scholarly journals The effects of forced activity on circulating catecholamines and pH and water content of erythrocytes in the toad

1987 ◽  
Vol 128 (1) ◽  
pp. 411-418
Author(s):  
B. L. Tufts ◽  
D. C. Mense ◽  
D. J. Randall
Keyword(s):  
Water Content ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
In Vivo Experiments ◽  
Beta Adrenergic Agonist ◽  
Toad Bufo ◽  
Adrenergic Effects

In vivo experiments were carried out to determine the effect of forced activity on circulating catecholamine levels, haematocrit, and the pH and water content of erythrocytes in the toad, Bufo marinus. In addition, the effect of the beta-adrenergic agonist isoproterenol on erythrocyte pH and water content was examined in vitro. Forced activity caused a significant decrease in both whole blood and erythrocyte pH, while haematocrit and circulating adrenaline and noradrenaline levels increased. Erythrocyte water content did not change following forced activity. Addition of isoproterenol to toad blood in vitro had no effect on either erythrocyte pH or water content. The apparent absence of beta-adrenergic effects on erythrocyte pH and water content in the toad is in sharp contrast to the response of teleost fish erythrocytes to beta-adrenergic stimulation. The significance of these differences is discussed.

Secretion of lingual lipase and amylase from rat lingual serous glands

1987 ◽  
Vol 253 (2) ◽  
pp. G217-G225 ◽  
Author(s):  
R. B. Field ◽  
A. R. Hand
Keyword(s):  
Protein Secretion ◽  
Major Salivary Gland ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Cholinergic Agonist ◽  
Significant Difference ◽  
The Media

The effects of various secretagogues on the release of lingual lipase and amylase from rat lingual serous glands was examined in vitro and in vivo. After incubation, the media and tissues were assayed for lingual lipase and amylase activity to determine percent of secretion. In vitro secretion of lingual lipase and amylase stimulated by the cholinergic agonist, carbamylcholine chloride (carbachol), was 28.3 +/- 1.7, 48.0 +/- 3.2, and 55.9 +/- 2.4% and 18.1 +/- 1.7, 26.4 +/- 3.0, and 28.0 +/- 2.5%, respectively, for 30-, 60-, and 90-min incubations. The beta-adrenergic agonist, isoproterenol, and the adenylate cyclase activator, forskolin, elicited very little secretion in vitro; the 90-min values with isoproterenol were 16.8 +/- 7.1% lingual lipase and 6.0 +/- 2.6% amylase. The alpha-adrenergic agonist, phenylephrine, did not stimulate enzyme secretion. Morphological assessment of incubated tissues revealed that carbachol induced a rapid and extensive degranulation of the acinar cells, while isoproterenol caused only minimal exocytosis. In vivo stimulation by the cholinergic agonist, pilocarpine, caused rapid secretion, with maximal secretion occurring by 1 h. In vivo secretion stimulated by isoproterenol was slow, but by 4 h secretion was comparable to that induced by pilocarpine. In vitro, there was a significant difference between the percentages of lingual lipase and amylase secreted, which could not be accounted for by the presence of proteases or microbial products or the lack of stability of the enzymes during the incubation period. Neurotransmitter regulation of protein secretion by the lingual serous (minor salivary) glands appears to be principally cholinergic in contrast to the beta-adrenergic stimulation of protein secretion by the parotid (major salivary) gland.

scholarly journals In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure

2013 ◽  
Vol 57 ◽  
pp. 47-58 ◽  
Author(s):  
Anuradha Guggilam ◽  
Kirk R. Hutchinson ◽  
T. Aaron West ◽  
Amy P. Kelly ◽  
Maarten L. Galantowicz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Volume Overload ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Cardiac Responses

scholarly journals Energy metabolism in trout red cells: consequences of adrenergic stimulation in vivo and in vitro

