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PubMed1990

Modulation of gonadotropin-releasing hormone neuronal activity as evidenced by uptake of fluorogold from the vasculature.

Peripheral injections of the tracer fluorogold (FG) and immunocytochemistry were used to study the modulation of gonadotropin-releasing hormone (GnRH) cell secretory activity in adult mice. Intraperitoneal administration of FG would make it available to all GnRH terminals outside the blood-brain barrier. The degree of capture of the dye would be linked to exocytotic (e.g., secretory) events at the nerve terminal. Single injections of tracer were made into intact mice of both sexes, and this resulted in the retrograde labeling of two-thirds of the GnRH cell bodies. Administration of identical doses to 3 week castrate mice revealed a reduction in the percentage of GnRH cells, with detectable FG, to 40% of the total. Castration did not diminish the number of GnRH cells visualized. When castrate animals received two doses of FG, the number of GnRH cells with tracer was increased to slightly greater than intact levels. This suggests that the secretory rate of individual GnRH cells might be reduced under conditions of castration. In addition, when ovariectomized females treated with estrogen and progesterone to induce luteinizing hormone (LH) surge were injected with FG just prior to that surge, over 80% of the GnRH neurons were robustly labeled with FG. These latter data are interpreted as representing GnRH neurons at maximally synchronized activity. This study suggests that peripheral administration of FG can be used in this species to follow alterations in neurosecretory rates.

Animals↗
PubMed2000

Social class, sex, and age differences in mucosal immunity in a large community sample.

There have been very few reports addressing levels and distribution of commonly used PNI measures in large community samples. In this study, we report such data for secretion rates of secretory immunoglobulin A (sIgA), as determined from saliva samples taken from 1971 subjects interviewed as part of the West of Scotland Twenty-07 survey of health in West Central Scotland. Univariate analyses of demographic variables found lower sIgA and salivary flow to be significantly related to poorer social class, increased age, and being female. Smokers also had lower sIgA but not lower salivary flow. Multivariate analysis showed that demographic variables were significant predictors of sIgA independently of each other and assay variation. Adding smoking status to the equation confirmed it as an independent predictor and also indicated that social class differences in sIgA are partly explicable in terms of smoking status. In view of reported associations between sIgA levels and stress, its role as a first line of mucosal defense, and its relevance to health, these first results from a large survey are of interest. Further work is now needed to explore which factors, including psychosocial ones, may be contributing to subgroup differences.

Adolescent↗
PubMed1994

Vasoactive intestinal polypeptide antiserum affects rat prolactin mRNA in 40-day but not 110-day diethylstilbestrol-induced prolactinoma tissue.

Experiments were designed to examine whether vasoactive intestinal polypeptide (VIP), a known stimulator of basal prolactin (PRL) secretion, regulates PRL gene expression in the rat diethylstilbestrol (DES)-induced prolactinoma model. The VIP-induced increase in PRL release could result from increased PRL synthesis and/or decreased PRL degradation. Male Fischer 344 rats were implanted with 10 mg DES pellets 40 or 110 days prior to obtaining the anterior pituitary glands for cell dispersal. Cells were incubated in 1:10 normal rabbit serum or VIP antiserum (AVIP). After incubation, cells were pelleted, washed, and pooled for total nucleic acid extraction. The rat PRL (rPRL) mRNA abundance was quantitated using a solution hybridization/ribonuclease protection assay. Supernatant was collected and analyzed for PRL content using radioimmunoassay. Results from this experiment reveal partial immunoneutralization of intrapituitary VIP significantly decreased PRL secretory rate by rapid reduction in rRPL mRNA in the 40-day tumors. However, in the 110-day tumors the rPRL mRNA steady-state levels were unchanged but the basal release of PRL continued to be decreased by AVIP. These results indicate VIP exerts its effects on PRL secretion through at least two mechanisms.

Animals↗
PubMed1986

Control of O2 supply to the pancreas during a vasopressin-induced vasoconstriction.

