In vivo effect of volume expansion on rectal gland function. II. Hemodynamic changes

1984 ◽  
Vol 246 (1) ◽  
pp. R67-R71
Author(s):  
R. J. Solomon ◽  
M. Taylor ◽  
R. Rosa ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Blood Flow ◽  
Volume Expansion ◽  
Energy Requirement ◽  
Fluid Secretion ◽  
Chloride Secretion ◽  
Secretory Response ◽  
Rectal Gland ◽  
Oxygen Extraction Ratio ◽  
Humoral Factors

Intravascular volume expansion causes a 300% increase in the rate of fluid secretion from, and blood flow to, the in vivo rectal gland of the spiny dogfish Squalus acanthias. Similar increases are also observed in explanted rectal glands perfused through a catheter from the dorsal aorta of a volume-expanded dogfish. Stimulation of rectal gland secretion by volume expansion is not associated with a change in the ratio of chloride secreted to oxygen consumed by the rectal gland and the oxygen extraction ratio, suggesting that an increase in blood flow is necessary to support the increased rate of chloride secretion. Perfusion of the explanted gland with bumetanide (10(-4) M) completely inhibits the secretory response to volume expansion but does not prevent the increase in blood flow. Bumetanide also inhibits dibutyryl adenosine 3',5'-cyclic monophosphate- and theophylline-induced increases in chloride secretion but does not inhibit the hyperemic response. Somatostatin inhibits the secretory response of the explanted gland to volume expansion but does not prevent the increase in blood flow. Although an increase in blood flow is necessary to support the increased energy requirement of enhanced transport, the secretory response and the increase in blood flow appear to be independently regulated and mediated, at least in part, by humoral factors.

In vivo effect of volume expansion on rectal gland function. I. Humoral factors

1984 ◽  
Vol 246 (1) ◽  
pp. R63-R66 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
J. S. Stoff ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Volume Expansion ◽  
Chloride Secretion ◽  
Ringer Solution ◽  
Squalus Acanthias ◽  
Humoral Factor ◽  
Rectal Gland ◽  
Host Fish ◽  
Humoral Factors ◽  
Gland Function

The spiny dogfish Squalus acanthias responds to volume expansion by increasing the rate of chloride secretion by its rectal gland. The response is elicited by intravascular infusion of either isotonic shark Ringer solution, a 1 M hypertonic sodium chloride solution, or an isotonic hyponatremic solution containing equal volumes of shark Ringer solution and 10% mannitol. The effect of volume expansion was evoked in explanted glands connected to a host fish only by the arterial supply, indicating that the response is mediated by a humoral factor. The explanted gland responded to theophylline (2.5 X 10(-3) M) and adenosine 3',5'-cyclic monophosphate (5 X 10(-4) M) by increasing the rate of secretion of chloride by an amount similar to that induced by volume expansion of the perfusing fish. Theophylline at concentrations (10(-6) to 5 X 10(-5) M) that are known to inhibit the effect of adenosine in isolated perfused glands failed to inhibit the effect of volume expansion on explanted glands. Somatostatin (4.5 X 10(-6) M), which inhibits the effect of vasoactive intestinal peptide (VIP) in the isolated perfused gland, completely prevented the secretory response to volume expansion in explanted glands. Volume expansion is a major stimulus for chloride secretion by the rectal gland. The effect is mediated by a humoral factor that appears to be VIP.

