Non-esterified fatty acids increase arterial pressure via central sympathetic activation in humans

John P. Florian, James A. Pawelczyk

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Previous studies have shown that acute increases in plasma NEFAs (non-esterified fatty acids) raise SVR (systemic vascular resistance) and BP (blood pressure). However, these studies have failed to distinguish between CNS (central nervous system) mechanisms that raise sympathetic activity and paracrine mechanisms that increase SVR directly, independent of CNS involvement. The aim of the present study was to directly determine whether the sympathetic nervous system contributes to the pressor response to NEFAs. On 2 days separated by at least 2 weeks, 17 lean healthy volunteers (ten male/seven female; age, 22 ± 1 years; body mass index, 23 ± 1 kg/m2; values are means ± S.E.M.) received a 4-h intravenous infusion of 20% Intralipid® or placebo (in a single-blind randomized balanced order). MSNA (muscle sympathetic nerve activity), HR (heart rate), BP (oscillometric brachial measurement) and Q̇(cardiac output; acetylene rebreathing) were measured before and throughout infusion. The change in HR (+8.2 ± 1.0 and +2.4 ± 1.2 beats/min), systolic BP (+14.0 ± 1.6 and +3.2 ± 2.5 mmHg) and diastolic BP (+8.2 ± 1.0 and - 0.1 ± 1.7 mmHg) were significantly greater after the 4-h infusion of Intralipid® compared with placebo (P < 0.001). The change in BP with Intralipid® resulted from an increase in SVR (Q̇/mean arterial pressure; P < 0.001) compared with baseline, without a change in Q̇. MSNA burst frequency increased during Intralipid® infusion compared with baseline (+4.9 ± 1.3 bursts/min; P < 0.05), and total MSNA (frequency x amplitude) was augmented 65% (P < 0.001), with no change during placebo infusion. Lipid infusion increased insulin, aldosterone and F2-isoprostane, but not leptin, concentrations. On the basis of the concomitant increase in BP, MSNA and SVR, we conclude that central sympathetic activation contributes to the pressor response to NEFAs.

Original languageEnglish (US)
Pages (from-to)61-69
Number of pages9
JournalClinical Science
Volume118
Issue number1
DOIs
StatePublished - Jan 1 2010

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Arterial Pressure
Fatty Acids
Blood Pressure
Vascular Resistance
Muscles
Placebos
Central Nervous System
Heart Rate
F2-Isoprostanes
Acetylene
Sympathetic Nervous System
Leptin
Aldosterone
Intravenous Infusions
Cardiac Output
Healthy Volunteers
Body Mass Index
Arm
Insulin
Lipids

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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abstract = "Previous studies have shown that acute increases in plasma NEFAs (non-esterified fatty acids) raise SVR (systemic vascular resistance) and BP (blood pressure). However, these studies have failed to distinguish between CNS (central nervous system) mechanisms that raise sympathetic activity and paracrine mechanisms that increase SVR directly, independent of CNS involvement. The aim of the present study was to directly determine whether the sympathetic nervous system contributes to the pressor response to NEFAs. On 2 days separated by at least 2 weeks, 17 lean healthy volunteers (ten male/seven female; age, 22 ± 1 years; body mass index, 23 ± 1 kg/m2; values are means ± S.E.M.) received a 4-h intravenous infusion of 20{\%} Intralipid{\circledR} or placebo (in a single-blind randomized balanced order). MSNA (muscle sympathetic nerve activity), HR (heart rate), BP (oscillometric brachial measurement) and Q̇(cardiac output; acetylene rebreathing) were measured before and throughout infusion. The change in HR (+8.2 ± 1.0 and +2.4 ± 1.2 beats/min), systolic BP (+14.0 ± 1.6 and +3.2 ± 2.5 mmHg) and diastolic BP (+8.2 ± 1.0 and - 0.1 ± 1.7 mmHg) were significantly greater after the 4-h infusion of Intralipid{\circledR} compared with placebo (P < 0.001). The change in BP with Intralipid{\circledR} resulted from an increase in SVR (Q̇/mean arterial pressure; P < 0.001) compared with baseline, without a change in Q̇. MSNA burst frequency increased during Intralipid{\circledR} infusion compared with baseline (+4.9 ± 1.3 bursts/min; P < 0.05), and total MSNA (frequency x amplitude) was augmented 65{\%} (P < 0.001), with no change during placebo infusion. Lipid infusion increased insulin, aldosterone and F2-isoprostane, but not leptin, concentrations. On the basis of the concomitant increase in BP, MSNA and SVR, we conclude that central sympathetic activation contributes to the pressor response to NEFAs.",
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Non-esterified fatty acids increase arterial pressure via central sympathetic activation in humans. / Florian, John P.; Pawelczyk, James A.

In: Clinical Science, Vol. 118, No. 1, 01.01.2010, p. 61-69.

Research output: Contribution to journalArticle

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N2 - Previous studies have shown that acute increases in plasma NEFAs (non-esterified fatty acids) raise SVR (systemic vascular resistance) and BP (blood pressure). However, these studies have failed to distinguish between CNS (central nervous system) mechanisms that raise sympathetic activity and paracrine mechanisms that increase SVR directly, independent of CNS involvement. The aim of the present study was to directly determine whether the sympathetic nervous system contributes to the pressor response to NEFAs. On 2 days separated by at least 2 weeks, 17 lean healthy volunteers (ten male/seven female; age, 22 ± 1 years; body mass index, 23 ± 1 kg/m2; values are means ± S.E.M.) received a 4-h intravenous infusion of 20% Intralipid® or placebo (in a single-blind randomized balanced order). MSNA (muscle sympathetic nerve activity), HR (heart rate), BP (oscillometric brachial measurement) and Q̇(cardiac output; acetylene rebreathing) were measured before and throughout infusion. The change in HR (+8.2 ± 1.0 and +2.4 ± 1.2 beats/min), systolic BP (+14.0 ± 1.6 and +3.2 ± 2.5 mmHg) and diastolic BP (+8.2 ± 1.0 and - 0.1 ± 1.7 mmHg) were significantly greater after the 4-h infusion of Intralipid® compared with placebo (P < 0.001). The change in BP with Intralipid® resulted from an increase in SVR (Q̇/mean arterial pressure; P < 0.001) compared with baseline, without a change in Q̇. MSNA burst frequency increased during Intralipid® infusion compared with baseline (+4.9 ± 1.3 bursts/min; P < 0.05), and total MSNA (frequency x amplitude) was augmented 65% (P < 0.001), with no change during placebo infusion. Lipid infusion increased insulin, aldosterone and F2-isoprostane, but not leptin, concentrations. On the basis of the concomitant increase in BP, MSNA and SVR, we conclude that central sympathetic activation contributes to the pressor response to NEFAs.

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