Effects of propranolol and pindolol on plasma ANP levels in humans at rest and during exercise

1989 ◽  
Vol 257 (2) ◽  
pp. R259-R264
Author(s):  
P. Bouissou ◽  
F. X. Galen ◽  
J. P. Richalet ◽  
M. Lartigue ◽  
F. Devaux ◽  
...  

In attempt to elucidate whether the beta-adrenoceptor is involved in the control of atrial natriuretic peptide (ANP) secretion, plasma immunoreactive ANP level was measured at rest, in recumbent and upright positions, and during graded maximal ergocycle exercise in nine healthy male subjects (23 +/- 0.5 years of age) treated for 3 days with nonselective beta-blockers propranolol (150 mg/day) or pindolol (15 mg/day) or with placebo. The effects of beta-blockers, which differ by their hemodynamic actions at rest because of the intrinsic sympathomimetic activity of pindolol, were compared. Maximal O2 consumption (VO2max) during beta-blockade was not significantly different from the placebo value. Resting heart rate was not affected by pindolol treatment but was decreased with propranolol (-10 beats/min). Both beta-blockers caused a reduction in heart rate at all the exercise intensities. Mean blood pressure was not affected by beta-blockade at rest but was significantly reduced during exercise. During placebo treatment, plasma ANP increased in response to exercise intensities greater than 65% of VO2max. At 100% VO2max plasma ANP was nearly doubled (101.5 +/- 14 pg/ml) compared with the basal value in upright position (56.6 +/- 15 pg/ml). beta-Blockade caused a marked elevation in plasma ANP at all the levels of activity. Despite different hemodynamic responses to pindolol and propranolol, both beta-blockers produced similar increases in the basal level of plasma ANP. These rises were maintained in the course of exercise tests, and no significant difference was found between propranolol and pindolol. We conclude that beta-adrenoceptor mechanisms are not directly responsible for tonic and exercise-induced ANP secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

2021 ◽  
Vol 7 (2) ◽  
pp. 00937-2020
Author(s):  
Silvia Ulrich ◽  
Stéphanie Saxer ◽  
Michael Furian ◽  
Patrick R. Bader ◽  
Paula Appenzeller ◽  
...  

The aim of the study was to investigate the pulmonary haemodynamic response to exercise in Central Asian high- and lowlanders.This was a cross-sectional study in Central Asian highlanders (living >2500 m) compared with lowlanders (living <800 m), assessing cardiac function, including tricuspid regurgitation pressure gradient (TRPG), cardiac index and tricuspid annular plane systolic excursion (TAPSE) by echocardiography combined with heart rate and oxygen saturation measured by pulse oximetry (SpO2) during submaximal stepwise cycle exercise (10 W increase per 3 min) at their altitude of residence (at 760 m or 3250 m, respectively).52 highlanders (26 females; aged 47.9±10.7 years; body mass index (BMI) 26.7±4.6 kg·m−2; heart rate 75±11 beats·min−1; SpO2 91±5%;) and 22 lowlanders (eight females; age 42.3±8.0 years; BMI 26.9±4.1 kg·m−2; heart rate 68±7 beats·min−1; SpO2 96±1%) were studied. Highlanders had a lower resting SpO2 compared to lowlanders but change during exercise was similar between groups (highlanders versus lowlanders −1.4±2.9% versus −0.4±1.1%, respectively, p=0.133). Highlanders had a significantly elevated TRPG and exercise-induced increase was significantly higher (13.6±10.5 mmHg versus 6.1±4.8 mmHg, difference 7.5 (2.8 to 12.2) mmHg; p=0.002), whereas cardiac index increase was slightly lower in highlanders (2.02±0.89 L·min−1versus 1.78±0.61 L·min−1, difference 0.24 (−0.13 to 0.61) L·min−1; p=0.206) resulting in a significantly steeper pressure–flow ratio (ΔTRPG/Δcardiac index) in highlanders 9.4±11.4 WU and lowlanders 3.0±2.4 WU (difference 6.4 (1.4 to 11.3) WU; p=0.012). Right ventricular-arterial coupling (TAPSE/TRPG) was significantly lower in highlanders but no significant difference in change with exercise in between groups was detected (−0.01 (−0.20 to 0.18); p=0.901).In highlanders, chronic exposure to hypoxia leads to higher pulmonary artery pressure and a steeper pressure–flow relation during exercise.