Atriopeptin stimulation of rectal gland function in Squalus acanthias

1985 ◽  
Vol 249 (3) ◽  
pp. R348-R354 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
D. Dorsey ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Volume Expansion ◽  
Epithelial Transport ◽  
Extracellular Volume ◽  
Chloride Secretion ◽  
Hormonal Control ◽  
Rectal Gland ◽  
Gland Function ◽  
Stimulation Of

The rectal gland of the shark plays a significant role in the homeostasis of extracellular volume. Regulation of rectal gland function is under hormonal control, but the precise identity of the humoral mediator is unknown. Atriopeptin stimulates rectal gland chloride secretion in vivo. This stimulation of epithelial transport is accompanied by systemic and local hemodynamic effects. Atriopeptin also stimulates chloride secretion by the in vitro perfused rectal gland, an effect that is not accompanied by hemodynamic changes. Extracts of shark heart, but not muscle, brain, kidney, or intestine, contain a heat-stable trypsin-sensitive substance capable of in vitro stimulation of rectal gland chloride secretion. Electron micrographic analysis reveals multiple neurosecretory-like granules in atrial cardiocytes that are only rarely seen in ventricular cardiocytes. By using the in vitro perfused gland as a biologic assay, serum obtained after extracellular volume expansion reveals the presence of a rectal gland stimulatory factor that is not present in serum before expansion. These results are consistent with the hypothesis that atriopeptin is present in shark cardiocytes and is released during volume expansion. The atriopeptin stimulates rectal gland chloride secretion, providing a negative feedback mechanism for the regulation of extracellular volume.

scholarly journals Rotavirus Infection Is Not Associated with Small Intestinal Fluid Secretion in the Adult Mouse

2006 ◽  
Vol 80 (22) ◽  
pp. 11355-11361 ◽  
Author(s):  
Shirin Kordasti ◽  
Claudia Istrate ◽  
Mahanez Banasaz ◽  
Martin Rottenberg ◽  
Henrik Sjövall ◽  
...  
Keyword(s):  
Fluid Secretion ◽  
Chloride Secretion ◽  
Potential Difference ◽  
Pathophysiological Mechanism ◽  
Rotavirus Infection ◽  
In Vivo Experiments ◽  
Adult Mice ◽  
Small Intestines

ABSTRACT In contrast to humans, adult but not infant small animals are resistant to rotavirus diarrhea. The pathophysiological mechanism behind this age-restricted diarrhea is currently unresolved, and this question was investigated by studying the secretory state of the small intestines of adult mice infected with rotavirus. Immunohistochemistry and histological examinations revealed that rotavirus (strain EDIM) infects all parts of the small intestines of adult mice, with significant numbers of infected cells in the ilea at 2 and 4 days postinfection. Furthermore, quantitative PCR revealed that 100-fold more viral RNA was produced in the ilea than in the jejuna or duodena of adult mice. In vitro perfusion experiments of the small intestine did not reveal any significant changes in net fluid secretion among mice infected for 3 days or 4 days or in those that were noninfected (37 ± 9 μl · h−1 · cm−1, 22 ± 13 μl · h−1 · cm−1, and 33 ± 6 μl · h−1 · cm−1, respectively) or in transmucosal potential difference (4.0 ± 0.3 mV versus 3.9 ± 0.4 mV), a marker for active chloride secretion, between control and rotavirus-infected mice. In vivo experiments also did not show any differences in potential difference between uninfected and infected small intestines. Furthermore, no significant differences in weight between infected and uninfected small intestines were found, nor were any differences in fecal output observed between infected and control mice. Altogether, these data suggest that rotavirus infection is not sufficient to stimulate chloride and water secretion from the small intestines of adult mice.

Primary role of volume expansion in stimulation of rectal gland function

1985 ◽  
Vol 248 (5) ◽  
pp. R638-R640 ◽  
Author(s):  
R. Solomon ◽  
M. Taylor ◽  
S. Sheth ◽  
P. Silva ◽  
F. H. Epstein
Keyword(s):  
Plasma Volume ◽  
Plasma Osmolality ◽  
Sodium Concentration ◽  
Chloride Secretion ◽  
Ringer Solution ◽  
Rectal Gland ◽  
Primary Role ◽  
Fourfold Increase ◽  
Gland Function

