Changes in endothelial actin cytoskeleton in venules with time after histamine treatment

1995 ◽  
Vol 269 (5) ◽  
pp. H1528-H1537 ◽  
Author(s):  
A. L. Baldwin ◽  
G. Thurston
Keyword(s):  
Endothelial Cells ◽  
Confocal Microscopy ◽  
Time Course ◽  
Relative Size ◽  
Fluorescein Isothiocyanate ◽  
Adherent Cells ◽  
Sprague Dawley ◽  
Filamentous Actin ◽  
Rhodamine Phalloidin ◽  
Sprague Dawley Rats

In this study the time course of development and recovery of histamine-induced venular leaks was followed in conjunction with rearrangement of endothelial actin fibers. The microvasculature of a single mesenteric window of anesthetized Sprague-Dawley rats was perfused with buffered saline, with or without 10(-4) M histamine, for 3-30 min. Fluorescein isothiocyanate (FITC)-albumin was added for the last 3 min. The microvasculature was perfusion fixed, stained with rhodamine phalloidin (for filamentous actin), and viewed using confocal microscopy. The number and relative size of FITC-albumin leaks per venule length were measured. After 3 min of histamine application focal leaks appeared in some of the venules. Most focal leaks were accompanied by local breaks in the endothelial peripheral actin rim. Larger leaks were also present, accompanied by greater disruption of the venular endothelial peripheral actin rim, diffuse F-actin staining, and adherent platelets and leukocytes. Few central actin fibers were visible even in endothelial cells associated with large leaks. After 10-15 min of histamine exposure, larger leaks were more abundant but with fewer adherent cells. Central actin fibers in endothelial cells increased in number, peaking after 20 min of histamine, while the diffuse actin staining declined. Leak area per micrometer of venule peaked at 10-15 min, but the numbers of leaks per micrometer did not vary significantly from 3 to 30 min. These data suggest that the central fibers are not involved with the phase of increasing permeability, but they may play a role in the structural and functional recovery of endothelial cells perturbed by histamine.

Distribution and metabolism of corticotropin-releasing factor in the rat

1986 ◽  
Vol 64 (6) ◽  
pp. 683-688 ◽  
Author(s):  
Bernard Candas ◽  
Josée Lalonde ◽  
Maurice Normand
Keyword(s):  
Time Course ◽  
Corticotropin Releasing Factor ◽  
Metabolic Clearance ◽  
Sprague Dawley ◽  
Rapid Injection ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
The Mean ◽  
The Moment ◽  
The One

To develop a mathematical model of the distribution and metabolism of rat corticotropin-releasing factor (rCRF), the time course of 125I-labelled rCRF in plasma was measured in male Sprague–Dawley rats (i) following a rapid injection of 24 ng rCRF/100 g body weight (BW), or (ii) following a rapid injection of 424 ng rCRF/100 g BW, or (iii) during an infusion at a rate ranging from 0.28 to0.73 ng rCRF∙min−1∙100 g BW−1. The comparison of the one-, two-, and three-compartment models shows that the two-pool structure fits better to the dynamics of CRF in plasma as measured in each rat. Following a rapid injection the decay curve occurs in a biphasic manner; the early phase of disappearance is 25 times faster than the late one. There is no significant difference between the estimates of the metabolic clearance rate following both amplitudes of injection (0.40 ± 0.06 and 0.48 ± 0.05 mL∙min−1∙100 g BW−1). The volume of the first pool, 16.8 ± 1.1 mL/100 g BW, is four times larger than the plasma volume. It would thus appear that CRF is rapidly distributed from plasma into several tissues which are represented in the first pool of the model. The mean residence time of every CRF molecule in the second compartment, from the moment of secretion to its elimination, is from three to four times longer than in the first one. It stays, on average, between 140 min and 3 h in the system before an irreversible exit. At steady state, the disposal rate represents only 3% of the CRF mass of the first compartment every minute. These results could explain the prolonged effects of CRF on pituitary-adrenocortical secretion.

