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(Hypertension. 1998;32:693-698.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Intralipid Enhances ₁-Adrenergic Receptor–Mediated Pressor Sensitivity

Adetola T. Haastrup; Konrad T. Stepniakowski; Theodore L. Goodfriend; ; Brent M. Egan

From the Division of Clinical Pharmacology, Departments of Pharmacology and Medicine, Medical University of South Carolina, Charleston, SC.

Correspondence to Brent M. Egan, MD, Division of Clinical Pharmacology, Medical University of South Carolina, 171 Ashley Ave, CSB 826H, Charleston, SC 29425. E-mail eganbm{at}musc.edu

Abstract—The dyslipidemia in obese hypertensive persons may contribute to their increased vascular -adrenergic receptor reactivity and tone. To further examine this notion, we conducted 2 studies of pressor sensitivity to phenylephrine, an ₁-adrenergic receptor agonist, in lean normotensive subjects. In the first study (n=6), pressor responses to phenylephrine were obtained before and during a saline and heparin infusion. On another day, pressor reactivity to phenylephrine was measured before and during infusion of 20% Intralipid at 0.5 mL · m^-2 · min^-1 with heparin at 1000 U/h to increase lipoprotein lipase activity and raise nonesterified fatty acids (NEFAs). In the second study (n=8), baseline reactivity to phenylephrine was obtained on 2 separate days and repeated after raising NEFAs and triglycerides either with 0.8 mL · m^-2 · min^-1 of 20% Intralipid alone or together with heparin. The infusion of saline and heparin did not significantly change plasma NEFAs from baseline (516±90 versus 512±108 µmol/L, respectively; P=NS) or the dose of phenylephrine required to raise mean blood pressure by 20 mm Hg ([PD_20PE]; 1.00±0.14 versus 0.95±0.10 µg · kg^-1 · min^-1, respectively, P=NS). Intralipid at 0.5 mL · m^-2 · min^-1 with heparin raised plasma NEFAs to 793±30 µmol/L per liter (P<0.05 versus baseline) and reduced PD_20PE from 1.01±0.10 to 0.80±0.09 µg · kg^-1 · min^-1 (P<0.05). Compared with baseline, Intralipid alone increased plasma NEFAs to 946±80 µmol/L (P<0.05), and NEFAs increased further with the addition of heparin to 2990±254 µmol/L (P<0.01). Despite an apparently greater increase of plasma NEFAs with Intralipid and heparin, Intralipid alone and together with heparin similarly reduced PD_20PE. Across all study conditions, changes in levels of triglycerides and NEFAs correlated with changes in mean arterial pressure responses to phenylephrine, especially at the 0.4-µg · kg^-1 · min^-1 infusion rate of phenylephrine (r=0.64, P<0.01 and r=0.54, P<0.01, respectively). These data suggest that raising levels of plasma NEFAs and/or triglycerides enhances ₁-adrenoceptor–mediated pressor sensitivity. The findings suggest that lipid abnormalities in obese hypertensives, which include elevated NEFAs and triglycerides, contribute to greater vascular ₁-adrenergic reactivity.

Key Words: fatty acids • phenylephrine • receptors, adrenergic • blood pressure

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