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PubMed1995

Distinct modes of melatonin secretion in normal men.

As for many hormones, melatonin levels in the blood suggest that it is discharged from the pineal gland in a pulsatile manner. Recently, the existence of short-term episodes, superimposed on the circadian pattern of circulating melatonin, has been questioned. Because plasma melatonin levels reflect not only the secretory process, but also the effects of distribution and degradation, secretory rates were estimated from peripheral levels, using a deconvolution procedure. Fourteen healthy volunteers were studied during the night, while sleeping in the dark (2300-0700), and seven of them subsequently were used in a replicate study. Plasma melatonin levels were measured at 10-min intervals by a direct, specific radioimmunoassay. Pulse analysis was performed using the computer program ULTRA. Approximately 30% more pulses were detected on the overall secretory were often superimposed on tonic basal secretion. Their number, amplitude, and distribution over time were variable depending on subjects. Also the mean melatonin secretory rate varied more than threefold across individuals. Despite the large interindividual variability, the subjects, who were used in replicate experiment, displayed a rather similar secretory profile. We conclude that in normal adult men, melatonin secretion undergoes two distinct secretory modes, in which episodic secretion is superimposed on tonic secretion in subject-dependent variable proportions.

Adult↗
PubMed1987

Biliary lipid secretion in the rat during infusion of increasing doses of unconjugated bile acids.

The aim of the present study was to examine the secretion of biliary components in rats during infusion of increasing doses of either deoxycholic acid, chenodeoxycholic acid or cholic acid and to test the hypothesis that biliary phospholipids may regulate the hepatic bile acid secretory capacity. Analysis of bile samples, collected every 10 min throughout the infusion period showed that there was an elevation of bile acid, phospholipid, cholesterol and alkaline-phosphodiesterase secretion, with all the bile acids, peaking and then gradually declining. Their secretory rates maximum differed and were inversely related to their detergent strength. However, the secretory rates maximum and total output of phospholipids and cholesterol were similar for all bile acids infused. The per cent contribution of phosphatidylcholine to total bile acid-dependent phospholipid secretion was reduced from 84% (in the pre-infusion period) to 59, 46 and 13% at the end of the cholic acid, chenodeoxycholic acid and deoxycholic acid infusions, respectively. This decrease in the per cent contribution of phosphatidylcholine was associated with an increase in the contribution of both sphingomyelin and phosphatidylethanolamine. The biliary phospholipid fatty acid pattern corroborated these changes in the phospholipid classes. Since sphingomyelin and phosphatidylethanolamine are major phospholipids in bile canalicular and other hepatocellular membranes, the marked increase in their secretion in bile during the infusion of high doses of bile acids may indicate solubilization of membrane phospholipids, resulting in membrane structural changes responsible for the reduced excretory function of the liver.

Animals↗
PubMed1978

Studies of renin-aldosterone axis in stable normotensive and hypertensive renal allograft recipients.

Functional aspects of the renin-aldosterone axis were investigated in long-term normotensive and hypertensive renal allograft recipients. Unstimulated plasma renin and aldosterone levels were within control range in all patients and rose significantly in response to sodium depletion. However, no difference in the stimulated renin and aldosterone values between normotensive and hypertensive patients was noted. Baseline aldosterone secretory rates were elevated in all patients, but were higher in hypertensive patients than in normotensive patients. In both groups sodium depletion failed to augment this already elevated aldosterone secretion rate. Possibly, changes in the body pool and/or metabolic clearance rate of aldosterone account for elevations in plasma levels despite a relatively fixed secretory rate, though the role played by the lack of normal innervation of the kidneys cannot be ignored. It is unknown whether these observations may be causal or affected by other presently unknown or unmonitored factors. This in part may reflect unfolding problems in the understanding of nonrenal transplant hypertension.

Adult↗
PubMed1980

Micropipette measurement of airway submucosal gland secretion. Autonomic effects.

