Adenosine‐induced respiratory stimulation in man depends on site of infusion. Evidence for an action on the carotid body?

Watt, Andrew; Reid, PG; Stephens,; Routledge, PA

doi:10.1111/j.1365-2125.1987.tb03081.x

Cited by 79 publications

(57 citation statements)

References 18 publications

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“…Since the response in MSNA did not differ significantly be tween LBNP and adenosine, involvement of the baroreflex could still account for the residual increase in MSNA but not for the residual heart rate response, since this was markedly different from the response to LBNP. Adenosine increases tidal volume Watt et al 1987;Smits et al 1987b) and thereby stimulates pulmonary stretch receptors. However, the heart rate response to adenosine is not affected by pulmonary denervation in humans, indicating that these receptors are not involved in the heart rate response to adeno sine (Morgan-Hughes et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Rongen¹,

Senn²,

Ando³

et al. 1997

Can. J. Physiol. Pharmacol.

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Adenosine increases heart rate and sympathetic nerve activity reflexively in conscious humans through several mechanisms. The purpose of this study was to assess the relative contributions of arterial baroreceptor unloading, carotid chemoreceptor stimulation, and other adenosine-sensitive afferent nerves to these responses. In 12 healthy men, the effect on blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA; peroneal nerve) of lower body negative pressure (LBNP; -15 mmHg (1 mmHg =133.3 Pa)) was compared with the effect of intravenous adenosine (35, 70, and 140 |ag*kg"1*min_1). In eight subjects, the highest dose was reinfused during 100% oxygen to suppress arterial chemoreceptors. Blood pressure reductions during LBNP and adenosine (140 jxg-kg'^min"1) were similar. HR did not change significantly during LBNP (+2 ± 2 beats/min; mean ± SE) but increased at the highest adenosine dose (+25 ± 3 beats/min; p < 0.05). MSNA increased significantly (p < 0.05) during both interventions (+255 ± 82 and +247 ± 5 8 units/100 beats for adenosine and LBNP, respectively), and there was no difference in the MSNA response to these two stimuli (p > 0.1). Oxygen inhibited adenosine-induced increases in HR and MSNA (from +305 ± 99 to +198 ± 75 units/100 beats and from +26 ± 4 to +18 ± 3 beats/min;p < 0.05 for both comparisons). The MSNA response to these combined stimuli was similar to that observed during LBNP. In contrast, the residual HR response (+18 ± 3 beats/min) was significantly greater than the response to LBNP (+2 ± 2 beats/min; p < 0.05). These data indicate that arterial baroreceptor unloading cannot account for the marked adenosine-induced increase in HR, but may be sufficient to explain its effect on MSNA. The effect of 100% oxygen confirms that stimulation of carotid chemoreceptors accounts for approximately one-third of the HR and MSNA response to adenosine. However, other mechanisms, such as stimulation of adenosine-sensitive afferent nerves in other vascular beds, are involved in the HR and possibly the MSNA response.Key words: adenosine, human, heart rate, sympathetic nervous system, baroreflex.Résumé : L 'adénosine augmente la fréquence cardiaque et l'activité nerveuse sympathique de manière réflexe chez les humains conscients et ce, par 1*intermédiaire de divers mécanismes. Le but de la présente étude a été d'évaluer l'influence sur ces réponses d'une décharge des barorécepteurs artériels, d'une stimulation des chémorécepteurs carotidiens, ainsi que d'autres nerfs afférents sensibles à Padénosine. Chez 12 hommes sains, on a comparé l'effet d 'une pression négative des membres inférieurs (PNMI; -15 mmHg (1 mmHg = 133,3 Pa)) avec celui de Padénosine intraveineuse (35, 70 et 140 jig-kg^-m ür1) sur la pression artérielle, la fréquence cardiaque (FC) et l'activité nerveuse sympathique musculaire (ANSM; nerf périonnier). Chez huit sujets, on a réinjecté la plus forte dose d'adénosine en présence de 100% d'oxygène afin de supprimer les chémorécepteurs artériels. Les réductions de press...

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Section: Discussionmentioning

confidence: 99%

Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Rongen¹,

Senn²,

Ando³

et al. 1997

Can. J. Physiol. Pharmacol.