In the anesthetized dog, the metabolic level of the pancreas was elevated by a secretin infusion (1.2 U/kg/hr iv), displaying a metabolic control of tissue oxygenation and blood flow. Question was raised how this system would response to a decrease in O2 supply, as induced by increasing doses of vasopressin (2-131 mU/kg, iv). These vasopressin administrations progressively diminished blood flow (down to 20%), as well as secretory rate (down to 7%) and O2 consumption (down to 33%). The O2 extraction was increased up to 227%. Capillary density, mitochondrial O2 consumption, capillary PO2 and cellular PO2 were calculated by simulating these data with the model of the metabolic control of tissue oxygenation. The changes mentioned above could be simulated adequately. These simulations revealed that a. in the pancreas vasopressin primarily increases arteriolar resistance; the inhibition of metabolism is secondary to the vasopressin-induced vasoconstriction. b. The pancreas responds with a small compensatory capillary recruitment (up to 29%), which in itself would increase tissue oxygenation. c. The main consequence of the lowering of blood flow is a dramatic decrease of mean capillary PO2 (down to 38%), as well as a lowering in mean cellular PO2 (down to 41%). This lowering of O2 supply to the tissue will slow down the metabolic rate, as evidenced by the decrease of the volume of the excretion.

Animals↗
PubMed1994

Low-dose hydrocortisone infusion attenuates the systemic inflammatory response syndrome. The Phospholipase A2 Study Group.

There is increasing evidence that the hypercortisolemia in inflammatory diseases suppresses the elaboration of proinflammatory cytokines, thus protecting the host from its own defence reactions. In severe sepsis and septic shock cortisol levels are usually elevated, but some patients may have relative adrenal insufficiency. This may contribute to the overwhelming systemic inflammatory response syndrome. We evaluated the impact of low-dose hydrocortisone infusion (10 mg/h) on the course of the systemic inflammatory response syndrome. This dose corresponds to a maximum secretory rate of cortisol achieved in corticotropin-stimulated healthy humans. In a prospective observational study 57 surgical patients with severe sepsis or septic shock were studied, of which in addition to the conventional treatment 12 patients were infused with low-dose hydrocortisone, and 45 were treated without any corticosteroid. In the longitudinal analysis the systemic inflammatory response--as judged by body temperature, cardiovascular response, and kinetics of inflammatory mediators such as phospholipase A2, C-reactive protein, and neutrophil elastase--started to differ in favor of the hydrocortisone-treated patients after 2 days of treatment (P < 0.05, Mann-Whitney U test). The difference disappeared after withdrawal of exogenous cortisol. Shock reversal was achieved in all patients treated with low-dose hydrocortisone. The data provide evidence that low-dose hydrocortisone infusion attenuates the systemic inflammatory response in human septic shock. From an immunological point of view a relative cortisol deficiency may contribute to the amplified immune response in systemic inflammatory diseases. A randomized clinical trial must clarify the impact of low-dose hydrocortisone infusion on the clinical course and outcome of septic shock patients.

Adrenal Insufficiency↗
PubMed1989

The hypoglycaemic and insulinotropic activity of Tinospora crispa: studies with human and rat islets and HIT-T15 B cells.

