Failure of chronic beta-adrenergic blockade to inhibit overfeeding-induced thermogenesis in humans

1989 ◽  
Vol 256 (3) ◽  
pp. R653-R658 ◽  
Author(s):  
S. L. Welle ◽  
K. S. Nair ◽  
R. G. Campbell
Keyword(s):  
Weight Maintenance ◽  
Resting Metabolic Rate ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Initial Reduction ◽  
Adrenergic Antagonist ◽  
Adrenergic Activity ◽  
Propranolol Treatment ◽  
Male Subjects

The effect of the beta-adrenergic antagonist propranolol on the increase in resting metabolic rate (RMR) induced by overfeeding was examined to determine whether increased beta-adrenergic activity contributes to this response. Six male subjects who were overfed with carbohydrate (1,600 excess kcal/day) for 10 days without drug treatment (control group) had increases (compared with values after 10 days of weight maintenance) in RMR after 6 days [0.24 +/- 0.06 kcal/min (22%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. Eight male subjects were given a weight-maintenance diet for 10 days with oral propranolol treatment (40-60 mg every 6 h) over the last 7 days of this period. Five of these subjects were then overfed for 10 days, and three remained on the weight-maintenance diet; propranolol treatment continued until the end of the study. Propranolol significantly reduced RMR (mean 9%) before the onset of overfeeding but did not prevent increases in RMR after 6 days [0.18 +/- 0.05 kcal/min (16%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. In the subjects who remained on the weight-maintenance diet throughout the study, there was no reversal of propranolol's initial reduction of RMR that would have falsely elevated the overfeeding effect. These data provide further evidence that the increase in RMR induced by overfeeding in humans is not mediated by increased beta-adrenergic activity.

Beta-adrenergic modulation of pulmonary transvascular fluid and protein exchange

1986 ◽  
Vol 60 (1) ◽  
pp. 266-274 ◽  
Author(s):  
F. L. Minnear ◽  
A. Johnson ◽  
A. B. Malik
Keyword(s):  
Control Group ◽  
Protective Effects ◽  
Beta Adrenergic ◽  
Intravascular Coagulation ◽  
Protein Clearance ◽  
Adrenergic Antagonist ◽  
Adrenergic Modulation ◽  
Pulmonary Arterial ◽  
Beta Adrenergic Agonist ◽  
Protein Exchange

We determined in anesthetized sheep whether isoproterenol, a beta-adrenergic agonist, prevents the increases in pulmonary fluid and protein exchange produced by thrombin-induced intravascular coagulation. Seven sheep were infused intravenously with 0.05 micrograms X kg-1 X min-1 isoproterenol before infusion of alpha-thrombin, and six sheep were infused with alpha-thrombin only and served as control subjects. The marked increases in pulmonary lymph flow and lymph protein clearance in the control thrombin group were attenuated (P less than 0.05) in the isoproterenol group in association with a higher pulmonary blood flow (P less than 0.05) and a lower pulmonary vascular resistance (P less than 0.05) in the isoproterenol group and with similar increases in pulmonary arterial and pulmonary arterial wedge pressures in both groups. The decreases in fluid and protein fluxes produced by isoproterenol are related to its beta-adrenergic properties because propranolol, a beta-adrenergic antagonist, blocked the protective effects of isoproterenol in a second group of sheep infused with propranolol, isoproterenol, and thrombin. Raising left atrial pressure to test for changes in vascular permeability increased protein flux to a much greater extent in the thrombin control group than in the isoproterenol group challenged with thrombin. The data suggest that isoproterenol attenuated the increase in fluid and protein fluxes produced by thrombin-induced intravascular coagulation by a permeability-decreasing mechanism.