Chloride secretion by the in vivo rectal gland of the shark is stimulated by the intravascular infusion of salt solutions of varying osmolar and sodium concentration. In a cross-perfused and denervated rectal gland, the infusion of a small amount of a hypertonic salt solution raises plasma osmolality but does not increase plasma volume in the donor fish. Under these conditions, rectal gland chloride secretion is not stimulated. A subsequent infusion of isotonic shark Ringer solution increases plasma volume 50%, decreases plasma osmolality, and produces a fourfold increase in chloride secretion and a threefold decrease in vascular resistance within the gland. Both the vasodilatory and secretory responses also follow the infusion of a hypotonic shark Ringer solution. The data further support the hypothesis that the rectal gland of the shark is involved in the regulation of intravascular volume rather than in osmoregulation.

scholarly journals Nitric oxide production duringVibrio choleraeinfection

1997 ◽  
Vol 273 (5) ◽  
pp. G1160-G1167 ◽  
Author(s):  
Edward N. Janoff ◽  
Hiroshi Hayakawa ◽  
David N. Taylor ◽  
Claudine E. Fasching ◽  
Julie R. Kenner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Epithelial Cells ◽  
Regional Blood Flow ◽  
Fluid Secretion ◽  
The United States ◽  
No Production ◽  
Loop Model ◽  
Ileal Loop

Vibrio cholerae induces massive intestinal fluid secretion that continues for the life of the stimulated epithelial cells. Enhanced regional blood flow and peristalsis are required to adapt to this obligatory intestinal secretory challenge. Nitric oxide (NO) is a multifunctional molecule that modulates blood flow and peristalsis and possesses both cytotoxic and antibacterial activity. We demonstrate that, compared with those in asymptomatic control subjects, levels of stable NO metabolites ([Formula: see text]/[Formula: see text]) are significantly increased in sera from acutely ill Peruvian patients with natural cholera infection as well as from symptomatic volunteers from the United States infected experimentally with V. cholerae. In a rabbit ileal loop model in vivo, cholera toxin (CT) elicited fluid secretion and dose-dependent increases in levels of[Formula: see text]/[Formula: see text]in the fluid ( P < 0.01). In contrast, lipopolysaccharide (LPS) elicited no such effects when applied to the intact mucosa. NO synthase (NOS) catalytic activity also increased in toxin-exposed tissues ( P< 0.05), predominantly in epithelial cells. The CT-induced NOS activity was Ca2+dependent and was not suppressed by dexamethasone. In conclusion, symptomatic V. cholerae infection induces NO production in humans. In the related animal model, CT, but not LPS, stimulated significant production of NO in association with increases in local Ca2+-dependent NOS activity in the tissues.

Is Calcium a Coronary Vasoconstrictor In Vivo? 

1998 ◽  
Vol 88 (3) ◽  
pp. 735-743 ◽  
Author(s):  
George J. Crystal ◽  
Xiping Zhou ◽  
Ramez M. Salem
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Coronary Blood Flow ◽  
Myocardial Oxygen Consumption ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Oxygen Extraction Ratio ◽  
Myocardial Oxygen Extraction ◽  
Dose Dependent

Background Calcium produces constriction in isolated coronary vessels and in the coronary circulation of isolated hearts, but the importance of this mechanism in vivo remains controversial. Methods The left anterior descending coronary arteries of 20 anesthetized dogs whose chests had been opened were perfused at 80 mmHg. Myocardial segmental shortening was measured with ultrasonic crystals and coronary blood flow with a Doppler flow transducer. The coronary arteriovenous oxygen difference was determined and used to calculate myocardial oxygen consumption and the myocardial oxygen extraction ratio. The myocardial oxygen extraction ratio served as an index of effectiveness of metabolic vasodilation. Data were obtained during intracoronary infusions of CaCl2 (5, 10, and 15 mg/min) and compared with those during intracoronary infusions of dobutamine (2.5, 5.0, and 10.0 microg/min). Results CaCl2 caused dose-dependent increases in segmental shortening, accompanied by proportional increases in myocardial oxygen consumption. Although CaCl2 also increased coronary blood flow, these increases were less than proportional to those in myocardial oxygen consumption, and therefore the myocardial oxygen extraction ratio increased. Dobutamine caused dose-dependent increases in segmental shortening and myocardial oxygen consumption that were similar in magnitude to those caused by CaCl2. In contrast to CaCl2, however, the accompanying increases in coronary blood flow were proportional to the increases in myocardial oxygen consumption, with the result that the myocardial oxygen extraction ratio remained constant. Conclusions Calcium has a coronary vasoconstricting effect and a positive inotropic effect in vivo. This vasoconstricting effect impairs coupling of coronary blood flow to the augmented myocardial oxygen demand by metabolic vascular control mechanisms. Dobutamine is an inotropic agent with no apparent direct action on coronary resistance vessels in vivo.