Abstract 637: Hydrogen Sulfide Acts on Endothelial Cells to Elicit Dilation.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Nancy L Kanagy ◽  
Jessica M Osmond ◽  
Olan Jackson-Weaver ◽  
Benjimen R Walker
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Hydrogen Sulfide ◽  
Mesenteric Arteries ◽  
Direct Effects ◽  
Sprague Dawley ◽  
Imaging Studies ◽  
Knock Out ◽  
Event Frequency ◽  
Sprague Dawley Rats

Hydrogen sulfide (H 2 S), produced by the enzyme cystathionine-γ lyase (CSE), dilates arteries by hyperpolarizing and relaxing vascular smooth muscle cells (VSMC) and CSE knock-out causes hypertension and endothelial dysfunction showing the importance of this system. However, it is not clear if H 2 S-induced VSMC depolarization and relaxation is mediated by direct effects on VSMC or indirectly through actions on endothelial cells (EC). We reported previously that disrupting EC prevents H 2 S-induced vasodilation suggesting H 2 S might act directly on EC. Because inhibiting large-conductance Ca 2+ -activated K + (BK Ca ) channels also inhibits H 2 S-induced dilation, we hypothesized that H 2 S activates EC BK Ca channels to hyperpolarize EC and increase EC Ca 2+ which stimulates release of a secondary hyperpolarizing factor. Small mesenteric arteries from male Sprague-Dawley rats were used for all experiments. We found that EC disruption prevented H 2 S-induced VSMC membrane potential ( E m ) hyperpolarization. Blocking EC BK Ca channels with luminal application of the BK Ca inhibitor, iberiotoxin (IbTx, 100 nM), also prevented NaHS-induced dilation and VSMC hyperpolarization but did not affect resting VSMC E m showing EC specific actions. Sharp electrode recordings in arteries cut open to expose EC demonstrated H 2 S-induced hyperpolarization of EC while Ca 2+ imaging studies in fluor-4 loaded EC showed that H 2 S increases EC Ca 2+ event frequency. Thus H 2 S can act directly on EC. Inhibiting the EC enzyme cytochrome P 450 2C (Cyp2C) with sulfaphenazole also prevented VSMC depolarization and vasodilation. Finally, inhibiting TRPV4 channels to block the target of the Cyp2C product 11,12-EET inhibited NaHS-induced dilation. Combined with our previous report that CSE inhibition decreases BK Ca currents in EC, these results suggest that H 2 S stimulates EC BK Ca channels and activates Cyp2C upstream of VSMC hyperpolarization and vasodilation.

Time course of peripheral heterothermy in a homeotherm

1980 ◽  
Vol 239 (1) ◽  
pp. R126-R129 ◽  
Author(s):  
R. T. Brown ◽  
J. G. Baust
Keyword(s):  
Room Temperature ◽  
Time Course ◽  
Temperature Fluctuations ◽  
Temperature Gradients ◽  
Tissue Temperature ◽  
Central Component ◽  
Sprague Dawley ◽  
Contralateral Limb ◽  
Sprague Dawley Rats ◽  
Peripheral Temperature

The integrity of the peripheral heterothermic response was monitored in adult Sprague-Dawley rats during cold acclimation. Subcutaneous peripheral temperature gradients were simultaneously recorded in the hindlimbs. One limb was exposed to room temperature (22 +/- 2 degrees C) while the contralateral limb was gradually cooled to 0 +/- 1 degrees C. Noncontrols were acclimated at 5 +/- 1 degrees C for periods up to 35 days. Controls responded to the cooling regimen (25 to 0 degrees C at 0.5 degrees C . min-1) in a "poikilothermic" manner indicating local cold-induced vasoconstriction (CIVC). CIVC was not released until tissue temperatures reached 22,3 +/- 2.5 degrees C whereupon nonpatterned limb temperature fluctuations, Lewis' hunting response, were often initiated. The hunting response occurred synchronously in the contralateral warmed limb despite its elevated temperature. The experiments revealed a progressive decrease in the intensity of heterothermy indicative of an earlier onset of cold-induced vasodilation as well as increased resistance to tissue cooling with increasing acclimation time. Following 21 days at 5 degrees C, limb exposure to 0 degrees C resulted in a 2-4 degrees C drop in tissue temperature. The time course of the diminution in peripheral heterothermy is discussed. In addition, evidence supporting the hypothesis of a central component in the regulation of the hunting response is presented.