Exercise gas exchange in asthmatics after beta-adrenergic blockade

1983 ◽  
Vol 55 (2) ◽  
pp. 529-533 ◽  
Author(s):  
D. Y. Sue ◽  
L. R. Van Meter ◽  
J. E. Hansen ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Cardiovascular Response ◽  
Minute Ventilation ◽  
Work Rate ◽  
Incremental Exercise ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Maximal Heart Rate ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist

Pharmacologic beta-adrenergic blockade reduces maximal heart rate (HR) during exercise but variable results have been reported for minute ventilation (VE), CO2 output (VCO2), and O2 uptake (VO2). A total group of 19 subjects with mild asthma was studied. We studied 16 subjects from the group who received placebo or pindolol, a beta-adrenergic antagonist, during 1-min incremental exercise on a cycle ergometer. During incremental exercise, HR, VE, VCO2, and VO2 were less after beta-blockade than after placebo at the same work rate below the anaerobic threshold. Maximal HR, VE, VO2, VCO2, and work rate were significantly less after beta-blockade. In addition, we studied six subjects from the group, including three who had also performed incremental exercise, during the steady state of constant-work cycling exercise. We found no difference in VE, VCO2, or VO2 although HR was less after beta-blockade. We conclude that beta-adrenergic blockade affects gas exchange by delaying the normal cardiovascular response to exercise. Decreased VE during incremental exercise is due to slowed delivery of CO2 load to the lungs rather than alterations in substrate, lung function, or ventilatory control.

Effects of physical training on adrenergic sensitivity in obesity

1983 ◽  
Vol 55 (6) ◽  
pp. 1811-1817 ◽  
Author(s):  
M. Krotkiewski ◽  
K. Mandroukas ◽  
L. Morgan ◽  
T. William-Olsson ◽  
G. E. Feurle ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Physical Training ◽  
Plasma Insulin ◽  
Beta Agonist ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
C Peptide ◽  
Adrenergic Antagonist ◽  
Adrenergic Nervous System

To examine the possibility that the decrease of hyperinsulinemia and blood pressure in obesity associated with physical training is mediated via adaptations in the adrenergic nervous system, a pure beta-adrenergic agonist (isoproterenol) or an alpha-adrenergic antagonist (phentolamine) was infused before and during an oral glucose tolerance test before and after physical training. A number of circulatory, metabolic, and endocrine factors under adrenergic control were followed. Physical training was associated with an augmented beta-agonist response in blood pressure, heart rate, blood glucose, plasma insulin, connecting (C) peptide, and pancreatic polypeptide (PP) but not in plasma glucagon and gastric inhibitory polypeptide. Physical training also resulted in higher values of C-peptide and PP values after alpha-adrenergic blockade. It was concluded that physical training probably is associated with an augmented sensitivity of the beta-adrenergic nervous system. This might also be the case with the alpha-adrenergic system. It was suggested that this in turn might be due to a decreased firing in the adrenergic nervous system leading secondarily to an increased sensitivity in the effector cells. It was hypothesized that such decreased firing could provide a background to explain lower blood pressure and plasma insulin after physical training.

Pituitary adenylate cyclase activating polypeptide stimulates release of peptide YY

1993 ◽  
Vol 264 (6) ◽  
pp. E933-E937
Author(s):  
T. Zhang ◽  
G. Gomez ◽  
N. Yanaihara ◽  
T. Mochizuki ◽  
J. C. Thompson ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Intravenous Administration ◽  
Vasoactive Intestinal Polypeptide ◽  
Peptide Yy ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Pituitary Adenylate Cyclase ◽  
Propranolol Treatment ◽  
Ganglionic Transmission

The purpose of these experiments was to examine the effects of the recently discovered gastrointestinal peptide, pituitary adenylate cyclase activating polypeptide (PACAP), and two structurally related peptides, vasoactive intestinal polypeptide and secretin, on release of peptide YY (PYY) in conscious dogs. Intravenous administration of PACAP-27 or -38 stimulated a dose-related release of PYY; PACAP-27 was more potent than PACAP-38. PACAP-stimulated release of PYY was inhibited significantly by atropine, whereas ganglionic or beta-adrenergic blockade with hexamethonium and propranolol treatment, respectively, did not affect PACAP-induced release of PYY significantly (P > 0.05). These results indicate that PACAP-induced release of PYY is cholinergic dependent and that beta-adrenergic tone and ganglionic transmission do not participate in PACAP-induced release of PYY. PACAP may play a role in the neural regulation of PYY release.