scholarly journals Mechanism and control of hyperosmotic NaCl-rich secretion by the rectal gland of Squalus acanthias

1983 ◽  
Vol 106 (1) ◽  
pp. 25-41 ◽  
Author(s):  
F. H. Epstein ◽  
J. S. Stoff ◽  
P. Silva
Keyword(s):  
Cyclic Amp ◽  
Chloride Secretion ◽  
Squalus Acanthias ◽  
Rectal Gland ◽  
Energetic Efficiency ◽  
Secondary Active Transport ◽  
Transport Pathway ◽  
Rectal Glands ◽  
And Control

Secretion of chloride from blood to lumen is accomplished in the rectal gland of elasmobranchs by a process of secondary active transport involving the co-transport of Cl- with Na+ across the basolateral membranes of rectal gland cells. Energy is provided by ATP via membrane Na-K-ATPase, which establishes an electrochemical gradient favouring Na+ influx into the cell. The involvement of K+ in the co-transport mechanism, so as to provide a ratio of 1 Na+:1 K+:2 Cl- entering the cell, would increase the energetic efficiency of the process, and is consistent with the Cl/O2 ration of 27–30 observed in secreting rectal glands. Secretion is stimulated by cyclic AMP (cAMP) and by vasoactive intestinal peptide (VIP) and adenosine, which activate adenylate cyclase. Activation of the gland in vivo probably occurs via VIP-secreting nerves as well as circulating agents; it is inhibited by somatostatin. Cyclic AMP probably stimulates chloride secretion by at least three mechanisms: (1) increasing chloride conductance across the luminal cell membrane, (2) enhancing the co-transport pathway for transmembrane movements of Na+, K+ and Cl- and (3) activating Na-K-ATPase.

A novel plant-derived inhibitor of cAMP-mediated fluid and chloride secretion

1999 ◽  
Vol 276 (1) ◽  
pp. G58-G63 ◽  
Author(s):  
S. E. Gabriel ◽  
S. E. Davenport ◽  
R. J. Steagall ◽  
V. Vimal ◽  
T. Carlson ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Ussing Chamber ◽  
Fluid Secretion ◽  
Chloride Secretion ◽  
Inhibitory Effect ◽  
Adult Mice ◽  
Dependent Inhibition ◽  
Chamber Studies

We have identified an agent (SP-303) that shows efficacy against in vivo cholera toxin-induced fluid secretion and in vitro cAMP-mediated Cl−secretion. Administration of cholera toxin to adult mice results in an increase in fluid accumulation (FA) in the small intestine (FA ratio = 0.63 vs. 1.86 in control vs. cholera toxin-treated animals, respectively). This elevation in FA induced by cholera toxin was significantly reduced (FA ratio = 0.70) in animals treated with a 100 mg/kg dose of SP-303 at the same time as the cholera treatment. Moreover, when SP-303 was administered 3 h after cholera toxin, a dose-dependent inhibition of FA levels was observed with a half-maximal inhibitory dose of 10 mg/kg. In Ussing chamber studies of Caco-2 or T84 monolayer preparations, SP-303 had a significant effect on both basal current and forskolin-stimulated Cl−current. SP-303 also induced an increase in resistance that paralleled the observed decrease in current. These data suggest that SP-303 has an inhibitory effect on cAMP-mediated Cl−and fluid secretion. Thus SP-303 may prove to be a useful broad-spectrum antidiarrheal agent.