Time course of airway hyperresponsiveness and remodeling induced by hyperoxia in rats

1995 ◽  
Vol 269 (2) ◽  
pp. L227-L233 ◽  
Author(s):  
J. L. Szarek ◽  
H. L. Ramsay ◽  
A. Andringa ◽  
M. L. Miller
Keyword(s):  
Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Time Course ◽  
Electrical Field Stimulation ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Electrical Field ◽  
Muscle Area ◽  
Sprague Dawley Rats ◽  
The Relationship

The purpose of this study was to answer two questions concerning hyperoxia-induced airway hyperresponsiveness: 1) What is the time course of the development of airway hyperresponsiveness? 2) What is the relationship between the increase in responsiveness and smooth muscle area? Segments of intrapulmonary bronchi were isolated from male Sprague-Dawley rats that had been exposed to 80-85% O2 for a period of 1, 3, 5, or 7 days and from aged-matched control animals that breathed room air. Hyperoxia increased the sensitivity (log concentration or frequency that elicited a half-maximal response) and reactivity (maximum tension developed) of the airways to electrical field stimulation (EFS) after 3, 5, and 7 days; sensitivity to acetylcholine was not affected, but reactivity was increased after 7 days. Hyperoxia increased smooth muscle area beginning 5 days after commencing the exposure. After normalizing tension responses to smooth muscle area, reactivity of the airways to the stimuli was not different between the two groups, but sensitivity to EFS was still increased. The increase in reactivity observed after 5 and 7 days of exposure can be explained by an increase in smooth muscle area that occurred at these time points. The fact that the sensitivity of the airways to EFS remained increased after normalization, together with the fact that the increase in airway responsiveness after 3 days of exposure occurred at a time when smooth muscle area was not different from control, suggests that mechanisms other than increased smooth muscle area contribute to the development of hyperoxia-induced airway hyperresponsiveness.

Distribution and metabolism of adrenocorticotropin in the rat

1979 ◽  
Vol 57 (9) ◽  
pp. 1024-1027 ◽  
Author(s):  
Maurice Normand ◽  
Josee Lalonde
Keyword(s):  
Standard Error ◽  
Time Course ◽  
Compartment Model ◽  
Sprague Dawley ◽  
Mean Values ◽  
Sprague Dawley Rats ◽  
Two Compartment Model ◽  
Rapid Fall ◽  
Significant Difference ◽  
Endogenous Release

The time course of plasma bioactive adrenocorticotropin (ACTH) concentrations measured following two rapid injections of the hormone at doses of 7.5 and 22.5 mU/100 g, iv, and one infusion over a period of 80 min at a rate of 1.3 mU/min per 100 g, to male Sprague–Dawley rats whose endogenous release of ACTH had been blocked, leads to the conclusion that the hormone is distributed in two compartments. Indeed, the rapid fall of plasma ACTH concentrations in the early minutes following either the injections or the stop of the infusion is followed by a much slower phase. There is no significant difference between the measurements and the two-compartment model outputs. The model represents, on the average, the mean values of the measurements plus or minus 1 standard error for the single injections and plus or minus 1.2 standard error for the infusion.

Nitric oxide and penile erection in streptozotocin-diabetic rats

1999 ◽  
Vol 96 (4) ◽  
pp. 365-371 ◽  
Author(s):  
Gil ARI ◽  
Yoram VARDI ◽  
John P. M. FINBERG
Keyword(s):  
Methyl Ester ◽  
Time Course ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
No Synthase ◽  
Sprague Dawley ◽  
Nerve Roots ◽  
Sprague Dawley Rats ◽  
Pithed Rats ◽  
Stimulation Of

