Effects on exercise tachycardia during forty-eight hours of a series of doses of atenolol, sotalol, and metoprolol

1981 ◽  
Vol 29 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Dean W G Harron ◽  
Kenneth Balnave ◽  
Charles D Kinney ◽  
Richard Wilson ◽  
Clive J Russell ◽  
...  
Keyword(s):  
Exercise Tachycardia

ADRENOCORTICAL RESPONSE TO NON-EXHAUSTIVE MUSCULAR EXERCISE

1972 ◽  
Vol 70 (1) ◽  
pp. 73-80 ◽  
Author(s):  
L. W. Raymond ◽  
J. Sode ◽  
J. R. Tucci
Keyword(s):  
Treadmill Exercise ◽  
Serum Cortisol ◽  
Treadmill Walking ◽  
Exhaustive Exercise ◽  
Muscular Exercise ◽  
Adrenocortical Response ◽  
Exercise Tachycardia ◽  
Before And After

ABSTRACT Treadmill walking produced a prompt reduction in serum cortisol in 10 of 12 healthy military men. In contrast, two subjects, with pre-exercise tachycardia and apprehension, showed an increase in serum cortisol with treadmill exercise. In each group, the changes produced by exercise were still evident 30 and 60 minutes after the 30-minute treadmill walk. Urine collected before and after exercise contained similar amounts of 11-hydroxy- and 17-hydroxycorticosteroid material. These results may be explained by an increase in cortisol utilization during exercise and/or by a change in its distribution. The data indicate that in the absence of psychic factors, non-exhaustive exercise is not associated with pituitary adrenocortical activation.

scholarly journals Effects of ICI 141,292 on exercise tachycardia and isoprenaline-induced beta-adrenoceptor responses in man.

1986 ◽  
Vol 21 (3) ◽  
pp. 249-258 ◽  
Author(s):  
TH Pringle ◽  
PC O'Connor ◽  
AJ McNeill ◽  
MB Finch ◽  
JG Riddell ◽  
...  
Keyword(s):  
Beta Adrenoceptor ◽  
Exercise Tachycardia

Penbutolol: Pharmacokinetics, effect on exercise tachycardia, and in vitro inhibition of radioligand binding

1988 ◽  
Vol 35 (6) ◽  
pp. 613-623 ◽  
Author(s):  
D. Brockmeier ◽  
P. Hajd� ◽  
W. Henke ◽  
E. Mutschler ◽  
D. Palm ◽  
...  
Keyword(s):  
Radioligand Binding ◽  
Exercise Tachycardia ◽  
In Vitro Inhibition

Haemodynamic Responses to Exercise and Acute β-Receptor Blockade in Renin Sub-Types of Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 493s-496s ◽  
Author(s):  
F. Burkart ◽  
F. R. Bühler ◽  
M. Pfisterer ◽  
B. E. Lütold ◽  
M. Küng
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin ◽  
Receptor Blockade ◽  
Control Mechanisms ◽  
Exercise Tachycardia ◽  
Adrenergic Control ◽  
Before And After ◽  
Pre Treatment ◽  
Β Receptor

1. Haemodynamic and renin responses to dynamic exercise before and after intravenous β-adrenoreceptor blockade with propranolol were compared in twenty-one patients with essential hypertension and either high (n = 7), normal (n = 7) or low plasma renin activity (n = 7). 2. Renin and heart-rate responses to exercise and β-receptor blockade diminished from high-renin to normal and to low-renin patients, effects which were blunted with increasing age. 3. Among the renin groups cardiac output, stroke volume, diastolic pulmonary artery pressure, systemic pressure and peripheral vascular resistance as well as their changes produced by exercise and acute β-receptor blockade were not significantly different. 4. Long-term anti-hypertensive propranolol effects correlated with the pre-treatment renin status, renin stimulation and its suppression by acute β-receptor blockade as well as with the exercise tachycardia and the patient's age. 5. The results suggest different adrenergic control mechanisms in renin sub-types of essential hypertension, age being a modulating factor.

