactosamine was able to decrease hepatic UDP-glucuronic acid (UDP-GA) levels by 85% and excretion of EE-17beta-glucuronide after administration of a tracer dose of [3H]EE by 40%. Uridine (0.9 g/kg b.wt. i.p.) coadministration reverted the effect of galactosamine on hepatic UDP-GA levels and restored the excretion of [3H]EE-17beta-glucuronide. When administered for 5 days, galactosamine itself did not alter any of the serum markers of liver injury studied (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase) or biliary secretory function. When coadministered with EE, galactosamine partially prevented the impairment induced by this estrogen in total bile flow, the bile-salt-independent fraction of bile flow, basal bile salt secretion, and the secretory rate maximum of tauroursodeoxycholate. Uridine coadministration partially prevented galactosamine from exerting its anticholestatic effects. In conclusion, galactosamine administration partially prevented EE-induced cholestasis by a mechanism involving decreased UDP-GA availability for subsequent formation of EE 17beta-glucuronide. The evidence thus supports the hypothesis that EE 17beta-glucuronide is involved in the pathogenesis of EE cholestasis.

Animals↗
PubMed1972

The effect of portacaval anastomosis on oral carbohydrate tolerance and on plasma insulin levels.

In patients with portal hypertension, plasma insulin levels were raised both fasting and after oral glucose or intravenous tolbutamide. This supports previous suggestions that resistance to endogenous insulin plays a major role in producing the impaired glucose tolerance found in chronic hepatic dysfunction. The operation of portacaval anastomosis was followed by impaired oral fructose tolerance, but did not significantly change oral glucose tolerance. Plasma insulin levels were unchanged by the operation, either fasting or following the stimulus of an oral glucose load or intravenous tolbutamide. The insulin response after operation was only higher after intensive pancreatic beta cell stimulation by a combination of glucose, tolbutamide, and glucagon. These results indicate that, in patients with hepatic dysfunction, little insulin is being removed by the liver from the portal blood except when the insulin secretory rate is unusually high.

Fasting↗
PubMed1972

Inhibition of pancreatic secretion in man by cigarette smoking.

Cigarette smoking has been linked to an elevated incidence of duodenal ulcer disease in smokers, although the mechanism is unclear. In 23 young normal subjects single or double secretin tests were performed during non-smoking and smoking periods. Cigarette smoking inhibited the secretion of pancreatic juice and bicarbonate in light smokers (< one pack/day for < three years). Heavy smokers (> one pack/day for > three years) exhibited depressed pancreatic secretory rates during non-smoking periods. Inhibition of pancreatic alkaline secretion by cigarette smoking could be the link between the habit and duodenal ulcer disease.

Adult↗
PubMed1977

Effect of fundic distension on gastric acid secretion in man.

The effect of distension of the fundus and body of the stomach on gastric acid secretion was studied in 26 patients with duodenal ulcer and six healthy subjects. Graded distension produced by inflating a rubber balloon to volumes of 150, 300, and 600 ml resulted in significant sequential increments of acid output. The secretory response outlasted stimulation by at least one hour. In both groups of subjects, the highest acid output obtainable with fundic distension amounted to just above 50% of the maximum secretory response evoked by intravenous infusion of pentagastrin. A significant correlation was found between the peak secretory rates observed during fundic distension and after pentagastrin stimulation. It is concluded that distension of the oxyntic gland area in man is a potent stimulus for gastric secretion of acid and that patients with duodenal ulcer are no more sensitive to this stimulus than healthy subjects.

Adult↗
PubMed1979

Secretion of biliary lipids in young Chilean women with cholesterol gallstones.

The early appearance of cholesterol gallstones is very common in Chile. To elucidate the mechanisms involved in this phenomenon, the size of the bile acid pool and the secretion of biliary lipids were studied in two groups of young women with normal weights and radiologically functioning gallbladders: nine with cholesterol gallstones and 14 healthy volunteers. The bile acid pool was similar in control and gallstone patients. The secretory rates of bile acids and phospholipids were comparable and significantly correlated in both groups. On the other hand, cholesterol output was higher in gallstone patients. In controls there was a significant correlation between the output of bile acids and cholesterol, but no correlation was found in the gallstone group. This study suggests that cholesterol hypersecretion into the bile is a major factor in the pathogenesis of cholesterol gallstone disease in young Chilean women with normal weights.