1990 ◽  
Vol 69 (2) ◽  
pp. 485-489 ◽  
Author(s):  
P. Van Nguyen ◽  
J. Cleroux ◽  
M. Peterson ◽  
F. H. Leenen

The effects of beta-blockade on acute exercise-induced changes in plasma lipoprotein levels were investigated in 12 healthy normotensive subjects by use of beta-blockers of three types: a nonselective agent, a beta 1-selective agent, and a nonselective agent with intrinsic sympathomimetic activity (ISA) or partial agonist activity. Each subject received each drug and a placebo for 1 wk each according to a randomized double-blind crossover design. After placebo, exercise caused 10-20% increases in total plasma cholesterol and the high-density lipoprotein (HDL)-cholesterol fraction. The total-to-HDL cholesterol ratio fell, particularly during the 30-min recovery phase. Pindolol treatment increased resting values of HDL cholesterol (from 43 +/- 4 to 48 +/- 4 mg/dl) and potentiated the response to exercise (to 59 +/- 5 vs. 51 +/- 4 mg/dl after placebo). The total-to-HDL cholesterol ratio was significantly lower after pindolol treatment than after placebo. In contrast, neither atenolol nor timolol affected exercise-induced changes in plasma lipoprotein levels. The effects of pindolol on other study parameters (exercise endurance and exercise-induced increases in systolic blood pressure, heart rate, and potassium) were similar to the effects of the nonselective agent, timolol. We conclude that the effects of pindolol on the plasma lipid profile are due to its ISA and that the process activated (possibly plasma lecithin-cholesterol acyltransferase activity) is under minimal sympathetic control and, therefore, sensitive to the expression of ISA both at rest and in response to exercise.


1993 ◽  
Vol 75 (1) ◽  
pp. 155-161 ◽  
Author(s):  
J. M. Overton

The purposes of this study were to determine the role of the sympathetic and parasympathetic nervous systems in producing the heart rate (HR) response to dynamic exercise in rats and to determine the effect of attenuation of the HR response to exercise on blood flow redistribution. Sprague-Dawley rats (n = 10) were instrumented with arterial and venous catheters and Doppler flow probes. Mean arterial pressure (MAP), HR, mesenteric blood flow (MBF), and iliac blood flow (IBF) were determined during four exercise tests. On 4 consecutive days, rats were treated with saline (SAL, 1 mg/kg iv), atropine methyl nitrate (ATR, 2 mg/kg), timolol maleate (TIM, 0.5 mg/kg), and combined timolol and atropine. One minute of mild exercise (10 m/min) produced an increase in HR of 90 +/- 6 beats/min after SAL treatment, which was significantly less than the increment after ATR (56 +/- 5 beats/min) or TIM (4 +/- 3 beats/min). For the remainder of graded exercise, ATR treatment produced a modest attenuation in the increment in HR and no effect on MAP, IBF, and MBF. At 30 m/min, TIM markedly blunted the exercise-induced increment in HR (SAL, 138 +/- 8 beats/min; TIM, 53 +/- 4 beats/min) and IBF (SAL, 324 +/- 33%; TIM, 197 +/- 33%) with no effect on MAP or MBF. The results suggest that 1) the sympathetic nervous system is an important mediator of exercise-induced tachycardia in rats and 2) exercised-induced hyperemia, but not MAP, is attenuated by nonselective beta-blockade during exercise in rats.


2017 ◽  
Vol 12 (5) ◽  
pp. 662-667 ◽  
Author(s):  
Matthijs T.W. Veltmeijer ◽  
Dineke Veeneman ◽  
Coen C.C.W. Bongers ◽  
Mihai G. Netea ◽  
Jos W. van der Meer ◽  
...  

Purpose:Exercise increases core body temperature (TC) due to metabolic heat production. However, the exercise-induced release of inflammatory cytokines including interleukin-6 (IL-6) may also contribute to the rise in TC by increasing the hypothalamic temperature set point. This study investigated whether the exercise-induced increase in TC is partly caused by an altered hypothalamic temperature set point.Methods:Fifteen healthy, active men age 36 ± 14 y were recruited. Subjects performed submaximal treadmill exercise in 3 randomized test conditions: (1) 400 mg ibuprofen and 1000 mg acetaminophen (IBU/APAP), (2) 1000 mg acetaminophen (APAP), and (3) a control condition (CTRL). Acetaminophen and ibuprofen were used to block the effect of IL-6 at a central and peripheral level, respectively. TC, skin temperature, and heart rate were measured continuously during the submaximal exercise tests.Results:Baseline values of TC, skin temperature, and heart rate did not differ across conditions. Serum IL-6 concentrations increased in all 3 conditions. A significantly lower peak TC was observed in IBU/APAP (38.8°C ± 0.4°C) vs CTRL (39.2°C ± 0.5°C, P = .02) but not in APAP (38.9°C ± 0.4°C) vs CTRL. Similarly, a lower ΔTC was observed in IBU/APAP (1.7°C ± 0.3°C) vs CTRL (2.0°C ± 0.5°C, P < .02) but not in APAP (1.7°C ± 0.5°C) vs CTRL. No differences were observed in skin temperature and heart-rate responses across conditions.Conclusions:The combined administration of acetaminophen and ibuprofen resulted in an attenuated increase in TC during exercise compared with a CTRL. This observation suggests that a prostaglandin-E2-induced elevated hypothalamic temperature set point may contribute to the exercise-induced rise in TC.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Ida Skrinde Leren ◽  
Jørg Saberniak ◽  
Eman Majid ◽  
Trine F Haland ◽  
Thor Edvardsen ◽  
...  