We describe a micropipette method for obtaining secretions from single submucosal gland ducts in vivo in cat tracheas. The secretory rate of 65 glands sampled under basal conditions in 16 animals varied from 3 to 30 nl/min (mean +/- SE, 9.05 +/- 0.60 nl/min) and varied 2 to 3-fold among glands sampled within an animal. Sequential samples collected from individual ducts during a 10-min period were highly repeatable (correlation coefficient, 0.96) and were remarkably constant for as long as 4 h. Vagal cooling decreased the secretory rate by a mean of 39% (n = 11, p less than 0.05). Stimulation of the cervical vagus nerves increased flow from 8.3 +/- 0.7 to 16.4 +/- 0.8 nl/min (n = 15, p less than 0.01), an effect that was abolished by intravenous injection of 0.5 mg of atropine sulfate/kg of body weight or by cooling of the vagus nerves, but not by 0.08 mg of phentolamine/kg given intravenously. Intravenous injection of 0.3 mg of phenylephrine/kg of body weight increased flow from 8.6 +/- 0.6 to 18.9 +/- 1.1 nl/min (n = 20, p less than 0.001), an effect that was prevented by phentolamine, but not by atropine. We conclude that cholinergic and alpha-adrenergic stimulation increases fluid secretion from feline submucosal glands.

Animals↗
PubMedDate not supplied

Inhibition of adrenal function in man by heparin or heparinoid Ro 1-8307.

Heparin and the heparinoid Ro 1-8307 inhibited the secretory rate of aldosterone in physiological or pathological aldosteronism to the level found in normal subjects on liberal sodium intake. In addition, these compounds inhibited corticosterone biosynthesis, although less markedly than that of aldosterone. Indications of interference with cortisol production have not been found. During drug treatment angiotensin, in doses of 5-10 ng/kg b.wt./min, did not stimulate aldosterone secretion. ACTH responsiveness of the adrenals--indicated by the fractional increases of both aldosterone and corticosterone secretory rates--remained unchanged. In two studies heparin had no consistent effect on plasma renin activity.

11-Hydroxycorticosteroids↗
PubMed1982

Effect of cervical and thoracic vagal stimulation on luminal serotonin release and regional blood flow in cats.

In acute experiments on 14 cats, the transected vagus nerves were stimulated at two levels (10 V, 5 ms, 10 Hz, 10 mA, 15 min). Fifteen-centimeter proximal jejunal segments were perfused with saline (1.0 ml/min). Basal luminal immunoreactive serotonin secretion averaged 206 +/- 67 ng/5 min. After stimulation of the vagus nerves, there was an immediate two- to threefold increase in the rate of secretion of immunoreactive serotonin into the lumen. There were no significant differences in the stimulated secretory rates that resulted from stimulation at the cervical or thoracic levels. Shortly after cessation of vagal stimulation, immunoreactive serotonin secretory rates returned to basal. Vagal nerve stimulation did not result in any change in peripheral or portal venous blood concentrations of serotonin. In 12 additional cats, the effects of stimulation of the vagus nerves at the cervical and thoracic levels on regional blood flow, as determined using the microsphere technique, were compared. Cervical vagal stimulation resulted in hypotension, bradycardia, decreased perfusion of the heart, kidney, and small and large bowels, but preservation of the perfusion of the fundus and antrum. In contrast, stimulation of the transected nerves in the chest stimulated gastric blood flow but did not alter either flow to other viscera or central hemodynamics.

Animals↗
PubMed1991

Analyzing pulsatile endocrine data in patients with chronic renal failure: a brief review of deconvolution techniques.

Deconvolution analysis provides an important new technique to evaluate underlying hormone secretory rates quantitatively based upon serially measured plasma hormone concentrations with or without prior knowledge of the half-time of hormone disappearance from the blood. Information about endocrine gland secretion is particularly important in chronic renal failure, wherein the decreased metabolic clearance rates of various hormones would otherwise confound the interpretation of plasma hormone concentrations. Here we review two particularly useful techniques of deconvolution, one of which is a waveform-defined algorithm and the other waveform independent. The first method can be used to estimate both hormone half-life and secretory rates in vivo. The second methodology allows calculation of in vivo hormone secretion rates without assuming any special form for the secretion event, but requires a priori knowledge of hormone half-life. We illustrate examples of these two deconvolution approaches, and discuss why the interpretations of hormone concentration measurements in earlier studies (where deconvolution methods were not employed) must be viewed with caution. Based on such considerations, additional investigations of in vivo hormone secretory pathophysiology will be required in children and adults with chronic renal failure.

