Developmental Changes of α1-Adrenergic Chronotropic Action on Human Sinus Node

Saitoh, Hirokazu; Nomura, Atsunobu; Osaka, Motohisa; Sasabe, Noriko; Atarashi, Hirotsugu; Hayakawa, Hirokazu

doi:10.1016/s0002-9149(99)80811-x

Cited by 15 publications

(9 citation statements)

References 14 publications

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“…10 Finally, a decrease in human a 1 -AR activity with age has also been suggested, because the a 1 -AR agonist phenylephrine appears to have less effect on heart rate with increasing patient age. 11 In summary, the present study indicates a substantial decrease in human atrial a 1 -AR expression with increasing age. The decline in cardiac a 1 -ARs with increasing age may contribute to the age-induced increase in cardiac morbidity and mortality.…”

Section: Low Expression Of a 1 -Adrenergic Receptors In The Aging Humsupporting

confidence: 57%

LOW EXPRESSION OF α₁‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

Kwatra¹,

Goldsmith²,

White³

et al. 2010

J American Geriatrics Society

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Section: Low Expression Of a 1 -Adrenergic Receptors In The Aging Humsupporting

confidence: 57%

LOW EXPRESSION OF α₁‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

Kwatra¹,

Goldsmith²,

White³

et al. 2010

J American Geriatrics Society

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“…The preload-dependent increase in HR demonstrated by Bainbridge (1) is excluded, since it relies on vagal transmission. Potentially, ␣-adrenergic receptors, which possess tachycardic function in young animals and humans (28), preserve the HR response to exercise when ␤-adrenergic and muscarinic receptors are inhibited. Alternatively, stretching of sinoatrial fibers, as induced during exercise by a higher preload, may increase their depolarization rate by activation of ion channels (5), but that remains to be established in humans.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia increases exercise heart rate despite combined inhibition of β-adrenergic and muscarinic receptors

Siebenmann

Rasmussen

Sørensen

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Hypoxia increases the heart rate response to exercise, but the mechanism(s) remains unclear. We tested the hypothesis that the tachycardic effect of hypoxia persists during separate, but not combined, inhibition of β-adrenergic and muscarinic receptors. Nine subjects performed incremental exercise to exhaustion in normoxia and hypoxia (fraction of inspired O2 = 12%) after intravenous administration of 1) no drugs (Cont), 2) propranolol (Prop), 3) glycopyrrolate (Glyc), or 4) Prop + Glyc. HR increased with exercise in all drug conditions (P < 0.001) but was always higher at a given workload in hypoxia than normoxia (P < 0.001). Averaged over all workloads, the difference between hypoxia and normoxia was 19.8 ± 13.8 beats/min during Cont and similar (17.2 ± 7.7 beats/min, P = 0.95) during Prop but smaller (P < 0.001) during Glyc and Prop + Glyc (9.8 ± 9.6 and 8.1 ± 7.6 beats/min, respectively). Cardiac output was enhanced by hypoxia (P < 0.002) to an extent that was similar between Cont, Glyc, and Prop + Glyc (2.3 ± 1.9, 1.7 ± 1.8, and 2.3 ± 1.2 l/min, respectively, P > 0.4) but larger during Prop (3.4 ± 1.6 l/min, P = 0.004). Our results demonstrate that the tachycardic effect of hypoxia during exercise partially relies on vagal withdrawal. Conversely, sympathoexcitation either does not contribute or increases heart rate through mechanisms other than β-adrenergic transmission. A potential candidate is α-adrenergic transmission, which could also explain why a tachycardic effect of hypoxia persists during combined β-adrenergic and muscarinic receptor inhibition.

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“…Although the rich sympathetic innervation of ventricles is widely recognized, as recently reviewed by Coote (39), there is accumulating evidence for dense parasympathetic innervation of this region and its functional significance in the control of ventricular rhythm, rate and contractility. In addition, a positive chronotropic response to α 1 -adrenergic stimulation has been reported in young individuals (287). However, the importance of parasympathetic regulation of ventricular function and α 1 -adrenoreceptor chronotropism during exercise in health and disease remains to be elucidated.…”

Section: Cardiac Autonomic Organizationmentioning

confidence: 99%

Autonomic Adjustments to Exercise in Humans

Fisher

Young

Fadel

2015

Comprehensive Physiology

226

253

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Autonomic nervous system adjustments to the heart and blood vessels are necessary for mediating the cardiovascular responses required to meet the metabolic demands of working skeletal muscle during exercise. These demands are met by precise exercise intensity-dependent alterations in sympathetic and parasympathetic nerve activity. The purpose of this review is to examine the contributions of the sympathetic and parasympathetic nervous systems in mediating specific cardiovascular and hemodynamic responses to exercise. These changes in autonomic outflow are regulated by several neural mechanisms working in concert, including central command (a feed forward mechanism originating from higher brain centers), the exercise pressor reflex (a feed-back mechanism originating from skeletal muscle), the arterial baroreflex (a negative feed-back mechanism originating from the carotid sinus and aortic arch), and cardiopulmonary baroreceptors (a feed-back mechanism from stretch receptors located in the heart and lungs). In addition, arterial chemoreceptors and phrenic afferents from respiratory muscles (i.e., respiratory metaboreflex) are also capable of modulating the autonomic responses to exercise. Our goal is to provide a detailed review of the parasympathetic and sympathetic changes that occur with exercise distinguishing between the onset of exercise and steady-state conditions, when appropriate. In addition, studies demonstrating the contributions of each of the aforementioned neural mechanisms to the autonomic changes and ensuing cardiac and/or vascular responses will be covered.

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Developmental Changes of α1-Adrenergic Chronotropic Action on Human Sinus Node

Cited by 15 publications

References 14 publications

LOW EXPRESSION OF α₁‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

LOW EXPRESSION OF α₁‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

Hypoxia increases exercise heart rate despite combined inhibition of β-adrenergic and muscarinic receptors

Autonomic Adjustments to Exercise in Humans

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Developmental Changes of α1-Adrenergic Chronotropic Action on Human Sinus Node

Cited by 15 publications

References 14 publications

LOW EXPRESSION OF α1‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

LOW EXPRESSION OF α1‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

Hypoxia increases exercise heart rate despite combined inhibition of β-adrenergic and muscarinic receptors

Autonomic Adjustments to Exercise in Humans

Contact Info

Product

Resources

About

LOW EXPRESSION OF α₁‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART

LOW EXPRESSION OF α₁‐ADRENERGIC RECEPTORS IN THE AGING HUMAN HEART