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1 Department of Medicine, University of Louisville, Louisville, KY, USA
2 VA Medical Center, Louisville, KY, USA
3 Department of Cardiopulmonary Science, Bellarmine University, Louisville, KY, USA
4 Department of Medicine, University of Louisville, Louisville, KY, USA; Department of Physiology, University of Louisville, Louisville, KY, USA
* To whom correspondence should be addressed. E-mail: j0yu0001{at}gwise.louisville.edu.
Bradykinin (BK) activates sympathetic afferents in the heart, intestine, and kidney, and alters hemodynamics. However, we know little about the influence of pulmonary sympathetic afferents on circulation. Activating pulmonary afferents by directly injecting stimulants into the lung parenchyma permits examining 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 (1µg/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 mm Hg) 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 Acetylcholine (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 decreased BP (31±3 mm Hg) when injected into the right atrium. Our data indicate that activating pulmonary sympathetic afferents reflexly suppresses hemodynamics.
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