Endocrine Glands↗
PubMed2005

Vildagliptin, a dipeptidyl peptidase-IV inhibitor, improves model-assessed beta-cell function in patients with type 2 diabetes.

AIMS/HYPOTHESIS: The dipeptidyl peptidase IV inhibitor, vildagliptin, increases levels of intact glucagon-like peptide-1 (GLP-1) and improves glycemic control in patients with type 2 diabetes. Although GLP-1 is known to stimulate insulin secretion, vildagliptin does not affect plasma insulin levels in diabetic patients, suggesting that more sophisticated measures are necessary to ascertain the influence of vildagliptin on beta-cell function. METHODS: This study examined the effects of 28-d treatment with vildagliptin (100 mg, twice daily; n = 9) vs. placebo (n = 11) on beta-cell function in diabetic patients using a mathematical model that describes the insulin secretory rate as a function of glucose levels (beta-cell dose response), the change in glucose with time (derivative component), and a potentiation factor, which is a function of time and may reflect the actions of nonglucose secretagogues and other factors. RESULTS: Vildagliptin significantly increased the insulin secretory rate at 7 mmol/liter glucose (secretory tone), calculated from the dose response; the difference in least squares mean (deltaLSM) was 101 +/- 51 pmol.min(-1).m(-2) (P = 0.002). The slope of the beta-cell dose response, the derivative component, and the potentiation factor were not affected. Vildagliptin also significantly decreased mean prandial glucose (deltaLSM, -1.2 +/- 0.4 mmol/liter; P = 0.01) and glucagon (deltaLSM, -10.7 +/- 4.8 ng/liter; P = 0.03) levels and increased plasma levels of intact GLP-1 (deltaLSM, +10.8 +/- 1.6 pmol/liter; P < 0.0001) and gastric inhibitory polypeptide (deltaLSM, +43.4 +/- 9.4 pmol/liter; P < 0.0001) relative to placebo. CONCLUSION: Vildagliptin is an incretin degradation inhibitor that improves beta-cell function in diabetic patients by increasing the insulin secretory tone.

Adamantane↗
PubMed1985

Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules.

We studied the effects of cyclic AMP (cAMP) on HCO-3 transport by rabbit cortical collecting tubules perfused in vitro. Net HCO-3 secretion was observed in tubules from NaHCO3- loaded rabbits. 8-Bromo-cAMP-stimulated net HCO-3 secretion, whereas secretion fell with time in control tubules. Both isoproterenol and vasopressin (ADH) are known to stimulate adenylate cyclase in this epithelium; however, only isoproterenol stimulated net HCO-3 secretion. The mechanism of cAMP-stimulated HCO-3 secretion was examined. If both HCO-3 and H+ secretion were to occur simultaneously in tubules exhibiting net HCO-3 secretion, cAMP might increase the net HCO-3 secretory rate by inhibiting H+ secretion, by stimulating HCO-3 secretion, or both. These possibilities were examined using basolateral addition of the disulfonic stilbene (4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS). In acidifying tubules from NH4Cl-loaded rabbits, DIDS eliminated HCO-3 reabsorption, a result consistent with known effects of DIDS as an inhibitor of H+ secretion. In contrast, cAMP left acidification (H+ secretion) intact. DIDS applied to HCO-3 secretory tubules failed to increase the HCO-3 secretory rate, indicating minimal H+ secretion in HCO-3 secreting tubules. Thus, inhibition of H+ secretion by cAMP could not account for the cAMP-induced stimulation of net HCO-3 secretion. cAMP-stimulated HCO-3 secretion was reversibly eliminated by 0 Cl perfusate, whereas luminal DIDS had no effect. Bath amiloride (1 mM) failed to eliminate cAMP-stimulated HCO-3 secretion when bath [Na+] was 145 mM or 5 mM. cAMP depolarized the transepithelial voltage. The collected fluid [HCO-3] after cAMP could be accounted for by electrical driving forces, suggesting that cAMP stimulates passive HCO-3 secretion. However, cAMP did not alter HCO-3 permeability measured under conditions expected to inhibit transcellular HCO-3 movement (0 Cl- solutions and bath DIDS). This measured HCO-3 permeability was not high enough to account, by passive diffusion, for the HCO-3 fluxes observed in Cl-containing solutions. We conclude the following: cAMP increased net HCO3- secretion by stimulating HCO3- secretion and not by inhibiting H+ secretion; this HCO3- secretion may have occurred by Cl-HCO3- exchange; Na+-H+ exchange appeared not to play a role in basolateral H+ extrusion under these conditions; and the stimulation of HCO3- secretion by isoproterenol, but not ADH, suggests the existence of separate cell cAMP pools or cellular heterogeneity in this cAMP response.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1999

Primary Sjögren's syndrome: salivary gland function and clinical oral findings.