In Malaysia, Tinospora crispa extract is taken orally by Type 2 (non-insulin-dependent) diabetic patients to treat hyperglycaemia. We have evaluated the claimed hypoglycaemic property by adding aqueous extract to the drinking water of normal and alloxan-diabetic rats. After one week, fasting blood glucose levels were significantly (p less than 0.01) lower and serum insulin levels were significantly (p less than 0.01) higher in treated diabetic animals (10.4 +/- 1.0 mmol/l and 12.8 +/- 1.1 muU/ml respectively) compared to untreated diabetic controls (17.4 +/- 1.7 mmol/l and 8.0 +/- 0.7 muU/ml respectively). The insulinotropic action of T. crispa was further investigated in vitro using isolated human or rat islets of Langerhans and HIT-T15 cells. In static incubations with rat islets and HIT-T15 B cells, the extract induced a dosage dependent stimulation and potentiation of basal and glucose-stimulated insulin secretion respectively. This insulinotropic effect was also evident in perifused human and rat islets and HIT-T5 B-cells. The observations that (i) in all three models insulin secretory rates rapidly returned to basal levels on removal of the extract and (ii) in rat islets, a second challenge with T. crispa induced an additional, stimulated response, are all consistent with physiological release of insulin by B cells. Moreover, the rate of HIT-T15 glucose utilisation was not affected by incubation with T. crispa, suggesting that the cells were viable throughout. These are the first studies to provide biochemical evidence which substantiates the traditional claims for an oral hypoglycaemic effect of Tinospora crispa, and which also show that the hypoglycaemic effect is associated with increased insulin secretion.

Animals↗
PubMed1992

Disparate effects of calcium channel blockers on pressure dependence of renin secretion and flow in the isolated perfused rat kidney.

Using the model of isolated perfused rat kidneys this study was performed to investigate whether or not voltage-operated calcium channels are essentially involved in the pressure control of renin secretion from the kidneys. At a perfusion pressure of 100 mm Hg (13.3 kPa) renin secretory rates were 4.2 +/- 0.7 (ng angiotensin I h-1) min-1 g-1. Stepwise reduction of renal perfusion pressure to 80, 60, and 40 mm Hg (10.6, 8.0, 5.3 kPa) resulted in an increase of renin release yielding a 30-fold stimulation at 40 mm Hg vs 100 mm Hg. Increasing the perfusion pressure above 100 mm Hg did not further significantly decrease renin secretion. The perfusate flow rate was also pressure-dependent. Flow rates increased linearly with pressure and reached a plateau at 100 mm Hg, which was maintained up to 160 mm Hg (21.3 kPa). The averaged flow rate at the plateau was 15.5 ml min-1 g-1. In the presence of the three different calcium antagonists nifedipine (5 microM), nitrendipine (3 microM) and verapamil (5 microM), myogenic autoregulation of flow was abolished as indicated by the rise of the pressure/flow curve between 40 and 160 mm Hg. At the same time, however, these calcium channel blockers did not alter the relationship between perfusion pressure and renin secretion. Moreover, the calcium channel agonist Bay K 8644 (5 microM) caused a strong and long-lasting vasoconstriction, without changing renin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1979

The action of physalaemin on electrolyte excretion by the mandibular and sublingual salivary glands of the rat.

The effect of physalaemin, an undecapeptide belonging to a family known collectively as the tachykinins, on water and electrolyte excretion of the mandibular and sublingual salivary glands of the rat has been investigated and compared to that of acetylcholine. Drugs were administered intravenously or by close-arterial infusion. Physalaemin is a powerful stimulant of fluid secretion by both glands although less potent than acetylcholine. The Na and K excretion patterns in physalaemin-evoked saliva resembled, but were by no means identical to those evoked by acetylcholine and other parasympathomimetic drugs: saliva evoked by physalaemin was considerably poorer in Na and K at all secretory rates. The HCO3 excretion curves, on the other hand, seemed to be identical to those evoked by parasympathomimetic drugs. From an analysis of the Na and K excretion patterns, it can be concluded, both for the mandibular and the sublingual glands, that physalaemin stimulated Na reabsorption and K secretion across the gland duct epitheluim, whereas acetylcholine has the opposite effect. These findings agree nicely with what has previously been demonstrated in vitro in the isolated perfused main excretory duct of the rat mandibular gland.

Acetylcholine↗
PubMed1987

Direct measurement of Na influx by 23Na NMR during secretion with acetylcholine in perfused rat mandibular gland.

