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      Differential contributions of cardiac, coronary and pulmonary artery vagal mechanoreceptors to reflex control of the circulation

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          Abstract

          Distinct populations of stretch‐sensitive mechanoreceptors attached to myelinated vagal afferents are found in the heart and adjoining coronary and pulmonary circulations. Receptors at atrio‐venous junctions appear to be involved in control of intravascular volume. These atrial receptors influence sympathetic control of the heart and kidney, but contribute little to reflex control of systemic vascular resistance. Baroreceptors at the origins of the coronary circulation elicit reflex vasodilatation, like feedback control from systemic arterial baroreceptors, as well as having characteristics that could contribute to regulation of mean pressure. In contrast, feedback from baroreceptors in the pulmonary artery and bifurcation is excitatory and elicits a pressor response. Elevation of pulmonary arterial pressure resets the vasomotor limb of the systemic arterial baroreflex, which could be relevant for control of sympathetic vasoconstrictor outflow during exercise and other states associated with elevated pulmonary arterial pressure. Ventricular receptors, situated mainly in the inferior posterior wall of the left ventricle, and attached to unmyelinated vagal afferents, are relatively inactive under basal conditions. However, a change to the biochemical environment of cardiac tissue surrounding these receptors elicits a depressor response. Some ventricular receptors respond, modestly, to mechanical distortion. Probably, ventricular receptors contribute little to tonic feedback control; however, reflex bradycardia and hypotension in response to chemical activation may decrease the work of the heart during myocardial ischaemia. Overall, greater awareness of heterogeneous reflex effects originating from cardiac, coronary and pulmonary artery mechanoreceptors is required for a better understanding of integrated neural control of circulatory function and arterial blood pressure.

          Abstract

          Abstract figure legend A schematic illustration of neural inputs to the cardiovascular control centre. The schema provides examples of typical afferent discharge, and related pressure traces, at several locations ( A) and depicts integration of vagal afferent signals arising from systemic arterial baroreceptors, pulmonary arterial baroreceptors, atrial volume receptors, coronary arterial receptors and ventricular receptors ( B). Impulse activity recorded from a pulmonary arterial receptor displays the familiar pattern associated with arterial baroreceptors. Atrial pattern type A displays a volley of impulses that corresponds with atrial systole and a decrease in atrial volume, whereas type B pattern corresponds to atrial diastole and filling of the atrium. Discharge from a coronary mechanoreceptor begins to rise before the aortic pressure and this corresponds the coronary perfusion pulse. Discharge from an unmyelinated vagal afferent increases briskly following injection of veratridine into the aortic root. The table summarizes fibre type, discharge pattern, activating stimuli and reflex effects. *Increase in vagal activity to the heart with no effect on sympathetic activity. #Increase in sympathetic activity to the heart with no effect on vagal activity or inotropy.

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          Pulmonary arterial pressure during rest and exercise in healthy subjects: a systematic review.

          According to current guidelines, pulmonary arterial hypertension (PAH) is diagnosed when mean pulmonary arterial pressure (Ppa) exceeds 25 mmHg at rest or 30 mmHg during exercise. Issues that remain unclear are the classification of Ppa values 30 mmHg during exercise is always pathological. We performed a comprehensive literature review and analysed all accessible data obtained by right heart catheter studies from healthy individuals to determine normal Ppa at rest and during exercise. Data on 1,187 individuals from 47 studies in 13 countries were included. Data were stratified for sex, age, geographical origin, body position and exercise level. Ppa at rest was 14.0+/-3.3 mmHg and this value was independent of sex and ethnicity. Resting Ppa was slightly influenced by posture (supine 14.0+/-3.3 mmHg, upright 13.6+/-3.1 mmHg) and age ( or = 50 yrs: 14.7+/-4.0 mmHg). Ppa during exercise was dependent on exercise level and age. During mild exercise, Ppa was 19.4+/-4.8 mmHg in subjects aged or = 50 yrs (p<0.001). In conclusion, while Ppa at rest is virtually independent of age and rarely exceeds 20 mmHg, exercise Ppa is age-related and frequently exceeds 30 mmHg, especially in elderly individuals, which makes it difficult to define normal Ppa values during exercise.
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            Sympathetic neural mechanisms in obstructive sleep apnea.