OBJECTIVE: To evaluate salivary gland function, saliva composition and oral findings in patients with primary Sjögren's syndrome (pSS) subdivided into patients with and without focus score > or = 1 (FS) and/or antibodies to SSA/SSB (AB) as well as in healthy controls. SUBJECTS AND METHODS: Unstimulated (UWS) and chewing stimulated (SWS) whole saliva, and stimulated parotid saliva (SPS) were collected in 16 patients fulfilling the European classification criteria for pSS subdivided into those with FS and/or AB (n = 8) and those without FS and AB (n = 8), and in age-matched (n = 14) and young healthy controls (n = 13). UWS and SWS were analysed for Na+ and K+. SPS was analysed for Na+, K+, statherin, and proline-rich proteins (PRPs). Sicca symptoms, DMFT/DMFS, plaque (PI) and gingival (GI) scores, periodontal pocket depth (PPD), and mucosal status were recorded. RESULTS: The young healthy controls had lower UWS as compared to the aged controls (P = 0.03). However, the aged controls had higher DMFT/DMFS (P < 0.001) and PI, GI and PPD (P < 0.01). Patients with FS and/or AB generally had lower saliva secretory rates than patients without FS and/or AB (P = 0.01 for UWS and SPS) and age-matched healthy controls (P = 0.001). There was no significant difference in the content of Na+ and K+, statherin and PRPs between groups. Patients with FS and/or AB had the highest frequency of oral mucosal changes and higher DMFT/DMFS than patients without FS and/or AB and healthy controls (P < 0.01). However, PI, GI, and PPD did not differ significantly. CONCLUSION: Patients with FS and/or AB had lower salivary secretory rates, higher DMFT/DMFS, and more oral mucosal changes than patients without FS and/or AB. Additionally, data suggest that salivary gland function in healthy individuals do not decrease with age.

Adult↗
PubMedDate not supplied

[Physiology and pathophysiology of the minor salivary glands].

Measurements of the secretory rates of the palatine and the parotid glands, assessing the electrolyte content of all salivary fractions and combined clinical biotic studies underline the clinical importance of the minor salivary glands. The minor salivary glands are shown to be organs whose function is decisively involved in symptoms such as xerostomia, stomatodynia, and what is known as "denture intolerance". Moreover, proper secretion of the palatine glands is of crucial importance for the physical retention of maxillary full dentures. There are no connections between secretory rates of major and minor salivary glands. The effect of certain drugs on salivary production and thus on the symptoms of hyposalivation seems to be considerable. Treatment methods for inadequate salivary secretion are outlined. The adaptive tendency of properly functioning palatine glands appears to be high. The fact that atrophic and dystrophic processes can be functionally compensated to a relatively high degree speaks for the dynamic capability of the glandular parenchyma. In view of the clinical relevance of the minor salivary glands it is mandatory that the functional principles and control mechanisms underlying their secretion be investigated in future studies.

Calcium Channel Blockers↗
PubMed1979

Pancreatitis as a complication of anticholinesterase insecticide intoxication.