Intracellular Na content (Nain) in the perfused rat mandibular gland was measured by using a 23Na NMR spectroscopy at 24 degrees C. An aqueous chemical shift reagent, dysprosium triethylenetetramine-N,N,N',N",N"'N"'-hexaacetic acid [Dy(TTHA)] was used in order to discriminate between the intracellular and the extracellular Na signal. The mandibular gland of rat was perfused arterially with a modified Krebs solution containing 10 mM Dy(TTHA). At rest, Nain was not changed by blocking the Na+/K+ ATPase with ouabain (1 mM) and atropine (3 microM), implying that, in the absence of stimulation, the spontaneous Na influx across the plasma membrane must have been negligibly small. Following onset of stimulation with acetylcholine (1 microM), Nain increased by 9.1 +/- 1.5 mmol/l intracellular fluid (mean +/- SEM, n = 13), and remained at this level during stimulation. In the initial phase of secretion (0-5 min), about 50 mmol/min/l intracellular fluid of Na was secreted into the luminal space (estimated from the secretory rate by assuming an isotonic primary secretion) but, in spite of the higher secretion rate, Nain increased only at an initial rate of 4.1 mmol/min/l intracellular fluid. During the steady phase of secretion (15-30 min) evoked by acetylcholine (1 microM), ouabain (1 mM) caused an increment of Nain of 44 +/- 8 mmol/l intracellular fluid (mean +/- SEM, n = 4). From the rate of Nain increment, the Na influx rate at the steady phase was estimated as 4.5 mmol/min/l intracellular fluid. These results suggest that the influx of Na is caused by stimulation with acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1984

Mammosomatotroph hyperplasia associated with acromegaly and hyperprolactinemia in a patient with the McCune-Albright syndrome. A histologic, immunocytologic and ultrastructural study of the surgically-removed adenohypophysis.

An 11-year-old girl, with the McCune-Albright syndrome, exhibited fibrous dysplasia of several bones, skin pigmentation, precocious puberty, growth hormone hypersecretion, acromegaly and hyper-prolactinemia. Histologic, immunocytologic and ultrastructural investigation of the surgically-removed pituitary showed massive mammosomatotroph hyperplasia. Since no adenoma was found, the abundance of these bihormonal cells, capable of producing both growth hormone and prolactin, was implicated in the causation of growth hormone and prolactin excess. Somatoliberin overproduction and/or somatostatin and dopamine deficiency could not account for the hypophysial abnormality, since changes in secretory rates of these hypothalamic hormones would lead to proliferation of mature somatotrophs and lactotrophs, rather than mammosomatotrophs. In our patient, a congenital hypothalamic malfunction might have been accompanied by hypersecretion of an unidentified releasing factor, resulting in pathologic differentiation of the pituitary and mammosomatotroph hyperplasia. Alternatively, mammosomatotroph hyperplasia may have been due to an inherent genetic or embryonic defect affecting primarily the pituitary. According to this interpretation, the pituitary lesion represented yet another developmental error in the setting of the McCune-Albright syndrome.

Acromegaly↗
PubMed1984

Stimulation of insulin secretion from isolated rat islets of Langerhans by melittin.

Melittin, an amphipathic polypeptide, stimulated the secretion of insulin from rat islets of Langerhans incubated in vitro. The secretory response was dose-dependent and saturable with half the maximal response elicited by a melittin concentration of 4 micrograms/ml. The response was rapid in onset, an increase in secretion occurring within 2 min of exposure of the islets to melittin (2 micrograms/ml). An enhanced secretory rate could be maintained for at least 40 min in the presence of melittin but declined steadily when the agent was removed. Stimulation of secretion by melittin occurred in the absence of glucose and in the presence of both 4 mM and 8 mM glucose but not in the presence of 20 mM glucose. The effect of melittin on secretion was dependent on the presence of extracellular calcium but was not inhibited by norepinephrine. The data suggest that melittin may be a valuable agent for further study of the role played by the B-cell plasma membrane in the regulation of insulin secretion.

Animals↗
PubMed1982

Histamine stimulation of digestive enzyme secretion by in vitro rabbit pancreas.