1989 ◽  
Vol 143 (1) ◽  
pp. 133-147 ◽  
Author(s):  
R. A. Ferguson ◽  
B. L. Tufts ◽  
R. G. Boutilier
Keyword(s):  
Ph Regulation ◽  
Red Cells ◽  
Red Cell ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Extracellular Acidosis ◽  
Metabolic Functions ◽  
The Face

beta-Adrenergic stimulation of salmonid red cells results in a rapid decrease (within 5 min) in the nucleotide triphosphate:haemoglobin ratio (NTP:Hb), which is thereafter maintained at a constant level, presumably through increased ATP turnover via matched aerobic metabolism and energy-consuming processes. Addition of the beta-adrenergic agonist isoproterenol to rainbow trout red cells in vitro leads to a rise in intracellular pH (pHi), a corresponding decrease in extracellular pH (pHe) and an increase in red cell oxygen consumption (MO2). Moreover, the extent to which red cell pHi is maintained constant in the face of an acute extracellular acidosis in vitro or in vivo is proportional to the adrenergically stimulated increase in red cell MO2. In the absence of oxygen, these red cells remain capable of pH regulation, but cannot maintain NTP:Hb constant. As a result, membrane and metabolic functions become uncoupled in the stimulated deoxygenated cells.

Inhibition of nitric oxide synthase augments myocardial contractile responses to beta-adrenergic stimulation

1996 ◽  
Vol 271 (6) ◽  
pp. H2646-H2652 ◽  
Author(s):  
J. F. Keaney ◽  
J. M. Hare ◽  
J. L. Balligand ◽  
J. Loscalzo ◽  
T. W. Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Myocardial Contractility ◽  
Adrenergic Stimulation ◽  
Maximum Increase ◽  
Beta Adrenergic ◽  
Before And After ◽  
Nos Inhibitor ◽  
Oxide Synthase

Recent in vitro evidence suggests a role for nitric oxide (NO) in the modulation of myocardial contractility. The specific role of NO in the control of cardiac function in vivo, however, remains unclear. We investigated the effect of NO synthase (NOS) inhibition on myocardial contractility in response to beta-adrenergic stimulation in autonomically blocked dogs. Intracoronary infusions of dobutamine (1-50 micrograms/min) and isoproterenol (0.1 and 0.5 microgram/min) were performed before and after the intracoronary administration of the specific NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Intracoronary dobutamine resulted in a dose-dependent increase in peak first derivative of pressure (dP/dtmax) to a maximum of 195 +/- 10% (P < 0.001). After inhibition of NOS with intracoronary L-NAME at rates of 0.1 and 1 mg/min, the response to dobutamine was significantly enhanced with dP/dtmax, increasing 276 +/- 17 and 317 +/- 26%, respectively (P < 0.001). Intracoronary isoproterenol resulted in a maximum increase in dP/dtmax of 116 +/- 15% (P < 0.001) that further increased to 154 +/- 17 and 157 +/- 18% after NOS inhibition with 0.1 and 1 mg/min L-NAME, respectively (both P < 0.002). L-NAME had no effect on baseline dP/dtmax but did produce a reduction in myocardial guanosine 3',5'-cyclic monophosphate content. These results suggest a role for NO in the control of myocardial contractility in response to beta-adrenergic stimulation in vivo.

scholarly journals Early activation of the cardiac CX3CL1/CX3CR1 axis delays β-adrenergic-induced heart failure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
M. Flamant ◽  
N. Mougenot ◽  
E. Balse ◽  
L. Le Fèvre ◽  
F. Atassi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protective Role ◽  
Cardiomyocyte Hypertrophy ◽  
Adrenergic Stimulation ◽  
Intramyocardial Injection ◽  
In Vivo Experiments ◽  
Concentric Hypertrophy