Severe pancreatitis and a pseudocyst occurred in a patient following accidental ingestion of an anticholinesterase insecticide, a substance not previously known to produce pancreatitis. Experiments were done to elucidate the mechanism. In one group of dogs the pancreatic duct was perfused and intraductal pressures were measured. The cholinesterase inhibitor 0,0-diethyl-0-(2-isopropyl-6-methyl-4-pyrimidinyl)phosphorothioate (25 mg/kg) caused a significant increase in the mean intraductal pressure from 12 +/- 2.4 to 27.8 +/- 5.9 cm saline. In a second group of dogs pancreatic secretory rates were measured. Anticholinesterase (75 mg/kg) in combination with secretin infusion (1 U/kg/hr) caused a significant increase in the secretin stimulated flow rate from 0.13 to 0.56 cc/min. Atropine (75 microgram/kg) abolished the anticholinesterase induced pressure and secretory rate increases. In a third group of dogs administration of cholinesterase inhibitor 75 mg/kg and secretin infusion 2 U/kg/hr resulted in acute pancreatic interstitial edema, acinar cell vacuolization, hyperamylasemia and hyperlipasemia. These results suggest that occurrence of pancreatitis as a complication of anticholinesterase insecticide intoxication is the result of hypersecretion and pharmacologic ductal obstruction.

Adult↗
PubMed1984

Studies on the kinetics of melatonin and N-acetylserotonin in the rat at mid-light and mid-dark.

The distribution and disappearance of melatonin and N-acetylserotonin after intravenous injection were studied at mid-light and mid-dark. Male rats were adapted under a photoperiod of 12 h light and 12 h dark cycle for a minimum of 1 week. After the intravenous injection of melatonin (10 micrograms), N-acetylserotonin (10 micrograms), or 3H-melatonin (76 ng), blood samples were collected at 1, 3, 5, 10, 20, 30, 45, 60, 75, 90, and 120 min. The concentrations of indoles in the plasma samples were determined by radioimmunoassay, while the radioactivity of 3H-melatonin was determined by scintillation counting. The distribution of melatonin and N-acetylserotonin followed a two-compartment model, showing an initial distribution phase followed by an elimination phase. The biological half-life of melatonin at mid-light and mid-dark were similar but the volume of distribution (V beta and Vc) and metabolic clearance rate (C1s) were greater at mid-dark than at mid-light. The estimated melatonin secretory rate at mid-dark was fivefold greater than that at mid-light. When 3H-melatonin was used, the half-life was significantly longer. A diurnal difference in the distribution was also evident in the N-acetylserotonin studies. The volume of distribution (V beta and Vc) was greater at mid-dark while the C1s was not significantly faster at mid-dark compared with that at mid-light. However, the estimated N-acetylserotonin secretory rate at mid-dark was eightfold greater than at mid-light.

Animals↗
PubMed1983

Similarities of Li+ and low Ca2+ in the modulation of secretion by parathyroid cells in vitro.

Parathyroid hormone (PTH) release from parathyroid cells in vitro was found to be stimulated by the presence of extracellular lithium ions through a specific secretory response which was comparable to that elicited by low extracellular Ca2+. Li+ (5-40 mM) caused a dramatic increase in the basal PTH secretory rate (up to 2.5-fold), as well as a further enhancement of the low Ca2+-stimulated PTH secretory rate (up to 0.5-fold). Cellular mediators commonly implicated in hormone release from endocrine cells, such as Ca2+ influx, cAMP, and changes in the activity of (Na+, K+) ATPase, were not involved in Li+-stimulated PTH release. The PTH secretory response induced by Li+ was fully maintained in the virtual absence of external Ca2+. Parathyroid cellular cAMP levels were unchanged in buffers varied with respect to both Li+ and Ca2+ and remained constant throughout the time course of Li+ uptake. Ouabain, in concentrations sufficient to block Na+, K+ activity, was also without effect on PTH release elicited by Li+. To identify the site and possible effectors of this stimulatory effect, experimental protocols were devised to modulate the level of intracellular Li+ at constant external Li+ concentrations. These results showed that the enhancement of PTH secretion by Li+ was independent of a 3-fold variation in intracellular Li+, but was directly related to the external Li+ concentration. This and previous evidence suggest that the regulation of PTH secretion by both lithium and calcium ions does not require their transmembrane influx but occurs instead in the parathyroid plasma membrane.

Animals↗
PubMed1982

The influence of calcium on the control of fluid secretion in the cockroach salivary gland.

When cockroach salivary glands are bathed in calcium-free medium the basal rate of fluid secretion increases from about 1 nl/min to about 10 nl/min; maintained dopamine stimulation elicits a further rise in secretory rate which gradually declines. Evidence is presented which indicates that magnesium is unable to substitute for calcium in this system. When calcium is returned to the bathing solution after a period of calcium deprivation there is a transient increase in secretory rate. Stimulation of the glands in certain conditions which inhibit the secretory response leads to some kind of calcium-dependent active state in the secretory cells which can outlast the interaction of the agonist with its receptors. It is concluded that stimulus-secretion coupling in this gland involves a calcium-dependent second messenger system.