Adult↗
PubMed1985

Acid and gastrin responses during intragastric titration in normal subjects and duodenal ulcer patients with G-cell hyperfunction.

Amino acid induced acid and gastrin responses during intragastric titration at pH 2.5 and 5.5 were compared in normal subjects and duodenal ulcer patients with G-cell hyperfunction. The latter were identified on the basis of raised basal or maximal acid outputs and increased gastrin responses to feeding. In normal subjects the mixed amino acid meal stimulated only modest increases in serum gastrin, and the highest observed increase was about 30% that after a standard meal. In contrast, in the G-cell hyperfunction group the highest gastrin concentrations were similar to those after a standard meal. In the G-cell hyperfunction group the increment in serum gastrin at pH 2.5 expressed as a proportion of that at pH 5.5 was 0.29 indicating that the capacity of acid to inhibit gastrin release was well established in these patients. Acid secretory rates were close to maximal at both pH 2.5 and 5.5 during intragastric titration in the ulcer patients, but in normal subjects acid output was about 50% maximal at 2.5 and close to maximal at 5.5. The results suggest that the enhanced gastrin response to feeding in G-cell hyperfunction patients is because of increased sensitivity to amino acid stimulation rather than to diminished acid-inhibitory mechanisms.

Adult↗
PubMed1981

Gastric inhibitory polypeptide stimulated secretion of somatostatinlike immunoreactivity from the stomach: inhibition by acetylcholine or vagal stimulation.

The possible involvement of gastric somatostatinlike immunoreactivity (SLI) in the acid inhibitory action of gastric inhibitory polypeptide (GIP) was studied in an isolated perfused rat stomach. GIP, in a dose of 5 or 50 ng/mL, caused a 4- and 12-fold increase in SLI secretion, respectively. At the higher dose level the stimulated secretory rate declined throughout the perfusion suggesting that secretion exceeded the capacity to synthesize SLI under excessive GIP stimulation. Acetylcholine (10 microM) or vagal stimulation (7 V, 10 Hz, 5 ms) completely inhibited GIP-stimulated SLI secretion. It is therefore proposed that the acid inhibitory activity of GIP is probably mediated via release of gastric SLI and this action is under cholinergic control.

Acetylcholine↗
PubMed1982

Inhibition of gastric H+ secretion, K+-ATPase and K+-phosphatase by estradiol in vivo and in vitro.

The effect of estrogen on the gastric acid secretion and H+-transporting enzymes, K+-ATPase and K+-phosphatase, were investigated in the rat. The maximum H+ secretory rate in response to 1 mM histamine was significantly reduced (P less than 0.05) in both the isolated gastric mucosa obtained from the rats treated with estradiol in vivo for 7 days and the mucosa directly incubated in vitro with estradiol. The inhibitory effect on the gastric enzyme activities in vitro showed a dose-dependent pattern of a noncompetitive type. The result suggested that estradiol may have a direct action on the gastric H+ secretion by inhibiting the H+ transport enzyme activities.

Adenosine Triphosphatases↗
PubMed1983

Origin of the decline in pancreatic amylase secretion with time in vitro.

The release of alpha-amylase (EC 3.2.1.1) into the medium bathing strips of rabbit pancreas decreased gradually with time in vitro so that after 3 h of incubation the secretory rate was only 20% of that seen initially. This decrease was not the result of an intrinsic loss of cellular responsiveness or viability, because a cholinergic agonist was still able to augment amylase secretion from the tissue after this incubation period to the same, or greater, degree than from "fresh" tissue. Rather, the inhibition of secretion was apparently due to the release of a nondialyzable substance from the tissue, which appears to be amylase itself. The observations that led to this conclusion are 1) replacing the bathing medium every 30 min eliminated the time-dependent decrease in enzyme secretion, 2) this replacement was ineffective if the tissue was separated from the medium by a dialysis membrane, and 3) adding an excess of the amylase substrate glycogen to the medium also prevented the falloff in amylase secretion, the effect of glycogen presumably being due to the formation of an enzyme-substrate complex in the medium. These observations are consistent with other observations that demonstrate that the rate of enzyme secretion by the pancreas depends on the rate of removal of product from the site of its secretion [Isenman and Rothman, Proc. Natl. Acad. Sci. USA 74: 4068-4072, 1977; Isenman and Rothman, Science 204: 1212-1215, 1979; Ho and Rothman, Am. J. Physiol. 242 (Gastrointest. Liver Physiol. 5): G32-G39, 1982].

Amylases↗