The purpose of this investigation was to study the time course, response to insulin and characteristics of erectile dysfunction in streptozotocin (STZ)-diabetic Sprague–Dawley rats, and the function of the NO-generating system in these animals. Copulation-induced and reflex erection were quantified in conscious Sprague–Dawley rats at different times after injection of STZ. The corporal vasodilatation response to nerve stimulation was studied by measuring the rise in corporal pressure in pithed rats following electrical stimulation of sacral spinal nerve roots. The activity of NO synthase was determined in corporal tissue by measuring the generation of [3H]citrulline from [3H]arginine. Copulation-induced erection was inhibited at 1 and 2 months after STZ treatment, but this could be prevented by a short (2-week) pretreatment with insulin. Reflex erection was inhibited at 1, 4, 6 and 9 months after STZ; at 6 months, this inhibition was also reversible by insulin pretreatment. Following pithing, the basal corporal pressure was elevated in diabetic rats. At 4 months after STZ, this increase was normalized by a 2-week, but not by a 1-week, pretreatment with insulin; however, at 9 months after STZ, insulin pretreatment did not normalize corporal pressure. The increase in corporal pressure caused by stimulation of sacral nerve roots in pithed rats was enhanced in diabetic animals. This enhancement was also normalized at 4 months, but not at 9 months, by 2 weeks of insulin treatment. The inhibition of the stimulation-induced increase in corporal pressure by NG-nitro-L-arginine methyl ester (5 mg/kg) was less following 9 months of diabetes, although NO synthase activity was normal in cavernosal tissue following 6–8 months of diabetes. In conclusion, STZ-induced diabetes caused changes in the erectile system that were initially reversible by a short insulin treatment, but which with time (more than 6 months) became irreversible. NO synthase activity in cavernosal tissue was normal, but the response to NG-nitro-L-arginine methyl ester was inhibited in long-term diabetes (9 months).

Renal memory after potassium adaptation: role of Na+-K+-ATPase

1988 ◽  
Vol 254 (6) ◽  
pp. F845-F850 ◽  
Author(s):  
S. K. Mujais
Keyword(s):  
Atpase Activity ◽  
Time Course ◽  
Base Line ◽  
Sprague Dawley ◽  
Membrane Transport Proteins ◽  
Sprague Dawley Rats ◽  
Potassium Adaptation ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

The present study was designed to explore the time course of the resolution of enhanced Na+-K+-ATPase activity in the cortical collecting tubule (CCT) and the parallel changes in renal K excretion that are characteristic of potassium adaptation. Potassium-adapted male Sprague-Dawley rats manifested an enhanced kaliuretic response to an acute intravenous load of KCl and a doubling of Na+-K+-ATPase activity in the CCT. Withdrawal of dietary K loading from these adapted rats was associated with a gradual resolution of these adaptive biochemical (t1/2 of Na+-K+-ATPase return to base line 48 h) and excretory changes. During this resolution phase, however, a temporal discrepancy was uncovered between the change in dietary K and the slower changes in enzyme activity and renal K excretion with a persistence of the enhanced kaliuresis leading to a negative K balance. We conclude that the slow inactivation, after withdrawal of K loading, of the increased membrane transport proteins of K adaptation, will manifest as a renal memory of the antecedent excretory requirements.

Regression of white adipose tissue in diabetic rats

1989 ◽  
Vol 257 (4) ◽  
pp. E547-E553 ◽  
Author(s):  
A. Geloen ◽  
P. E. Roy ◽  
L. J. Bukowiecki
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Protein Content ◽  
Cell Number ◽  
Diabetic Rats ◽  
Total Protein Content ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Wet Weight

The effects of long-term diabetes (4 wk) on the development of parametrial (PWAT) and retroperitoneal (RWAT) white adipose tissues were studied in young Sprague-Dawley rats (170-200 g) injected with a single dose of streptozotocin (75 mg/kg). Diabetes stopped animal growth and totally abolished the normal increases in the wet weight, total protein content, and cellularity (estimated by DNA content) of PWAT and RWAT. Remarkably, the prolonged lack of insulin induced a progressive decrease of the cellularity of RWAT to levels that were lower than those of the initial controls. It also resulted in a marked reduction of adipocyte size. The tiny adipocytes seen in diabetic animals were characterized by the presence of multilocular triglyceride droplets. In general, the decreases in cell number, cell size, and protein content were more pronounced in RWAT than in PWAT. Quantitative cellular frequency studies revealed that adipocytes, and possibly also endothelial cells, contribute to the decrease in RWAT cellularity. The results demonstrate that 1) diabetes inhibits proliferative activity in adipose tissue, 2) total cell number reduction may occur in adipose depot of young growing rats, 3) this effect is depot dependent, and 4) the turnover of adipocytes and endothelial cells is relatively slow (several weeks).

