Transient Increases In Blood Pressure After Spontaneous Bursts Of Muscle Sympathetic Nerve Activity: Contributions Of Cardiac Output And Systemic Vascular Conductance

Abstract

Previously, a latency of 5.5 seconds between the occurrence of a burst of muscle sympathetic nerve activity (MSNA) and the subsequent peak arterial blood pressure (BP) response was reported. Although this BP increase was thought to be primarily due to peripheral vasoconstriction, beat-to-beat vascular conductance measures were not made. Furthermore, a transient cardio-acceleration was observed following MSNA bursts. However, whether an increase in cardiac output contributes to the BP response is unknown. PURPOSE: To assess the beat-to-beat fluctuations in cardiac output (CO) and systemic vascular conductance (SVC) following a spontaneous burst of MSNA. METHODS: In 7 young men, BP (finger photoplethysmography), stroke volume (SV; Modelflow), heart rate (HR; ECG) and MSNA (microneurography) were continuously measured during 30 minutes of supine rest. Beat-to-beat fluctuations in BP, CO (HR × SV) and systemic vascular conductance (SVC; CO/MAP) were characterized for 15 cardiac cycles following each individual MSNA burst using signal averaging to identify the temporal pattern for each variable and a peak response was calculated. RESULTS: A significant rise in diastolic BP was observed following each burst of MSNA with a peak increase of 4.35 ± 0.5 mmHg (+6.6 ± 0.7%; p<0.05) occurring at a latency of 5.4 ± 0.2 s. Within the first 2 cardiac cycles following an MSNA burst, the immediate (1.7 ± 0.05 s) increase in BP was associated with a 0.49 ± 0.10 L (+10 ± 0.03%; p<0.05) increase in CO. SVC was also transiently increased with CO during this initial period but then subsequently decreased by -0.005 ml·min-1mmHg-1 (-8.1 ± 0.4%; p<0.05), reaching a maximum reduction around the time of the peak increase in BP. CONCLUSIONS: These preliminary findings indicate that spontaneous bursts of MSNA consistently produce elevations in BP that appear to be mediated by alterations in both CO and SVC. The initial rise in BP is associated with an increase in CO that transitions to peripheral vasoconstriction, noted by the significant fall in SVC at the time of the peak BP response. Thus, it appears that both central and peripheral adjustments contribute to the transient rise in BP following a spontaneous burst of MSNA.