scholarly journals Maximal exercise responses to acute and chronic beta-adrenergic blockade in healthy male subjects

1988 ◽  
Vol 20 (6) ◽  
pp. 570???573 ◽  
Author(s):  
SARAH M. JILKA ◽  
MICHAEL J. JOYNER ◽  
JOYCE M. NITTOLO ◽  
JONI K. KALIS ◽  
J. ANDREW TAYLOR ◽  
...  
Keyword(s):  
Maximal Exercise ◽  
Adrenergic Blockade ◽  
Healthy Male ◽  
Beta Adrenergic ◽  
Male Subjects

Effect of the beta-adrenergic blockade on intestinal lactate production and glycogen concentration in dogs infused with hexoses

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Michael O. Allen ◽  
Toyin M. Salman ◽  
Abdul Rasak A. Alada ◽  
Adeyemi F. Odetayo ◽  
Eli B. Patrick ◽  
...  
Keyword(s):  
Lactate Production ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Glycogen Concentration ◽  
Glucose Levels ◽  
Group I ◽  
Significant Difference ◽  
Pretreated Group ◽  
The Difference

Abstract Objectives To investigate effect of beta adrenergic blockade on intestinal lactate production and glycogen concentration in dogs infused with hexoses. Methods Experiments were carried out on 35 fasted male anaesthetized dogs weighing between 9 and 16 kg. The animals were divided into 7 (5 dogs per group) groups. Group I dogs served as control and infused with normal saline, groups II-IV were intravenously infused with glucose (1.1 mg/kg/min), fructose (1.1 mg/kg/min) and galactose (1.1 mg/kg/min) respectively while groups V-VII animals were pretreated with propranolol (0.5 mg/kg) and were infused with glucose, fructose or galactose respectively. A vein draining the proximal segment of the jejunum was cannulated along with right and left femoral arteries and veins. Glucose uptake was calculated as the product of jejunal blood flow and the difference between arterial and venous glucose levels (A-V glucose), part of the jejunum tissue was homogenized for estimation of glycogen concentration, and plasma lactate was assayed using lactate colorimetric kit. Results The result showed significant increase in venous lactate production in response to glucose (78.30 ± 4.57 mg/dl), fructose (60.72 ± 1.82 mg/dl) and galactose (71.70 ± 1.30 mg/dl) when compared with the control group (51.75 ± 1.32 mg/dl) at (p<0.05) with no significant difference in animals pretreated with propranolol. There was no significant difference in glycogen concentration (p>0.05) in animals infused with hexoses only compared with propanolol pretreated group. Conclusions Results suggests that one of the possible fates of the enormous amount of glucose taken up by the intestine is conversion to lactate and not glycogen and β-adrenergic receptor does not affect it.

Propranolol does not impair exercise oxygen uptake in normal men at high altitude

1986 ◽  
Vol 61 (5) ◽  
pp. 1935-1941 ◽  
Author(s):  
L. G. Moore ◽  
A. Cymerman ◽  
S. Y. Huang ◽  
R. E. McCullough ◽  
R. G. McCullough ◽  
...  
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Hemoglobin Concentration ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
O2 Uptake ◽  
Compensatory Mechanisms ◽  
Beta Adrenergic ◽  
Propranolol Treatment ◽  
Normal Men