scholarly journals Metabolic and Kinetic Considerations in the Use of [125I]HIPDM for Quantitative Measurement of Regional Cerebral Blood Flow

1985 ◽  
Vol 5 (1) ◽  
pp. 86-96 ◽  
Author(s):  
G. Lucignani ◽  
A. Nehlig ◽  
R. Blasberg ◽  
S. Patlak ◽  
L. Anderson ◽  
...  
Keyword(s):  
Time Course ◽  
Quantitative Measurement ◽  
Single Photon ◽  
Photon Emission ◽  
Sprague Dawley ◽  
Diffusion Limitations ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Metabolic Products ◽  
Metabolic Degradation

The metabolic degradation and the kinetics of the cerebral uptake of N, N, N'-trimethyl- N'-(2-hydroxy-3-methyl- 5-[125I]iodobenzyl)-1, 3-propanediamine ([125I]HIPDM) have been studied in conscious, adult male Sprague-Dawley rats to determine its suitability as a tracer for the quantitative measurement of regional CBF (rCBF). rCBF was calculated by the indicator fractionation and the tissue equilibration methods in experiments of different durations up to 1 h. The values of rCBF obtained with [125I]HIPDM were compared with those obtained in concurrent measurements with [14C]iodoantipyrine in the same animals. Results of the experiments demonstrate that [125I]HIPDM is an inadequate tracer for use with the indicator fractionation method and that any method that employs [125I]HIPDM for the determination of rCBF must take into account its metabolic degradation, diffusion limitations, and bidirectional flux across the blood-brain barrier. With the tissue equilibration method, consistent determinations of rCBF may be possible with [125I]HIPDM by measurement of the time course of its concentration in arterial blood, corrected for the presence of 125I-labeled metabolic products, and its concentration in the brain at any time up to 1 h after its administration. The method may be adapted to measure rCBF in humans by means of single-photon emission tomography with [123I]HIPDM.

scholarly journals 5-Hydroxytryptamine (5HT) Receptors in the Heart Valves of Cynomolgus Monkeys and Sprague-Dawley Rats

2005 ◽  
Vol 53 (5) ◽  
pp. 671-677 ◽  
Author(s):  
Chandikumar S. Elangbam ◽  
Ruth M. Lightfoot ◽  
Lawrence W. Yoon ◽  
Donald R. Creech ◽  
Robert S. Geske ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Heart Valves ◽  
Cell Types ◽  
Positive Staining ◽  
Normal Heart ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Positive Immunostaining ◽  
5Ht2c Receptor ◽  
Polymerase Chain

5-Hydroxytryptamine-2B receptor (5HT2BR) stimulation is known to cause fibroblast mitogenesis, and the mitogenic effect has been proposed to trigger valvular heart disease in humans. In this study, we used real-time polymerase chain reaction (TaqMan) to quantify transcript levels of 5HT2B, 5HT2C, and 5HT1B receptors and immunohistochemistry (IHC) to detect the tissue localization of these receptors in the normal heart valves of cynomolgus (CM) monkeys and Sprague-Dawley (S-D) rats. In both species, positive immunostaining was noted for 5HT1B and 5HT2B receptors in mitral, tricuspid, aortic, and pulmonary valves, and the cell types showing positive staining were interstitial cells and endothelial cells lining the valve leaflet. In CM monkeys, 5HT2CR was expressed only in the endothelial cells lining the leaflet, whereas S-D valves were negative for this receptor. IHC results were correlated with 5HT2B and 5HT1B receptor transcripts for all four valves. However, 5HT2C receptor transcripts were lower than 5HT2B or 5HT1B in all CM monkey valves, whereas 5HT2C transcripts were below the level of detection in any of the S-D rat valves. Our data showed the expression of 5HT2B, 5HT1B, and 5HT2C receptors in the normal heart valves of CM monkeys and S-D rats, and IHC and TaqMan techniques may be used to study the potential mechanism of compounds with 5HT2BR agonist activity.

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