Introduction: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inheritable arrhythmogenic disease, and typically presents as syncope or sudden cardiac death during exercise. Beta blockers are first choice therapy but little is known about antiarrhythmic effects of different beta blockers in CPVT. Nadolol has shown superior antiarrhythmic effect in other cardiomyopathies. Hypothesis: We hypothesized that nadolol is superior to selective beta blockers in arrhythmia protection in CPVT patients. Methods: We included 34 CPVT patients (age 34±19 yrs, 44% female, 88% RYR2 mutation positive). We serially performed 2 bicycle exercise tests in each patient; 1)>6 weeks on maximum tolerated dose of selective beta blockers. 2)>6 weeks on maximum tolerated dose of nadolol. We recorded resting and maximum heart rate (HR), HR at first arrhythmia and the most severe arrhythmia occurring. Arrhythmic window was defined as the difference between maximum HR and HR at first arrhythmia. Severity of arrhythmias was scored as arrhythmic score: no arrhythmias (0point), single ventricular extra systoles (1point), bigemini (2points), couplets (3points) and nonsustained VT (4points). Results: Resting HR was similar on nadolol and selective beta blockers (54±10bpm vs. 56±14bpm, p=0.50), while maximum heart rate was lower on nadolol (122±21bpm vs. 139±24bpm, p<0.01). First arrhythmias occurred at similar HR at both exercise tests (113±21bpm vs. 113±19bpm, p=1.0). Consequently, arrhythmic window was smaller during nadolol treatment (17±10bpm vs. 32±26bpm, p=0.03) (Figure) and also the arrhythmic score was lower than on selective beta blockers (1.1±1.2 vs. 2.4±0.9, p<0.01). Conclusion: Arrhythmic score was lower on nadolol compared to selective beta blockers. Also, arrhythmic window, representing the span of heart rates where arrhythmias may occur and progress in severity, was smaller. This suggests that nadolol should be the beta blocker of choice in CPVT patients.


1984 ◽  
Vol 22 (01) ◽  
pp. 35-40
Author(s):  
E. E. van der Wall ◽  
M. J. van Eenige ◽  
S. Scholtalbers ◽  
W. den Hollander ◽  
E. C. Visser ◽  
...  

SummaryIn an experimental study in 50 dogs the myocardial uptake of free fatty acids (FFAs) after beta-blockade was determined using radioiodinated heptadecanoic acid as a metabolic tracer. All 4 beta-blockers used (metoprolol, timolol, propranolol and pindolol) lowered the uptake of FFAs in the normal canine heart. Uptake of FFAs was also diminished after coronary artery occlusion per se, but administration of beta-blockers exerted little additional influence on the uptake of FFAs. This observation was qualitatively parallelled by the uptake of 201T1 in concomitant experiments. Plasma FFA levels were increased by pindolol (non-selective with intrinsic sympathomimetic activity), not changed by metoprolol (a cardioselective betablocking agent) and lowered by timolol and propranolol (both nonselective compounds). The extent of ischemic tissue, as reflected by uptake of iodoheptadecanoic acid and 201T1, was diminished by metoprolol but not by other beta-blockers. Regional distribution of both tracers, as shown in the endo-epicardial uptake ratios, was hardly influenced by beta-blockade, except for a small increase of 201T1 uptake in non-occluded endocardium. Uptake of 201T1 as well as of iodoheptadecanoic acid in the ischemic area was increased by metoprolol, timolol and propranolol and decreased by pindolol. We conclude that beta-blocking agents confer different effects on myocardial uptake and metabolism of FFAs which might possibly be related to their different inherent properties.


1973 ◽  
Vol 36 (2) ◽  
pp. 639-645 ◽  
Author(s):  
G. Harley Hartung

Heart rates of 30 male Ss were monitored prior to, during, and in recovery from a standard treadmill walk. 10 Ss were trained distance runners and were considered trained in the specific work studied. 10 Ss were conditioned swimmers but were doing a type of work for which they were not trained. The runners had significantly better mean endurance times (time to heart rates 110, 130, 150, and 170) than the swimmers, even though both had previously undergone extensive endurance training. The swimmers did not perform significantly better than a group of nontrained Ss except to heart rate 130. In recovery to heart rate 130, there was no significant difference among the means of the three groups. The only significant difference among group means to final recovery heart rate was between the runners and the nontrained group.


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