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Bradykinin causes hypotension by activating pulmonary sympathetic afferents in the rabbit

Departments of ¹Medicine and ²Physiology and Biophysics, University of Louisville, Louisville 40292; ³Veterans Affairs Medical Center, Louisville 40206; ⁴Cardiopulmonary Science, Bellarmine University, Louisville, Kentucky 40205

Submitted 1 July 2002 ; accepted in final form 28 March 2003

Bradykinin (BK) activates sympathetic afferents in the heart, intestine, and kidney, and it alters hemodynamics. However, we know little about the influence of pulmonary sympathetic afferents on circulation. Activation of pulmonary afferents by directly injecting stimulants into the lung parenchyma permits examination of reflexes that originate in the lung without confounding effects from the systemic circulation. In the present study, we tested the hypothesis that pulmonary sympathetic afferents exert a significant influence on hemodynamics. We examined reflex effects of injecting BK (1 µg/kg in 0.1 ml) into the lung parenchyma on circulation in anesthetized, open-chest, artificially ventilated rabbits. BK significantly decreased mean arterial blood pressure (BP) (27 ± 3 mmHg) and heart rate (19 ± 4 beats/min). Both effects remained after bilateral vagotomy. To rule out possible direct systemic vasodilation by BK, we examined renal sympathetic nerve activity (RSNA) in response to BK injection and examined BP responses to injection of ACh (0.1 ml of 10^-4 M). BK suppressed the RSNA before and after vagotomy. ACh did not change BP when injected into the lung parenchyma, but it decreased BP (31 ± 3 mmHg) when injected into the right atrium. Our data indicate that activating pulmonary sympathetic afferents reflexly suppresses hemodynamics.

lung receptors; lung reflex; depressor effect; bradycardia

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