Sympatho‐Excitation in Pulmonary Hypertension: The Potential Role of Pulmonary Arterial Baroreceptors: An Acute Physiologic Intervention Study

Background and Objective Sympathetic nerve activity is heightened in pulmonary arterial hypertension (PAH), promotes deleterious pulmonary vascular and right ventricular remodelling, and is associated with worsened exercise capacity and mortality. Pulmonary arterial baroreceptors, activated by increased pulmonary arterial pressure and distension, could drive muscle sympathetic nerve activity (MSNA) in pulmonary hypertension (PH). We hypothesised that pulmonary arterial baroreceptor unloading using nebulised iloprost as a pulmonary arterial vasodilator would lower MSNA in clinically stable treated PAH and chronic thromboembolic PH (CTEPH) patients. Methods In eleven PH patients (9 PAH, 2 CTEPH; 6 female; age 54 ± 14 years) common peroneal nerve microneurography was performed to record MSNA ( n = 9) at baseline (10 min) and immediately following iloprost nebulisation (10 min). Concurrent measures of cardiorespiratory physiology and pulmonary haemodynamics (transthoracic echocardiography) were obtained. Results Iloprost reduced systolic pulmonary artery pressure (50 ± 19 mmHg baseline vs. 44 ± 15 mmHg iloprost; p = 0.040), and increased right ventricular outflow tract acceleration time (RVOT AT; 99 ± 15 ms baseline vs. 117 ± 16 ms iloprost; p < 0.001). Although no overall change was seen in MSNA ( p > 0.05), the magnitude of change in MSNA burst size was inversely associated with the increase in RVOT AT (R 2 = 0.667, p = 0.0133). Conclusion These findings provide evidence suggestive of possible pulmonary arterial baroreceptor influence of MSNA burst amplitude in some PH patients. Pulmonary arterial baroreceptor activation may be a contributory mechanism to adverse sympatho‐excitation in PH.