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“…1 Intravenous adenosine produces vasodilatation in coronary and noncoronary vascular beds, which typically decreases mean blood pressure (BP) a -10% to -15% during stable hyperemia. 2 Nevertheless, observational 3,4 and experimental studies [5][6][7] have observed a large interpatient variability in the BP response to intravenous adenosine, with most patients developing mild hypotension, whereas in others, BP profoundly decreases during stable hyperemia. The possible relevance of these varying BP responses to intravenous adenosine for stenosis assessment with FFR, however, has been barely addressed in the literature.…”

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confidence: 99%

Low Coronary Microcirculatory Resistance Associated With Profound Hypotension During Intravenous Adenosine Infusion

Echavarría‐Pinto

Gonzalo

Ibáñez

et al. 2014

Circ: Cardiovascular Interventions

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“…The value calculated on placebo for the mean slope of the regression of ventilation upon PET,CO 2 Hyperoxic, hypercapnic responses were studied in an attempt to elucidate central adenosine-related mechanisms. The carotid bodies in animals [12,13], and also probably in humans [4,5], are stimulated directly by adenosine. Centrally-mediated respiratory depression by adenosine has also been observed in animals [14].…”

Section: Discussionmentioning

confidence: 99%

“…These drugs would be expected to enhance and attenuate adenosine-related mechanisms, respectively. The presence of hyperoxia is important in these experiments as, under these conditions, afferent activity from the carotid bodies (a site at which exogenous [4,5] and endogenous [3] adenosine may stimulate breathing) is attenuated.…”

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confidence: 99%

The effect of dipyridamole and theophylline on hypercapnic ventilatory responses: the role of adenosine

Griffiths

Christie²,

Parsons³

et al. 1997

Eur Respir J

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The purine nucleoside, adenosine, has been implicated as a neuromodulator in central respiratory depression during prolonged exposure to hypoxia. It may also be a mediator of hypoxic hyperpnoea, acting on the carotid bodies. As there may be adenosine-sensitive mechanisms of hypoxic respiratory control, we sought to determine whether adenosine might be involved as a respiratory modulator in another central but non-oxygen-related control mechanism, the ventilatory response to hyperoxic hypercapnia.Twelve normal subjects were studied following 3 days of oral treatment with placebo, dipyridamole (which potentiates adenosine effects by inhibiting cellular uptake), and theophylline (a specific adenosine antagonist of cell surface receptors). The drugs were given in a random order, double-blind fashion. Resting endtidal carbon dioxide tension (PET,CO 2 ) and the maximum rate of isometric inspiratory pressure change at the mouth ((dP/dt )max), an index of respiratory drive, were determined in all subjects on each treatment. Hyperoxic, hypercapnic ventilatory responses were determined in seven of these subjects using a rebreathing technique. For each hypercapnic response, minute ventilation (V 'E) and (dP/dt )max were plotted against PET,CO 2 breath-by-breath.Resting PET,CO 2 breathing room air was lower with theophylline (5.47 (SD 0.21) kPa) than with placebo (5.74 (0.26) kPa) or dipyridamole (5.86 (0.34) kPa), with no significant drug differences in resting (dP/dt )max. However, neither the slope nor the PET,CO 2 intercept of the relationship between ventilation or respiratory drive and PET,CO 2 were altered by the study drugs under hyperoxic conditions. We conclude that endogenous adenosine-related mechanisms are unlikely to be involved in determining either the sensitivity or the threshold of the ventilatory response to carbon dioxide under hyperoxic conditions. However, in normoxia, a centrally-acting, tonic, adenosine-mediated, respiratory modulation is not ruled out.

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Adenosine‐induced respiratory stimulation in man depends on site of infusion. Evidence for an action on the carotid body?

Cited by 79 publications

References 18 publications

Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Comparison of hemodynamic and sympathoneural responses to adenosine and lower body negative pressure in man

Low Coronary Microcirculatory Resistance Associated With Profound Hypotension During Intravenous Adenosine Infusion

The effect of dipyridamole and theophylline on hypercapnic ventilatory responses: the role of adenosine

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