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The sympathetic nervous system contributes to the pressor response to plasma fatty acids
Author(s) -
Florian John Paul,
Pawelczyk Jim
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a891
Subject(s) - medicine , blood pressure , sympathetic nervous system , placebo , heart rate , pressor response , endocrinology , autonomic nervous system , microneurography , vascular resistance , hemodynamics , mean arterial pressure , cold pressor test , anesthesia , cardiology , baroreflex , alternative medicine , pathology
Previous studies have shown that acute increases in plasma free fatty acids (FFA) raise systemic vascular resistance (SVR) and blood pressure (BP). However, these studies fail to distinguish between central nervous system (CNS) mechanisms that raise sympathetic activity and peripheral (paracrine) mechanisms that increase SVR directly independent of CNS involvement. On 2 days separated by at least 2 wks 15 lean, healthy volunteers (9M/6F; 22.3±0.9 yrs; BMI: 23.2±0.7; mean±SEM) received a 4‐hr iv infusion of Intralipid 20% or placebo (single‐blind, randomized, balanced order). Muscle sympathetic nerve activity (MSNA), heart rate (HR), BP (brachial auscultation), and cardiac output (Q, C2H2 rebreathing) were measured before and throughout infusion. The change in HR (+10.2±1.6 vs. +3.1±1.2 beats/min), systolic BP (+15.6±1.2 vs. +2.5±2.6 mmHg), and diastolic BP (+8.9±1.1 vs. −0.9±1.9 mmHg) was significantly greater after the 4‐hr infusion of Intralipid vs. placebo (p<.001). The change in BP with Intralipid resulted from an increase in SVR (mean BP/Q; p=0.014), without a change in Q. MSNA augmentation tended to increase during Intralipid infusion vs. baseline (+5.2±1.8; p=.053), with no change following placebo infusion. Based on the concomitant increase in BP, SVR, and possibly MSNA, we conclude that central sympathetic activation contributes to the pressor response to FFA. Support ‐ ACSM FRG, NIH MO1RR10732