Interactive effect of acetylcholine and norepinephrine on the sinoatrial node of the trained rat

Bolter, Chris P.; Sanders, W.D

doi:10.1016/0165-1838(88)90011-2

Cited by 2 publications

(1 citation statement)

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“…The concentration response relationship of isolated atria and hearts to the βadrenoceptor agonists, isoproterenol and norepinephrine, demonstrates no changes in maximal response or sensitivity of response to agonist (Bolter and Atkinson, 1988;. Nor is there a change in responsiveness to atropine or a combination of atropine and norepinephrine (Bolter and Sanders, 1988). The current data support the hypothesis that training produces a lowering of the intrinsic heart rate via mechanisms that do not depend upon the continual presence of a humoral substance, and furthermore, appear to be mediated by the sympathetic nervous system.…”

Section: Exercisementioning

confidence: 96%

Alterations in intrinsic heart rate in endotoxemia

Wearden¹

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After much early debate, it is now well recognized that the origin of the heart beat is myogenic, or intrinsic, to the heart. It has been felt that the intrinsic heart rate (IHR) is constant and that the observed heart rate is controlled by tonal alterations in the activity of the autonomic nervous system in response to various stimuli. Some investigators have recognized, however, that the intrinsic heart rate (IHR) can be altered in certain conditions. Sepsis, or the host response to bacterial infection, is recognized as a stress to the host that results in decreased myocardial contractility and tachycardia. Some previous work has suggested that this tachycardia may exist outside the tonal regulation of the autonomic nervous system, raising the possibility of an elevation of the IHR. Utilizing an E. coli lipopolysaccharide (LPS) endotoxin model of sepsis in the rat, this work demonstrates an elevation of the IHR in sepsis. The experimental evidence further suggests that the β-adrenoceptor participates in the induction of the elevation in IHR early in the septic process. By sixteen hours after LPS administration the β-adrenoceptor is, however, no longer required for the ongoing elevation of IHR. It is also demonstrated that the elevation in IHR is more prolonged than the contractile dysfunction induced by LPS. iii Dedication To Andrea, Andrew, Mara and Luke Without your support this would not have been possible Without your unconditional love this would all be meaningless

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Section: Exercisementioning

confidence: 96%