            Blood pressure, heart rate, sympathetic nerve activity, and polysomnography were recorded during wakefulness and sleep in 10 patients with obstructive sleep apnea. Measurements were also obtained after treatment with continuous positive airway pressure (CPAP) in four patients. Awake sympathetic activity was also measured in 10 age- and sex-matched control subjects and in 5 obese subjects without a history of sleep apnea. Patients with sleep apnea had high levels of nerve activity even when awake (P < 0.001). Blood pressure and sympathetic nerve activity did not fall during any stage of sleep. Mean blood pressure was 92 +/- 4.5 mmHg when awake and reached peak levels of 116 +/- 5 and 127 +/- 7 mmHg during stage II sleep (n = 10) and rapid eye movement (REM) sleep (n = 5), respectively (P < 0.001). Sympathetic activity increased during sleep (P = 0.01) especially during stage II (133 +/- 9% above wakefulness; P = 0.006) and REM (141 +/- 13%; P = 0.007). Peak sympathetic activity (measured over the last 10 s of each apneic event) increased to 299 +/- 96% during stage II sleep and to 246 +/- 36% during REM sleep (both P < 0.001). CPAP decreased sympathetic activity and blood pressure during sleep (P < 0.03). We conclude that patients with obstructive sleep apnea have high sympathetic activity when awake, with further increases in blood pressure and sympathetic activity during sleep. These increases are attenuated by treatment with CPAP.
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              Increased sympathetic nerve activity in pulmonary artery hypertension.

              This study tested the hypothesis that sympathetic nerve activity is increased in pulmonary artery hypertension (PAH), a rare disease of poor prognosis and incompletely understood pathophysiology. We subsequently explored whether chemoreflex activation contributes to sympathoexcitation in PAH. We measured muscle sympathetic nerve activity (MSNA) by microneurography, heart rate (HR), and arterial oxygen saturation (Sao(2)) in 17 patients with PAH and 12 control subjects. The patients also underwent cardiac echography, right heart catheterization, and a 6-minute walk test with dyspnea scoring. Circulating catecholamines were determined in 8 of the patients. Chemoreflex deactivation by 100% O(2) was assessed in 14 patients with the use of a randomized, double-blind, placebo-controlled, crossover study design. Compared with the controls, the PAH patients had increased MSNA (67+/-4 versus 40+/-3 bursts per minute; P<0.0001) and HR (82+/-4 versus 68+/-3 bpm; P=0.02). MSNA in the PAH patients was correlated with HR (r=0.64, P=0.006), Sao(2) (r=-0.53, P=0.03), the presence of pericardial effusion (r=0.51, P=0.046), and NYHA class (r=0.52, P=0.033). The PAH patients treated with prostacyclin derivatives had higher MSNA (P=0.009), lower Sao(2) (P=0.01), faster HR (P=0.003), and worse NYHA class (P=0.04). Plasma catecholamines were normal. Peripheral chemoreflex deactivation with hyperoxia increased Sao(2) (91.7+/-1% to 98.4+/-0.2%; P<0.0001) and decreased MSNA (67+/-5 to 60+/-4 bursts per minute; P=0.0015), thereby correcting approximately one fourth of the difference between PAH patients and controls. We report for the first time direct evidence of increased sympathetic nerve traffic in advanced PAH. Sympathetic hyperactivity in PAH is partially chemoreflex mediated and may be related to disease severity.
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                Author and article information

                Contributors
                j.p.moore@bangor.ac.uk
                Journal
                J Physiol
                J Physiol
                10.1111/(ISSN)1469-7793
                TJP
                jphysiol
                The Journal of Physiology
                John Wiley and Sons Inc. (Hoboken )
                0022-3751
                1469-7793
                29 August 2022
                15 September 2022
                29 August 2022
                : 600
                : 18 ( doiID: 10.1113/tjp.v600.18 )
                : 4069-4087
                Affiliations
                [ 1 ] School of Human and Behavioural Sciences Bangor University Bangor UK
                [ 2 ] Department of Sport Science University of Innsbruck Innsbruck Austria
                [ 3 ] Leeds Insititute for Cardiovascular and Metabolic Medicine University of Leeds Leeds UK
                Author notes
                [*] [* ] Corresponding author J. Moore: School of Human and Behavioural Sciences, Bangor University, Bangor LS57 2PZ, UK. Email: j.p.moore@ 123456bangor.ac.uk

                Author information
                https://orcid.org/0000-0002-4244-8220
                https://orcid.org/0000-0002-0357-6561
                https://orcid.org/0000-0002-9007-1130
                Article
                TJP15208
                10.1113/JP282305
                9544715
                35903901
                e5883788-9275-4415-8f24-eaa25b8dd624
                © 2022 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 October 2021
                : 19 July 2022
                Page count
                Figures: 7, Tables: 0, Pages: 19, Words: 13474
                Funding
                Funded by: Medical Research Council , doi 10.13039/501100000265;
                Funded by: British Heart Foundation , doi 10.13039/501100000274;
                Categories
                Topical Review
                Topical Review
                Custom metadata
                2.0
                15 September 2022
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.0 mode:remove_FC converted:07.10.2022

                Human biology
                baroreceptor reflex,cardiovascular control,sympathetic nerve activity,vagal afferent

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