EFFECTS OF ALPHA-ADRENERGIC STIMULATION AND BLOCKADE ON PLASMA PARATHYROID HORMONE CONCENTRATIONS IN COWS

1978 ◽  
Vol 88 (3) ◽  
pp. 535-544 ◽  
Author(s):  
J. W. Blum ◽  
A. Guillebeau ◽  
U. Binswanger ◽  
P. Kunz ◽  
M. Da Prada ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Fatty Acid ◽  
Parathyroid Hormone ◽  
Free Fatty Acid ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Later Phase ◽  
Immunoreactive Parathyroid Hormone

ABSTRACT Experiments were designed to investigate responses of immunoreactive parathyroid hormone (PTH) during alpha-adrenergic stimulation and blockade in cows. Alpha-adrenergic agonists (methoxamine, phenylephrine and noradrenaline, the beta-adrenergic action of which was blocked by propranolol) did not change PTH and free fatty acid levels, whereas they characteristically increased the blood pressure and decreased the heart rate. In contrast, alpha-adrenergic blockade by phentolamine progressively increased PTH levels. The elevated PTH concentrations, associated with increased plasma noradrenaline and free fatty acid levels, rising heart rate and decreasing blood pressure, indicated that all these changes can be related to a beta-adrenergic stimulatory mechanism. Beta-adrenergic stimulation was presumably responsible for the initial elevation of PTH concentrations, whereas, during the later phase of the phentolamine infusions, a concomitant hypocalcaemia probably also produced a stimulatory effect.

scholarly journals Beta-adrenergic Receptor Blockade Effects on Cardio-pulmonary Exercise Testing

2021 ◽  
Author(s):  
Kevin Forton ◽  
Michel Lamotte ◽  
Alexis Gillet ◽  
Martin Chaumont ◽  
Van De Borne Philippe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Single Dose ◽  
Adrenergic Receptor ◽  
Adrenergic Blockade ◽  
Receptor Blockade ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Chronotropic Response ◽  
Adrenergic Receptor Blockade

Abstract Background: Beta-blockers are increasingly prescribed while the effects of beta-adrenergic receptor blockade on cardio-pulmonary exercise test (CPET) derived parameters remain under-studied. Methods: 21 young healthy adults repeated 3 CPET at an interval of 7 days at the same time of the day. The tests were performed 3 hours after a random, double blind, cross-over single dose intake of placebo, 2.5 mg bisoprolol or 5 mg bisoprolol. Gaz exchange, heart rate and blood pressure were measured at rest and during cyclo-ergometric CPET.Results: Maximal workload and VO2max were unaffected by the treatment, with maximal respiratory exchange ratio > 1.15 in all tests. A beta-blocker dose-dependent effect reduced resting and maximal blood pressure and heart rate and the chronotropic response to exercise, evaluated by the heart rate/VO2 slope (placebo: 2,9 ± 0,4 beat/ml/kg; 2,5 mg bisoprolol: 2,4 ± 0,5 beat/ml/kg; 5 mg bisoprolol: 2,3 ± 0,4 beat/ml/kg, p<0.001). Ventilation efficiency measured by the VE/VCO2 slope and the ventilatory equivalent for CO2 at the ventilatory threshold were not affected by beta1-receptor blockade. Post-exercise chronotropic recovery measured after 1 min was enhanced under beta1-blocker (placebo: 26 ± 7 bpm; 2,5 mg bisoprolol: 32 ± 6 bpm; 5 mg bisoprolol: 33 ± 6 bpm, p<0.01).Conclusion: The present results suggest that a single dose of bisoprolol does not affect metabolism, respiratory response and exercise capacity. However, beta-adrenergic blockade dose-dependently reduced exercise hemodynamic response by lowering the pressure and chronotropic responses.

Effect of aerobic conditioning on cardiovascular response to isometric exercise

1982 ◽  
Vol 52 (5) ◽  
pp. 1257-1260 ◽  
Author(s):  
B. J. Morgan ◽  
H. L. Brammell ◽  
D. L. Sable ◽  
M. L. Morton ◽  
L. D. Horwitz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Cardiovascular Response ◽  
Isometric Exercise ◽  
Adrenergic Blockade ◽  
Isometric Handgrip ◽  
Double Product ◽  
Beta Adrenergic ◽  
Aerobic Conditioning

The response to isometric handgrip exercise (IHE) and isometric quadriceps exercise (IQE) (30% maximum voluntary contraction held 3 min) was studied before and after 5 wk of aerobic training. Training exercises involved only the lower extremities. Seventeen healthy unconditioned males aged 21--35 yr were subjects. During training nine subjects received propranolol in doses that provided a high degree of beta-adrenergic blockade; eight received a placebo. All subjects were tested before training or drug and after training, 3--5 days off drug. With IGE after training, the placebo group had lower maximum heart rate (91 +/- 4 to 79 +/- 5 beats/min, P less than 0.05), systolic blood pressure (151 +/- 5 to 139 +/- 4 mmHg, P less than 0.05), and double product (heart rate x systolic blood pressure) (138 +/- 10 x 10(2) to 110 +/- 7 x 10(2), P less than 0.05). The response to IQE in the propranolol group was unchanged after training. Heart rate, systolic blood pressure, and double product with IHE was unchanged in either group after training. Aerobic conditioning can modify the hemodynamic response to isometric exercise. This effect is specific for the trained muscle group and is prevented by beta-adrenergic blockade.