The effects of adrenalectomy and autonomic blockades on the exercise tachycardia in conscious rats

2010 ◽  
Vol 155 (1-2) ◽  
pp. 59-67 ◽  
Author(s):  
Rie Wakasugi ◽  
Tomoko Nakamoto ◽  
Kanji Matsukawa
Keyword(s):  
Conscious Rats ◽  
Exercise Tachycardia

Observations on Some Properties of a Long-Acting Preparation of Propranolol

1979 ◽  
Vol 57 (s5) ◽  
pp. 409s-411s ◽  
Author(s):  
R. G. Shanks ◽  
J. D. Neill ◽  
W. J. Leahey ◽  
M. P. S. Varma
Keyword(s):  
Healthy Subjects ◽  
Slow Release ◽  
Peak Effect ◽  
Exercise Tachycardia ◽  
Repeated Dosing ◽  
Long Acting

1. The effects of 160 mg of propranolol and 160 mg of a long-acting (LA) formulation of propranolol were studied in healthy subjects. 2. Both drugs reduced an exercise tachycardia but the peak was less and the 24 h effect greater after long-acting propranolol than after propranolol. 3. These differences were maintained on repeated dosing for 8 days. 4. In contrast to single doses of 400 mg of sotalol, 160 mg of oxprenolol and 160 mg of slow-release oxprenolol, the peak effect of long-acting propranolol was less and that at 24 h was greater.

Reduction of exercise tachycardia in man after propranolol, atenolol and bisoprolol in comparison to beta-adrenoceptor occupancy

1987 ◽  
Vol 8 (suppl M) ◽  
pp. 3-8 ◽  
Author(s):  
A. Wellstein ◽  
D. Palm ◽  
G. G. Belz ◽  
R. Butzer ◽  
R. Polsak ◽  
...  
Keyword(s):  
Beta Adrenoceptor ◽  
Exercise Tachycardia

Modulation of exercise tachycardia by vasopressin in the nucleus tractus solitarii

1997 ◽  
Vol 273 (4) ◽  
pp. R1271-R1282 ◽  
Author(s):  
Daniel L. Dufloth ◽  
Mariana Morris ◽  
Lisete C. Michelini
Keyword(s):  
Brain Stem ◽  
Acute Exercise ◽  
Treadmill Exercise ◽  
Nucleus Tractus Solitarii ◽  
Male Rats ◽  
Exercise Tachycardia ◽  
Pressor Responses ◽  
Exercise Induced ◽  
Response To Exercise

Our objective was to study the role of vasopressinergic synapses at the nucleus tractus solitarii (NTS) in the modulation of exercise-induced tachycardia. We evaluated the effect of NTS administration of vasopressin (AVP) or vasopressin antagonist (AVPant) on heart rate (HR) and mean arterial pressure (MAP) responses during dynamic exercise in male rats with chronic arterial and NTS cannulas. Sedentary (S) and trained (T) animals were tested at three or four exercise levels (from 0.4 up to 1.4 km/h) after NTS injection of AVP or AVPant 20–30 min before treadmill exercise. Plasma and regional brain levels of AVP were measured in separate groups of S and T rats at rest and immediately after acute exercise. When administered into the NTS, exogenous AVP (20 pmol) caused a small but significant decrease in baseline HR and potentiated the tachycardiac response to mild to moderate exercise intensities (on average, increases of 35–46 beats/min over control tachycardic response). The potentiation of exercise tachycardia by AVP was long lasting and more pronounced in T than in S rats. Even 2 days after NTS AVP injection, there was evidence for an alteration in the HR response to exercise. Mediation by V1 receptors was supported by the blunted tachycardiac response to exercise after administration of a V1 antagonist d(CH2)5Tyr MeAVP into the NTS in both T and S rats (average reductions of 23–34 and 13–19 beats/min below control tachycardia, respectively). No changes were observed in baseline MAP or the exercise-induced pressor responses. There were specific changes in brain stem AVP levels that were related to the exercise treatment. T rats showed a marked increase in dorsal and ventral brain stem AVP content after acute exercise. There were no changes in hypothalamus, median eminence, posterior pituitary, or plasma AVP. These data indicate that vasopressinergic synapses and V1 receptors in the NTS are involved in the potentiation of tachycardic response to exercise. The vasopressinergic mechanism operates in both S and T rats, but training alters the sensitization of V1receptors by AVP.

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