Diquat-Induced Intestinal Secretion in the Anaesthetized Rat

1992 ◽  
Vol 11 (6) ◽  
pp. 524-529 ◽  
Author(s):  
John M. Rawlings ◽  
John R. Foster ◽  
Jon R. Heylings
Keyword(s):  
Structural Damage ◽  
Fluid Transport ◽  
Mammalian Species ◽  
Intestinal Secretion ◽  
Fluid Secretion ◽  
Transport Processes ◽  
Secretory Response ◽  
Anaesthetized Rats ◽  
Anaesthetized Rat

1 Diquat (1,1'-ethylene-2,2'-bipyridilium) is a non-selective desiccant herbicide which, when administered orally to mammalian species, causes significant secretion of fluid into the lumen of the gastrointestinal tract. In order to characterize this secretory response in more detail the effect of sublethal doses of diquat dibromide (DQBr2) on intestinal secretion was investigated in vivo in the jejunum of anaesthetized rats. 2 Ligated segments of jejunum (10 cm) which were prepared in groups of up to five animals were filled with 500 μl of isosmotic DQBr2 solutions with concentrations ranging from 1-100 mM and maintained in the anaesthetized rat for 1, 2 or 3 h; in control experiments a solution of 100 mM NaBr was used. 3 It was found that while all of the fluid instilled into the segments was absorbed in the control experiments, there was both a dose- and time-dependent secretory response to DQBr2. Maximal fluid secretion occurred after treatment with 50 mM DQBr2 for 3 h. 4 Histological assessment of the jejunum revealed an increase in cell exfoliation and evidence of luminal distension after incubation with DQBr2. However, no structural damage to the mucosa could be seen to account for the fluid secretion. 5 The model described provides a quantitative means of evaluating intestinal secretion and may be used for elucidating the mechanism by which diquat alters fluid transport processes.

scholarly journals Dissociation of local nitric oxide concentration and vasoconstriction in the presence of cell-free hemoglobin oxygen carriers

Blood ◽  
2006 ◽  
Vol 108 (10) ◽  
pp. 3603-3610 ◽  
Author(s):  
Amy G. Tsai ◽  
Pedro Cabrales ◽  
Belur N. Manjula ◽  
Seetharama A. Acharya ◽  
Robert M. Winslow ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Blood Volume ◽  
Volume Expansion ◽  
Molecular Volume ◽  
Oxygen Carriers ◽  
Systemic Hemodynamic ◽  
Study Objective ◽  
Blood Volume Expansion

Abstract Cell-free hemoglobin's (CFH) high affinity for nitric oxide (NO) could limit CFH's use as an oxygen-carrying blood replacement fluid because it scavenges NO, causing vasoconstriction and hypertension. However, the extent to which perivascular NO levels change following intravascular administration of hemoglobin (Hb) with different molecular dimensions correlates with vasoconstrictive responses in the microcirculation is unknown. The study objective was to determine vasoconstrictive effects following bolus infusions of (1) αα cross-linked Hb; (2) polymerized bovine Hb; or (3) polyethylene glycol-decorated Hb (PEG-Hb), by measurements of in vivo microvessel diameter, blood flow, perivascular NO concentration, and systemic hemodynamic parameters. All CFHs caused reductions in perivascular NO levels, not correlated to microvascular responses. PEG-Hb (largest molecular volume) maintained blood flow, while the others caused vasoconstriction and reduced perfusion. All solutions increased mean arterial pressure due to vasoconstriction and blood volume expansion, except for PEG-Hb, which increased blood pressure due to blood volume expansion and maintenance of cardiac output. In conclusion, perivascular NO reduction is similar for all Hb solutions because NO binding affinities are similar; however, effects on vascular resistance are related to the type of molecular modification, molecular volume, and oxygen affinity.

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