Increased Sympathetic Nerve Activity in Pulmonary Artery Hypertension

Abstract

Background-This study tested the hypothesis that sympathetic nerve activity is increased in pulmonary artery hypertension (PAH), a rare disease of poor prognosis and incompletely understood pathophysiology. We subsequently explored whether chemoreflex activation contributes to sympathoexcitation in PAH. Methods and Results-We measured muscle sympathetic nerve activity (MSNA) by microneurography, heart rate (HR), and arterial oxygen saturation (SaO 2 ) in 17 patients with PAH and 12 control subjects. The patients also underwent cardiac echography, right heart catheterization, and a 6-minute walk test with dyspnea scoring. Circulating catecholamines were determined in 8 of the patients. Chemoreflex deactivation by 100% O 2 was assessed in 14 patients with the use of a randomized, double-blind, placebo-controlled, crossover study design. Sympathetic hyperactivity in PAH is partially chemoreflex mediated and may be related to disease severity.

Outcomes of β-blocker use in pulmonary arterial hypertension: a propensity-matched analysis

“…Attention has recently been focused on neurohormonal alterations in PAH patients and abnormalities of the sympathetic nervous system, similar to those described in left ventricular dysfunction [5,6,17]. Our clinical findings correlate with the accumulating evidence of sympathetic overactivation in patients with …”

“…In contrast, recent evidence indicates that there is an excessive sympathetic activation in PAH patients [5,6] which may portend a worse prognosis [6][7][8]. Attention has also focused on the diverse role of β-blockers on RV function in PAH patients.…”

Impairment of Autonomic Nervous System Activity in Patients With Pulmonary Arterial Hypertension: A Case Control Study

“…32,33 In a recent interesting study, increased sympathetic nerve activity has been shown in PAH, suggesting that the mechanism may partially explained by chemo-reflex mediation. 34 On the other hand, increased plasma levels of catecholamines have been found in patients with pulmonary hypertension and right heart failure, [35][36][37] as well as increased oxidative stress and low synthesis of cAMP indicating beta 2 -adrenoreceptor desensitization. 36,37 Furthermore, carvedilol administration in a small cohort of patients with pulmonary hypertension has shown positive effects in their clinical status because of beta 2 -adrenoreceptor resensitization.…”

Hyponatremia Predicts Right Heart Failure and Poor Survival in Pulmonary Arterial Hypertension

“…HN in LHF reflects nonosmotic release of vasopressin consequent to activation of the sympathetic and renin-angiotensin-aldosterone system axes (7,8), and thus a low serum sodium reflects neurohormonal axis activation in these patients, as well as in other hypervolemic hyponatremic states such as cirrhosis and nephrotic syndrome (6,7,21). Importantly, neurohormonal activation has also been demonstrated in patients with PAH, and occurs in proportion to the degree of RV dysfunction (22,23). Thus, it is tempting to speculate that the HN observed in our patients with PAH resulted from neurohormonal activation in response to their more advanced RV dysfunction and that HN is not simply a marker but in fact a consequence of more advanced RV function and hemodynamics in patients with PAH.…”