AbstractWe recently highlighted a novel potential protective paracrine role of cardiac myeloid CD11b/c cells improving resistance of adult hypertrophied cardiomyocytes to oxidative stress and potentially delaying evolution towards heart failure (HF) in response to early β-adrenergic stimulation. Here we characterized macrophages (Mφ) in hearts early infused with isoproterenol as compared to control and failing hearts and evaluated the role of upregulated CX3CL1 in cardiac remodeling. Flow cytometry, immunohistology and Mφ-depletion experiments evidenced a transient increase in Mφ number in isoproterenol-infused hearts, proportional to early concentric hypertrophy (ECH) remodeling and limiting HF. Combining transcriptomic and secretomic approaches we characterized Mφ-enriched CD45+ cells from ECH hearts as CX3CL1- and TNFα-secreting cells. In-vivo experiments, using intramyocardial injection in ECH hearts of either Cx3cl1 or Cx3cr1 siRNA, or Cx3cr1−/− knockout mice, identified the CX3CL1/CX3CR1 axis as a protective pathway delaying transition to HF. In-vitro results showed that CX3CL1 not only enhanced ECH Mφ proliferation and expansion but also supported adult cardiomyocyte hypertrophy via a synergistic action with TNFα. Our data underscore the in-vivo transient protective role of the CX3CL1/CX3CR1 axis in ECH remodeling and suggest the participation of CX3CL1-secreting Mφ and their crosstalk with CX3CR1-expressing cardiomyocytes to delay HF.

Filter paper equilibration as a novel technique for in vitro studies of the composition of airway surface fluid

1992 ◽  
Vol 263 (2) ◽  
pp. L243-L248 ◽  
Author(s):  
L. Joris ◽  
P. M. Quinton
Keyword(s):  
Filter Paper ◽  
Ringer Solution ◽  
Adrenergic Stimulation ◽  
Tracheal Mucosa ◽  
Beta Adrenergic ◽  
Minor Elements ◽  
Tracheal Tissue ◽  
Water Saturated ◽  
Beta Adrenergic Agonist

We describe techniques which we developed to study the composition and regulation of airway surface fluid (ASF). ASF from isolated equine tracheal mucosa was absorbed onto or equilibrated with small strips of ashless filter paper after timed incubations in a water-saturated, 37 degrees C environment. After expression of the fluid from the paper, constant-volume aliquots of the samples were pipetted with a microvolumetric pipette on a filmed grid, together with standards containing known concentrations for Na, Cl, K, Ca, S, and P. Analysis of the microdroplets by dispersive X-ray microanalysis on a scanning electron microscope demonstrated that ASF from "unstimulated" tracheal tissue is significantly altered compared with the Ringer solution which was used to rinse the mucosal surface before incubation, in that Na is significantly decreased (approximately 130 mM), whereas K is significantly increased (approximately 16 mM). Furthermore, when a beta-adrenergic agonist (isoproterenol 10(-4) M) was added to the serosal surface, the Na concentration significantly increased to values which approached Ringer solution (146 +/- 5.3 mM) and were significantly different compared with the Na values obtained in unstimulated tissues. In contrast, Na remained unchanged after addition of a cholinergic agonist (metacholine, 10(-4) M) to the serosal side of the tissue; however, as with beta-adrenergic stimulation, most other minor elements and especially K significantly decreased compared with their values in unstimulated tissue. These results clearly suggest that ASF composition is clearly controlled by active transport of the airway epithelium and may be influenced by neurohumoral stimulation.

scholarly journals In Vivo and In Vitro Effects of Adrenergic Stimulation on Chloride/Bicarbonate Exchange in Rainbow Trout Erythrocytes

1988 ◽  
Vol 140 (1) ◽  
pp. 301-312
Author(s):  
B. L. TUFTS ◽  
R. A. FERGUSON ◽  
R. G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
Erythrocyte Membrane ◽  
Ph Gradient ◽  
Exhaustive Exercise ◽  
Adrenergic Stimulation ◽  
In Vivo Experiments ◽  
In Vitro Effects

In vitro and in vivo experiments were carried out to determine the effect of catecholamines on erythrocytic chloride/bicarbonate exchange in the rainbow trout. A further modified boat assay is described and was used to measure bicarbonate flux through intact erythrocytes. Catecholamines had no significant effect on the bicarbonate flux in vitro. The erythrocytes were sensitive to adrenergic stimulation, however, since the agonists used caused a decrease in the pH gradient across the erythrocyte membrane. Exhaustive exercise was associated with an increase in bicarbonate flux through the intact erythrocytes. The mechanism for this increase is not clear, but it is evidently not adrenergic in origin.