Histamine (10(-3) M) was found to stimulate pancreatic enzyme secretion from in vitro isolated rabbit pancreas preparations. Histamine produced a peak and then a sustained stimulated secretory rate. Secretion of amylase, lipase, trypsinogen, chymotrypsinogen, and total radio active protein were all found to be stimulated. Although fluid output was slightly increased by histamine, enzyme concentrations in secretion were elevated. This, along with the observed sustained release rate, rules out washout effects. Histamine produced a significant response at 10(-5) M with ED50 being about 3 x 10(-5) M and maximal responses produced by 10(-3) M. Histamine stimulation can be blocked with mepyramine (10(-4) or 10(-5) M) or mepyramine in combination with cimetidine. The observed behavior of the pancreas suggests a similarity with pepsinogen secretion in the stomach.

Amylases↗
PubMed1983

Gastric bleeding and gastric secretion with sulindac and naproxen.

We have examined concurrent gastric secretory rates and bleeding by a gastric wash technique during treatment with naproxen, sulindac, and placebo. Twelve subjects, in each of 4 treatment periods, took either placebo, sulindac 200 mg, naproxen 250 mg, or naproxen 375 mg, twice a day for four days. Of the resultant 192 days (12 subjects, 4 drugs, 4 days/drug), two thirds of all days showed bleeding at a rate less than 0.5 ml/day; this low rate of bleeding was seen with all treatments. In spite of this minor bleeding, we were able to show statistically significantly less bleeding with placebo than with drugs; placebo never resulted in a maximum rate of bleeding for any subject. Distinctions between drugs on the basis of bleeding, however, were not possible. Correlations between outputs of acid and chloride were not significantly affected by any of these drugs. In contrast to previous results with aspirin, no correlation between rates of bleeding and gastric secretion could be established. The low water solubility of these drugs at the pH of gastric contents may account for their causing very little bleeding. In effect, the greater the gastric secretion of acid the less the absorption through the gastric mucosa.

Aspirin↗
PubMed1988

Lactoferrin secretion in alcoholic pancreatic disease.

Lactoferrin, a nonenzyme protein normally secreted in small amounts in pancreatic juice, has been reported by several investigators to be secreted in large amounts in chronic pancreatitis. Whether this increased secretion first occurs at an early or late stage of alcoholic pancreatic disease is unknown. In this study we measured lactoferrin and enzyme outputs in duodenal juice from 10 healthy subjects and three groups of alcoholic subjects: asymptomatic chronic alcoholics without evidence, clinically or biochemically, of pancreatitis (10), those recovered from acute pancreatitis (8), and those with established chronic pancreatitis (8). A multilumen, marker-perfused duodenal catheter was used to aspirate basal pancreatic secretions at the ligament of Treitz. The mean ( +/-SE) lactoferrin concentration in duodenal juice for the four groups of subjects was: healthy, 0.7 +/- 0.1 micrograms/ml; asymptomatic alcoholics, 5.5 +/- 1.5 micrograms/ml; alcoholics who had recovered from acute pancreatitis, 7.4 +/- 0.8 micrograms/ml; and alcoholics with chronic pancreatitis 7.1 +/- 1.9 micrograms/ml. The three groups of alcoholics each had a greater lactoferrin concentration than the normals (P less than 0.005). The output of lactoferrin in the four groups paralleled the concentration in that the three groups of alcoholics had a significantly greater output: healthy subjects, 3.4 +/- 0.5 micrograms/kg/hr; asymptomatic alcoholics, 25.7 +/- 7.4 micrograms/kg/hr; alcoholics recovered from acute pancreatitis, 80.1 +/- 27 micrograms/kg/hr; and alcoholics with chronic pancreatitis, 90.9 +/- 32 micrograms/kg/hr. The output of chymotrypsin and trypsin in the four groups of subjects revealed increased secretory rates in the asymptomatic alcoholics and the alcoholics recovered from acute pancreatitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1988

Duodenal instillation of pancreatin does not abolish steatorrhea in patients with pancreatic insufficiency.