Decreased maximal O2 uptake (VO2max) and stimulation of the sympathetic nervous system have been previously shown to occur at high altitude. We hypothesized that tachycardia mediated by beta-adrenergic stimulation acted to defend VO2max at high altitude. Propranolol treatment beginning before high-altitude (4,300 m) ascent reduced heart rate during maximal and submaximal exercise in six healthy men treated with propranolol (80 mg three times daily) compared with five healthy subjects receiving placebo (lactose). Compared with sea-level values, the VO2max fell on day 2 at high altitude, but the magnitude of fall was similar in the placebo and propranolol treatment groups (26 +/- 6 vs. 32 +/- 5%, P = NS) and VO2max remained similar at high altitude in both groups once treatment was discontinued. During 30 min of submaximal (80% of VO2max) exercise, propranolol-treated subjects maintained O2 uptake levels that were as large as those in placebo subjects. The maintenance of maximal or submaximal levels of O2 uptake in propranolol-treated subjects at 4,300 m could not be attributed to increased minute ventilation, arterial O2 saturation, or hemoglobin concentration. Rather, it appeared that propranolol-treated subjects maintained O2 uptake by transporting a greater proportion of the O2 uptake with each heartbeat. Thus, contrary to our hypothesis, beta-adrenergic blockade did not impair maximal or submaximal O2 uptake at high altitude due perhaps to compensatory mechanisms acting to maintain stroke volume and cardiac output.

cAMP can raise or lower cardiac actomyosin ATPase activity depending on alpha-adrenergic activity

1994 ◽  
Vol 267 (2) ◽  
pp. H431-H442 ◽  
Author(s):  
G. McClellan ◽  
A. Weisberg ◽  
S. Winegrad
Keyword(s):  
Atpase Activity ◽  
Phosphatase Activity ◽  
Oxygen Tension ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
C Protein ◽  
Actomyosin Atpase ◽  
Enzymatic Function ◽  
Adrenergic Antagonist ◽  
Adrenergic Activity

Adenosine 3',5'-cyclic monophosphate (cAMP) or beta-adrenergic stimulation has been shown to increase actomyosin adenosinetriphosphatase (ATPase) activity in cardiac muscle. Because the major catecholamine transmitters have both alpha- and beta-adrenergic activity, the possibility of a role for alpha-adrenergic stimulation in the regulation of ATPase activity has been investigated. Histochemical measurement of actomyosin ATPase activity in quickly frozen rat hearts has been used as the assay of enzymatic function of the contractile proteins. The dose-response curve of ATPase activity to cAMP shows an increase in ATPase activity at a threshold concentration of 0.01 microM, a peak effect at 0.5–1.0 microM, and a decline beyond 1.5 microM to a level below control at 10 microM cAMP. Kinetic studies varying ATP concentration from 0.5 to 10 mM indicated the existence of multiple forms of actomyosin ATPase activity in the absence of cAMP and only one form with a higher maximum velocity in the presence of 1 microM cAMP. Apparently cAMP raises the enzymatic activity of the individual actomyosin molecule rather than increasing the number of active molecules. The addition of an alpha-adrenergic blocker had no significant effect in the absence of added cAMP, but in the presence of the cyclic nucleotide, 1 microM prazosin always produced a negative effect on ATPase activity. Over the entire range of 0.01–10 microM, cAMP lowered ATPase activity when the alpha-adrenergic antagonist was present. The integrity of the cAMP regulatory system was sensitive to the tissue oxygen tension at the time the heart was quickly frozen. At certain oxygen tension, the stimulatory component of the cAMP regulation was observed without any inhibitory component, suggesting that there are two relatively independent parts of the regulatory mechanism, an inhibitory and a stimulatory. In the presence of gamma-labeled [32P]ATP, 32P was incorporated into several proteins, including the inhibitory subunit of troponin (TNI), C protein, and the regulatory light chain of myosin. cAMP (1 microM) caused an increase in 32P labeling of TNI and C protein. The addition of prazosin with cAMP caused a decrease in the overall level of phosphorylation with specific dephosphorylation of C protein and TNI, the former to a degree similar to the decrease in actomyosin ATPase activity, the latter to a greater degree. These results indicate that alpha-adrenergic activity modulates the balance between kinase and phosphatase activity in the presence of cAMP, probably by inhibiting phosphatase activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute effect of epinephrine on muscle proteolysis in perfused rat hindquarters