Animals↗
PubMed1999

Evaluation of LH secretory dynamics during the rat proestrous LH surge.

The preovulatory luteinizing hormone (LH) surge results from the integration of complex interactions among gonadal steroids and hypothalamic and pituitary hormones. To evaluate changes in LH secretory dynamics that occur during the rat LH surge, we have 1) obtained frequently sampled serum LH concentration time series, 2) used both waveform-dependent and waveform-independent convolution analyses, and 3) independently assessed proestrous LH half-life and basal non-gonadotropin-releasing hormone (GnRH)-dependent LH secretion during the LH surge. Waveform-independent pulse analysis revealed a 24-fold increase in the maximal pulsatile LH secretory rate attained during late proestrus compared with early proestrus. A 15-fold increase was quantified for the mean LH secretory rate. In complementary analyses, we applied a measured LH half-life of 17 +/- 2.7 min and a median basal LH secretion rate of 0.0046 microgram. l-1. min-1 for convolution analysis, revealing a 16-fold increase in the mass of LH released/burst and more than sixfold rise in the amplitude of the secretory peaks. Evaluation of the approximate entropy of the LH surge profiles was performed, showing an increase in the orderliness of the LH release process during the surge. We conclude that both quantitative (mass/burst) and qualitative (approximate entropy) features of LH release are regulated during the proestrous LH surge.

Animals↗
PubMed1981

Possible physiological advantages of parietal cell vagotomy.

Parietal cell vagotomy (PCV) without drainage is associated with the lowest mortality of any operation currently being widely used for the elective treatment of duodenal ulcer. There are fewer gastrointestinal complaints of the type observed after more orthodox gastric operations. Diarrhea and dumping may occur after PCV in approximately 5 percent of patients, and when these complaints do occur they are milder and more easily controlled than after other types of operation. This improvement is attributed to retention of the peristaltic action of the antrum and an intact pyloric sphincter, which together, permit gastric emptying that is more normal than that which occurs with any other gastric procedure. There is insufficient evidence to indicate that retention of antral innervation exerts an inhibitory or a stimulatory effect on acid secretion which would be either beneficial or detrimental to the duodenal ulcer patients. The acid secretory rates are reduced effectively by PCV and equal the reductions that follow truncal vagotomy and drainage. Acid secretory rates increase during the first postoperative year and then remain rather constant with time. This observation and the reports that the rate of recurrent ulcers after 2 to 4 years follow-up is two to four percent, suggests that PCV is a highly effective procedure.

Duodenal Ulcer↗
PubMed1993

Adaptive changes of hepatic bile salt transport in a model of reversible interruption of the enterohepatic circulation in the rat.

The reversibility and time course of the adaptive changes in hepatic bile salt transport related to modifications of the bile salt enterohepatic circulation and bile salt pool size have not been previously studied. For this reason a model of reversible interruption of entero-hepatic circulation was characterized in unrestrained rats, which allowed the study of changes in hepatic bile salt transport following bile salt pool depletion and subsequent restoration by either the de novo synthesis of bile acids or i.v. administration of exogenous taurocholate. Rats subjected to biliary drainage for 24 h through a transduodenal common bile duct cannula, followed by removal of the cannula and restoration of the enterohepatic circulation were studied at 24, 48 and 72 h. Neither light and electron microscopy examination nor plasma biochemical parameters showed evidence of necrosis, fibrosis, cholestasis or inflammatory changes. Maximum taurocholate secretory rate decreased to 50% following 24-h bile salt depletion. After restoration of the enterohepatic circulation maximum taurocholate secretory rate progressively increased to normal values at 72 h, following the normalization of the bile salt pool size, which had a similar composition compared with controls. The same effect was obtained when the native bile salt pool was substituted with exogenous taurocholate. Thus, adaptive down-regulation of hepatic bile salt transport capacity is a reversible process, related to restoration of entero-hepatic circulation and normalization of bile salt pool size.

Adaptation, Physiological↗