Many believe that intragastric deactivation of lipase accounts for the frequent failure of orally ingested pancreatic enzymes to normalize fat absorption in patients with pancreatic insufficiency. To test this hypothesis, we measured fat absorption from a large test meal in six patients with pancreatic insufficiency after we had instilled Viokase directly into the postcibal duodenum in two doses, one to deliver lipase at about 10% of normal secretory rates and the other at four times this rate. Direct duodenal instillation of neither the low nor the high dose of Viokase, nor the low dose of Viokase plus sodium bicarbonate, normalized fat absorption from the test meal; none of these duodenal instillations significantly improved fat absorption over that after the test meal plus orally ingested Viokase. Despite these various treatments, the patients excreted an average of 25.5 g of dietary fat as opposed to 2.1 g excreted by six normal subjects after the same meal. We conclude that more than just intragastric destruction of lipase underlies the frequent failure of orally ingested pancreatin to normalize fat absorption in pancreatic insufficiency.

Celiac Disease↗
PubMed1992

Effect of a restricted diet on the in vitro glucose-induced insulin release of aging rats.

To study the effect of a sudden loss of body weight on the beta-cell function of aging rats, basal and glucose-induced insulin secretion was measured in pancreatic islets obtained from young (2-month-old), adult (12-month-old) and aging (24-month-old) rats, either fed ad libitum or fed a restricted diet (50% caloric restriction). Basal insulin secretion was similar in islets of young, adult and older rats. Glucose stimulated insulin release was significantly reduced in aging rats as compared to young animals. Animals fed a restricted diet showed a prolonged and higher secretory rate during first phase release when compared to animals fed ad libitum.

Aging↗
PubMed1978

Gastrin stimulated H+ secretion in amphibian gastric mucosa: effect of tetrodotoxin.

The role of neural mechanisms in gastrin stimulated H+ secretion was studied using amphibian gastric fundic mucosa. Spontaneously secreting mucosae were converted to resting state (zero H+ secretory rate) using Burimamide. Following removal of burimamide, 3 X 10(-6) M tetrodotoxin did not block gastrin stimulation of H+ secretion indicating that neural mechanisms are not required.

Animals↗
PubMedDate not supplied

Glucagon and insulin secretion during acid-base alterations.

Previously, we reported that change from the normal pH of 7.4 surrounding the islet cells to 7.8 results in a decreased B-cell response to 16.6 mM glucose, 10 mM arginine or 400 micrograms/ml tolbutamide. In the present report we studied the effect of modifications in the extracellular pH on glucose- and arginine-induced glucagon and insulin secretion by the perfused rat pancreas. It was found that at pH 7.8, arginine-induced glucagon secretion was significantly greater than at pH 7.4. On the other hand, the switch from pH 7.4 to 7.8 in a pancreas already stimulated by either low glucose or arginine, produced fast and transient glucagon release. Sequential extracellular pH changes from 7.4 to 7.8 and back to 7.4 in the presence of 8.3 mM glucose and a 5 mM arginine stimulus demonstrated that A- and B-cells rapidly modify their secretion in response to extracellular alkalosis in opposite directions. While glucagon output was enhanced (mean secretory rates at pH 7.4, 0.692 +/- 0.042 ng/min and 0.948 +/- 0.57 at pH 7.8), insulin secretion was clearly reduced (72.6 +/- 6.2 ng/min and 35.7 +/- 2.8 ng/min at pH 7.4 and 7.8, respectively). The above observations, together with our previously reported data, indicate that extracellular pH plays an important role in the regulation of glucagon and insulin release. Particularly, extracellular alkalosis enhances A-cell response to 2.3 mM glucose and 5 mM arginine while partially inhibiting B-cell secretion in the perfused rat pancreas.

Acid-Base Imbalance↗