1996 ◽  
Vol 270 (6) ◽  
pp. E961-E967 ◽  
Author(s):  
M. Kadowaki ◽  
T. Kamata ◽  
T. Noguchi
Keyword(s):  
Perfusion Pressure ◽  
Initial Rate ◽  
Sharp Decrease ◽  
Acute Effect ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Intracellular Pool ◽  
Beta Adrenoceptor ◽  
Adrenergic Activity ◽  
Rate Infusion

An acute and direct effect of epinephrine (Epi) on muscle proteolysis was investigated using a single-pass mode of rat hindquarter perfusion. The rate of tyrosine (Tyr) release at > 30 min with cycloheximide was regarded as the muscle proteolytic rate. Infusion of Epi (500 nM) to the hindquarters of fed rats led to a sharp decrease in the Tyr release to 50% within 5 min, accompanied by an increase in perfusion pressure and edema around the perfused tissues. To clarify the mechanism, alpha- and beta-antagonists were used together with Epi. A mixture of 10 microM prazosin and 10 microM yohimbine (alpha-adrenergic blockade) before or after Epi infusion completely prevented the edema development and resulted in a new steady state to 80% of the initial rate. On the contrary, 100 microM propranolol (a beta-antagonist) with Epi did not abolish the edema and caused fluctuation in Tyr release. Whether the above results are affected by changes in Tyr transport at the plasma membrane was tested by measuring Tyr efflux from the perfused muscle. Only a beta-adrenergic blockade significantly reduced the rate constant of Tyr efflux from the intracellular pool by 13%. These results suggested that the suppression of Tyr release by alpha-adrenergic activity was mainly due to the effect on Tyr efflux, whereas that by beta-adrenergic activity was not at the Tyr transport level but at the proteolysis level, demonstrating that Epi directly inhibits proteolysis of skeletal muscle via the beta-adrenoceptor.

Effect of short- and long-term beta-adrenergic blockade on lipolysis during fasting in humans

1989 ◽  
Vol 257 (1) ◽  
pp. E65-E73 ◽  
Author(s):  
S. Klein ◽  
E. J. Peters ◽  
O. B. Holland ◽  
R. R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Lean Body Mass ◽  
Body Mass ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Healthy Human ◽  
Beta Adrenergic ◽  
Triglyceride Fatty Acid ◽  
Propranolol Treatment ◽  
Oral Propranolol

Stable isotope tracers and indirect calorimetry were used to evaluate the importance of beta-adrenergic stimulation of lipolysis and triglyceride-fatty acid cycling during fasting in healthy human volunteers. Each subject was studied after 12 and 84 h of fasting both with and without propranolol infusion (protocol 1) and when oral propranolol treatment was given throughout fasting (protocol 2). In protocol 1, the rates of appearance of glycerol and palmitic acid increased from 3.04 +/- 0.19 and 1.78 +/- 0.17 mumol.kg lean body mass-1.min-1, respectively, after 12 h of fasting to 5.28 +/- 0.31 and 3.47 +/- 0.15 mumol.kg lean body mass-1.min-1, respectively, after 84 h of fasting (P less than 0.005). The rate of triglyceride-fatty acid cycling increased from 97 +/- 8 to 169 +/- 5 mumol/min (P less than 0.005). Intravenous propranolol infusion decreased the rate of lipolysis after both 12 and 84 h of fasting, but the magnitude of the antilipolytic effect was much greater after 84 h (P less than 0.005). In protocol 2, the rate of lipolysis and triglyceride-fatty acid cycling was still increased by fasting despite beta-adrenergic blockade with oral propranolol. This study demonstrates that beta-adrenergic stimulation contributes to the mobilization of fat during fasting. However, other mechanism(s) can increase lipolysis and triglyceride-fatty acid cycling when beta-adrenergic receptors are continuously blocked.

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