Plasma cyclic nucleotide levels in exercise-induced asthma.

Abstract

It is known that sympatho-adrenal control of airways is increased in asthma since blockade can cause severe bronchoconstriction in asthmatic individuals. It has not been established whether an altered catecholamine response to exercise plays any part in the production of the common symptom of exercise-induced asthma (EIA). We have investigated this indirectly by measuring arterial plasma cyclic nucleotide levels in 10 subjects with EIA and five normal subjects. Cyclic AMP, which in this context reflects fi stimulation, rose significantly by 25-4 % in the normal subjects during exercise, while there was no significant change during or after exercise ( < 5 %) in the asthmatic subjects. Cyclic GMP rose significantly after exercise in the asthmatic subjects. Six normal subjects repeated the protocol before and after inhalation of salbutamol aerosol, 1600 Htg daily for 18 days. This did not reduce the cAMP response to exercise, and we conclude that the diminished cAMP response of the asthmatic subjects was not caused by their medication. The results may indicate either impaired catecholamine production or endogenous fi receptor hyporesponsiveness in some asthmatic subjects and this may contribute to the development or EIA.

CSF Concentrations of cAMP and cGMP Are Lower in Patients with Creutzfeldt-Jakob Disease but Not Parkinson's Disease and Amyotrophic Lateral Sclerosis

“…Because of the profound degeneration of brain tissue, the decreased synthesis seems to be more likely. There is no concentration gradient between CSF and blood because they contain similar concentrations of cAMP and cGMP [44] . This fact makes an increased diffusion of the cyclic nucleotides into the blood unlikely that could result from an impairment of the blood-CSF-barrier in the choroid plexus.…”

Mechanisms of exercise‐induced asthma

“…Support for this view has been provided by studies demonstrating reduced sympathetic response to exercise in asthmatics than in normal subjects, and correction of this reduced sympathetic response by prior treatment of subjects with inhaled noradrenaline attenuated the bronchoconstrictor response to exercise [112-1141. However, other studies have failed to demonstrate any difference in the sympathetic response to exercise between asthmatic and normal subjects, or any rise in the catecholamines either during exercise or hypertonic challenge [70,115]. Recently, it was suggested that the catecholamine response to exercise may be mediated through release of atrial natriuretic peptide (ANP) which has been shown to dilate asthmatic airways.…”

Comparison between the effects of inhaled isoprenaline and fenoterol on plasma cyclic AMP and heart rate in normal subjects.

“…Other factors which may increase plasma cyclic AMP in normal subjects include stress, and strenuous exercise sufficient to increase the level of circulating catecholamines (Lin, 1978;Hartley et al, 1981); prolonged fasting may increase plasma cyclic AMP if continued for over 24 h (Mjos et al, 1977), and there is a small circadian variation in plasma cyclic AMP concentration during the day with a fall at night in phase with the diurnal fluctuation in endogenous catecholamine secretion (Mikuni et al, 1978). Plasma concentration of cyclic AMP is thought to originate as leakage of intracellular cyclic AMP into the extracellular space (Broadus et al, 1970(Broadus et al, , 1971.…”