Effects of chronic beta-adrenergic blockade on exercise training in dogs

1988 ◽  
Vol 64 (5) ◽  
pp. 1960-1967 ◽  
Author(s):  
E. E. Wolfel ◽  
J. Lindenfeld ◽  
J. Smoak ◽  
L. D. Horwitz
Keyword(s):  
Heart Rate ◽  
Submaximal Exercise ◽  
Peak Exercise ◽  
Exercise Heart Rate ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Exercise Time ◽  
Adrenergic Blocker

To assess the role of beta-adrenergic stimulation in cardiovascular conditioning we examined the effects of a beta-adrenergic blocker, propranolol, in mongrel dogs during an 8-wk treadmill-training program. Seven dogs were trained without a drug (NP), six were trained on propranolol 10 mg.kg-1.day-1 (P), and five served as caged controls (C). Effective beta-adrenergic blockade was documented by a decrease in peak exercise heart rate of 54 +/- 11 (SE) beats/min (P less than 0.05) and a one-log magnitude of increase in the isoproterenol-heart rate dose-response curve. Testing was performed before drug treatment or training and again after training without the drug for 5 days. Submaximal exercise heart rate decreased similarly in both NP and P (-26 +/- 4 NP vs. -25 +/- 9 beats/min P, P less than 0.05 for both) but peak heart rate decreased only with NP (-33 +/- 9 beats/min, P less than 0.05). Treadmill exercise time increased similarly in both groups: 3.4 +/- 0.6 min in NP and 3.0 +/- 0.2 min in P (both P less than 0.05). Blood volume also increased after training in both groups: 605 +/- 250 ml (26%) in NP and 377 +/- 140 ml (17%) in P (both P less than 0.05). Submaximal exercise arterial lactates were reduced similarly in both groups but peak exercise lactate was reduced more in NP (-1.4 +/- 0.3 NP vs -0.3 +/- 0.12 mmol/l P, P less than 0.05). Lactate threshold increased in both groups but the increase was greater in NP (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The cardiovascular and metabolic effects of epinephrine in man and their modification by beta adrenergic blocking agents

1969 ◽  
Vol 47 (2) ◽  
pp. 213-216 ◽  
Author(s):  
W. A. Mahon ◽  
D. J. Campbell
Keyword(s):  
Blood Pressure ◽  
Metabolic Effects ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Epinephrine Infusion ◽  
Beta Adrenergic ◽  
Blocking Agents ◽  
Adrenergic Blocking ◽  
Beta Adrenergic Blocking Agents ◽  
Adrenergic Blocking Agents

Normal adult patients were infused with epinephrine in a dose of 0.15 μg/kg per minute given intravenously before and after beta adrenergic blockade with propranolol, 0.1 mg/kg and butoxamine 1 mg/kg. Epinephrine produced a significant rise of heart rate, cardiac output, and blood pressure and an elevation of free fatty acids and glucose. The beta adrenergic blocking agents reversed all these effects with the exception that a rise in systolic blood pressure occurred. These findings are consistent with the hypothesis that a rise in free fatty acid is mediated by beta adrenergic stimulation whereas the rise in blood glucose produced by epinephrine is probably due to alpha adrenergic stimulation. In man, the beta adrenergic effects of butoxamine include a reversal of most of the cardiovascular as well as the metabolic effects produced by epinephrine infusion.

Effects of α-adrenergic stimulation and blockade on parathyroid hormone responses to β-adrenergic agonists in cattle

1982 ◽  
Vol 100 (4) ◽  
pp. 539-542 ◽  
Author(s):  
J. W. Blum ◽  
J. A. Fischer ◽  
U. Binswanger
Keyword(s):  
Heart Rate ◽  
Parathyroid Hormone ◽  
Plasma Levels ◽  
Heart Rate Response ◽  
Adrenergic Blockade ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Hormone Responses

Abstract. Experiments were designed to investigate the effect of α-adrenergic stimulation on parathyroid hormone (PTH) responses to isoproterenol (ISO). In addition, PTH responses to adrenaline (A) and hypocalcaemia were studied with and without α-adrenergic blockade by phentolamine. Infusions of phenylephrine (a 'pure' α-adrenergic agonist) did not modify basal PTH levels and PTH responses to ISO infusions, whereas the heart rate response to ISO was reduced (P < 0.05). The results demonstrate that α-adrenergic stimulation by phenylephrine does not reduce PTH responses to β-adrenergic agonists. In response to phentolamine the heart rate increased and plasma levels of Ca and Ca++ decreased. Plasma PTH concentrations were slightly but not significantly raised and PTH responses to adrenaline (P < 0.05), but not to hypocalcaemia, were enhanced. The potentiation of PTH responses to A in the presence of phentolamine may have been due to inhibition of α-adrenergic properties of A. It may have been also, in part, the consequence of the hypocalcaemia, which is known to augment PTH responses to A.

