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The lungs as receptor sites for cardiovascular regulation.
Author(s) -
JT Shepherd
Publication year - 1981
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.63.1.1
Subject(s) - medicine , receptor , cardiology
The heart and lungs contain numerous receptors that, when activated, can modulate the behavior of the heart and blood vessels. However, the separate roles of these two organs in causing the reflex circulatory adjustments are difflicult to assess. Present evidence indicates that the lungs can tonically inhibit the vasomotor center and that lung inflation causes a reflex decrease in blood pressure as a result of dilatation of systemic vessels, bradycardia and a negative inotropic effect on the ventricles. This lung inflationvasodepressor reflex is due to activation of low-threshold pulmonary stretch receptors, subserved by vagal afferents. The inhibition exerted by the lungs on the limb and kidney vessels is similar during normocapnia but, in certain species, the inhibition of the renal vessels becomes much greater during hypercapnia. Thus, receptors in the lungs may preserve renal blood flow during respiratory acidosis and therefore contribute to the restoration of acid-base balance. The lung inflation reflex also modulates the response to activation of the arterial chemoreceptors by attenuating the chemoreceptor-induced bradycardia and peripheral vasoconstriction. During diving, the annulment of the pulmonary depressor reflex by the reflex respiratory arrest permits the full expression of the trigeminal reflex and chemoreflex so that the arterial blood pressure is maintained by constriction of systemic vessels and the available oxygen is distributed to the mnost vulnerable systems, the brain and lungs. Other lung receptors can also affect the cardiovascular system in abnormal circumstances. Juxtapulmonary capillary receptors linked to nonmedullated vagal afferents can he activated by pulmonary congestion to cause reflex bradycardia, tachypnea and depression of the somatic nervous system. Mechanoreceptors in the pulmonary arteries, when activated with pressure up to 60 mm Hg, cause systemic hypotension and occasional bradycardia; with higher pressures, the systemic pressure increases. Some mechanoreceptors in the lung parenchyma, which increase their discharge with lung inflation, are subserved by medullated fibers that pass in the sympathetic nerves to the spinal cord. Their function is unknown.

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