DOES NORMOXIC PULMONARY VASODILATATION RATHER THAN HYPOXIC VASOCONSTRICTION ACCOUNT FOR THE PULMONARY PRESSOR RESPONSE TO HYPOXIA?

doi:10.1016/S0140-6736(78)90138-1

The Lancet

Volume 311, Issue 8062, 4 March 1978, Pages 476-477

https://doi.org/10.1016/S0140-6736(78)90138-1 Get rights and content

Abstract

A mediator of the pulmonary pressor response to hypoxia has not been found. The pressor phenomenon could be explained if the pulmonary vasodilatation present during normoxia were maintained by a vasodilator substance such as bradykinin. Ventilation of the lungs with air or oxygen causes the release of bradykinin which is rapidly inactivated in the lungs. Inhibition of the inactivating enzyme prevents the development of pulmonary hypertension in response to chronic hypoxia. Bradykinin is formed in the blood and is also present in alveolar macrophages, which arise from precursors in hæmatopoietic tissue. Formation of bradykinin by granulocytes is critically dependent on the local oxygen tension. The enzyme which inactivates bradykinin also converts angiotensin I to angiotensin II and thus provides a mechanism for interaction between the pulmonary and systemic vasculatures. The rate of inactivation of bradykinin may be altered by small changes in pH. It is postulated that when bradykinin production is reduced during hypoxia the higher tone of the pulmonary vascular smooth muscle, maintained by numerous constrictor stimuli, asserts itself.

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HypothesisDOES NORMOXIC PULMONARY VASODILATATION RATHER THAN HYPOXIC VASOCONSTRICTION ACCOUNT FOR THE PULMONARY PRESSOR RESPONSE TO HYPOXIA?

Abstract

Am. J. Cardiol.

Pediatrics, Springfield

Circulation Res.

J. Physiol.

J. Physiol.

Prog. Resp. Res.

J. Physiol.

Foetal and Neonatal Physiology

Circulation Res.

Am. Rev. resp. Dis.

Fedn Proc.

J. clin. Invest.

Am. Rev. resp. Dis.

Hypothesis
DOES NORMOXIC PULMONARY VASODILATATION RATHER THAN HYPOXIC VASOCONSTRICTION ACCOUNT FOR THE PULMONARY PRESSOR RESPONSE TO HYPOXIA?