Perceived exertion and gas exchange after calcium and beta-blockade in atrial fibrillation

1987 ◽  
Vol 63 (1) ◽  
pp. 97-104 ◽  
Author(s):  
J. Myers ◽  
J. E. Atwood ◽  
M. Sullivan ◽  
S. Forbes ◽  
R. Friis ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Blood Pressure ◽  
Heart Rate ◽  
Gas Exchange ◽  
Perceived Exertion ◽  
Maximal Exercise ◽  
Adrenergic Blockade ◽  
Channel Blockade ◽  
Calcium Channel Blockade ◽  
Beta Adrenergic

Nine male patients (mean age 65 yr) with chronic atrial fibrillation underwent maximal exercise testing during placebo, beta-adrenergic (celiprolol, 600 mg), or calcium (diltiazem, 30 or 60 mg four times daily) channel blockade. The results were analyzed to determine which factors most closely related to ratings of perceived exertion (RPE) during exercise. Heart rate (HR), blood pressure (BP), oxygen uptake (VO2), minute ventilation (VE), and carbon dioxide production (VCO2) were evaluated at rest, 3.0 mph/0% grade, the gas exchange anaerobic threshold (ATge), 80% of placebo maximal O2 uptake, and maximal exercise. Both beta-adrenergic and calcium channel blockade significantly reduced heart rate and systolic blood pressure relative to placebo; these effects were more profound during beta-adrenergic blockade and as exercise progressed. Correlation coefficients and estimates of slope were derived for changes in RPE during exercise vs. changes in HR, VO2, VE, and VCO2 during the three treatments (r = 0.76 to 0.92, P less than 0.001). Although RPE was significantly correlated with HR during placebo and diltiazem therapy (r = 0.45, P less than 0.01), this was not the case during beta-adrenergic blockade (r = 0.31, NS). Slope of the regression lines between RPE and VO2, VE, and VCO2 did not differ between the three treatments. Slope of the regression lines between RPE and HR differed only during calcium channel blockade. Because the presence of atrial fibrillation and beta-adrenergic blockade altered the associations between RPE, VO2, and HR, these results suggest that VE is more closely related to RPE than the other parameters.

Cardiac responses to acute insulin-induced hypoglycemia in humans

1990 ◽  
Vol 258 (6) ◽  
pp. H1775-H1779 ◽  
Author(s):  
B. M. Fisher ◽  
G. Gillen ◽  
D. A. Hepburn ◽  
H. J. Dargie ◽  
B. M. Frier
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Cholinergic Blockade ◽  
Arterial Blood ◽  
Blood Pressure Responses

The effects of acute hypoglycemia on the heart and cardiovascular system were examined in humans using radioisotopic techniques, complemented by measurement of heart rate and blood pressure. The heart rate increased from 62 +/- 3 to 87 +/- 3 beats/min in response to hypoglycemia; this increase was accompanied by a significant increase in systolic blood pressure, a fall in diastolic blood pressure, with no change in the mean arterial blood pressure. The left ventricular ejection fraction increased from 47 +/- 3 (SE) to 72 +/- 5% in response to hypoglycemia. The increases in heart rate and ejection fraction were abolished during parenteral nonselective beta-adrenergic blockade with propranolol but were unaffected by either alpha-adrenergic blockade with phentolamine or cholinergic blockade with atropine. During beta-adrenergic blockade, there were significant increases in diastolic and mean arterial blood pressure in response to hypoglycemia. During alpha-adrenergic blockade the systolic, diastolic, and mean arterial pressures fell significantly after hypoglycemia. The blood pressure responses to hypoglycemia were unaffected by cholinergic blockade. Thus the increases in ejection fraction and in heart rate in response to hypoglycemia are mediated by beta-adrenoreceptors, whereas the blood pressure responses to hypoglycemia are mediated by alpha- and by beta-adrenoreceptors.

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.

scholarly journals Association of Serum–Free Fatty Acid Level With Reduced Reflection Pressure Wave Magnitude and Central Blood Pressure

Hypertension ◽  
2014 ◽  
Vol 64 (6) ◽  
pp. 1212-1218 ◽  
Author(s):  
Yasuharu Tabara ◽  
Yoshimitsu Takahashi ◽  
Takahisa Kawaguchi ◽  
Kazuya Setoh ◽  
Chikashi Terao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Pressure Wave ◽  
Acid Level ◽  
Free Fatty Acid Level ◽  
Central Blood Pressure ◽  
Fatty Acid Level ◽  
Serum Free Fatty Acid ◽  
Serum Free
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