Lung inflation activates low-threshold pulmonary stretch receptors to cause a reflex decrease in blood pressure, bradycardia, and negative inotropic effects, modulating cardiovascular regulation.
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 restora- tion 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. Dur- ing diving, the annulment of the pulmonary depressor reflex by the reflex respiratory arrest permits the full ex- pression of the trigeminal reflex and chemoreflex so that the arterial blood pressure is maintained by constric- tion of systemic vessels and the available oxygen is distributed to the mnost vulnerable systems, the brain and lungs.
JT Shepherd (1981) conducted a review in Cardiovascular regulation. Lung inflation activates low-threshold pulmonary stretch receptors to cause a reflex decrease in blood pressure, bradycardia, and negative inotropic effects, modulating cardiovascular regulation.