Blood Pressure Responses to Catecholamines during Beta-Adrenergic Blockade with Propranolol in Hypertensive Subjects

CHEST Journal ◽  
1977 ◽  
Vol 71 (1) ◽  
pp. 38-43 ◽  
Author(s):  
Nicholas D. Vlachakis ◽  
Daisy DeGuia ◽  
Milton Mendlowitz
Keyword(s):  
Blood Pressure ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Blood Pressure Responses

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.

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.

Effects of epinephrine and norepinephrine on blood pressure of totally perfused dogs

1959 ◽  
Vol 197 (3) ◽  
pp. 607-612 ◽  
Author(s):  
J. E. Kendrick
Keyword(s):  
Blood Pressure ◽  
Pressor Response ◽  
Adrenergic Blockade ◽  
Constant Flow ◽  
Ganglionic Blockade ◽  
Depressor Response ◽  
Blood Pressure Responses

A pump, capable of maintaining a constant flow output against pressure heads up to 200 mm Hg, has been utilized to completely replace the heart in dogs. Epinephrine and norepinephrine (0.5–10.0 µg/kg) were given in over 50 totally perfused animals. Comparable doses of these agents produced blood pressure responses essentially identical both in magnitude and character. Following adrenergic blockade by Dibenzyline, the pressor response to both epinephrine and norepinephrine was greatly reduced or abolished. The response to epinephrine after adrenergic blockade was quite often a depressor response. The depressor phase never occurred in response to norepinephrine. Sympathetic ganglionic blockade potentiated the pressure responses to both epinephrine and norepinephrine to approximately the same degree.

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 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.

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.

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