Effect of exercise on lipolytic sensitivity in endurance-trained athletes

1995 ◽  
Vol 78 (6) ◽  
pp. 2201-2206 ◽  
Author(s):  
S. Klein ◽  
E. F. Coyle ◽  
R. R. Wolfe
Keyword(s):  
High Intensity ◽  
Lipolytic Activity ◽  
Whole Body ◽  
Adrenergic Stimulation ◽  
Epinephrine Infusion ◽  
Beta Adrenergic ◽  
Ergometer Exercise ◽  
Plasma Ffa

Studies performed in vitro suggest that an acute bout of exercise increases the lipolytic response to beta-adrenergic stimulation. We evaluated the effect of exercise on lipolytic sensitivity in vivo in five endurance-trained athletes. The rate of appearance (Ra) of glycerol in plasma, an index of whole body lipolysis, was determined during 60 min of epinephrine infusion (0.015 microgram.kg-1.min-1) on two occasions: 1) at basal resting conditions and 2) 90 min after completing 1 h of high-intensity (70% O2 uptake) cycle ergometer exercise. Total glycerol Ra during epinephrine infusion in the basal state (352 +/- 35 mumol.kg-1. 60 min-1) was not significantly different from the value obtained after high-intensity exercise (439 +/- 58 mumol.kg-1. 60 min-1). However, the increase in glycerol Ra above baseline during epinephrine infusion was lower after (30 +/- 16 mumol.kg-1. 60 min-1) than before (148 +/- 28 mumol.kg-1. 60 min-1) exercise because of the high postexercise baseline value (P < 0.05). Mean plasma free fatty acid (FFA) concentration was lower during exercise than during epinephrine infusion despite a greater rate of lipolysis during exercise. The slope of change in plasma FFA with respect to glycerol RA was lower during exercise (0.0171 +/- 0.006) than during epinephrine infusion (0.0835 +/- 0.018) (P < 0.05). We conclude that a single bout of intense exercise does not increase in vivo lipolytic sensitivity to beta-adrenergic stimulation in endurance-trained athletes. In addition, plasma FFA concentration represents the balance between plasma FFA inflow and tissue uptake and cannot be used as an index of lipolytic activity during certain physiological conditions, such as exercise.

Changes in beta-adrenergic responsiveness of rats during chronic cold exposure

1980 ◽  
Vol 49 (6) ◽  
pp. 923-929 ◽  
Author(s):  
C. C. Barney ◽  
M. J. Katovich ◽  
M. J. Fregly ◽  
P. E. Tyler
Keyword(s):  
Heart Rate ◽  
Cold Exposure ◽  
Chronic Exposure ◽  
Cardiovascular Responses ◽  
Time Dependent ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Heart Rates ◽  
Beta Adrenergic Agonist

Administration of isoproterenol (50 micrograms/kg sc) to rats that had been exposed to cold (6 degrees C) for 10, 15, and 25 days was accompanied by a greater increase in tail skin and colonic temperatures than in controls kept at 25 degrees C. Administration of isoproterenol (8 micrograms/kg sc) to cold-treated rats (1, 3, 5, 7, 14, and 28 days) increased heart rates above that of controls. However, resting unstimulated heart rates of cold-treated rats were also increased above that of controls after 1, 3, 5, and 7 days of cold exposure but were not different from controls after 14 and 28 days. Cold exposure also led to time-dependent increases in the weights of heart, adrenals, and interscapular brown fat. Thus, chronic exposure of rats to cold is accompanied by an increase in responsiveness of both heart rate and tail skin and colonic temperatures to beta-adrenergic stimulation. The results also suggest that increases in responsiveness to a beta-adrenergic agonist may not occur at the same time for the different beta-adrenergic-mediated metabolic and cardiovascular responses in cold-treated rats.

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