Mechanism of lipid enhancement of α1-adrenoceptor pressor sensitivity in hypertension

Gadegbeku, Crystal A.; Shrayyef, Muhammad; Taylor, Timothy P.; Egan, Brent M.

doi:10.1097/01.hjh.0000234119.63519.5a

Cited by 9 publications

(14 citation statements)

References 37 publications

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“…In contrast to our finding of preserved cardiovagal BRS in the face of acute hyperlipidemia, two previous humans studies reported impairments using an identical infusion protocol (8,9). There are at least several differences between these previous studies and ours that may help to explain the discrepant findings.…”

Section: Discussioncontrasting

confidence: 99%

“…Second, baroreflex dysfunction may contribute to increased sympathetic outflow at rest due to an impaired ability of the baroreflexes to tonically restrain sympathetic outflow. Although these previous studies (8,9) are important, they do not provide evidence that systematic changes in baroreflex function occurred since only the cardiac arm, and not the sympathetic arm of the baroreflex, was studied.…”

mentioning

confidence: 93%

“…In addition to the possibility that acute hyperlipidemia elicits sympathoexcitation at rest, several previous studies in humans have observed impaired cardiac baroreflex function after acute hyperlipidemia (8,9). Impaired baroreflex function may be important in several different regards.…”

mentioning

confidence: 99%

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Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans

Monahan¹,

Dyckman²,

Ray³

2007

Journal of Applied Physiology

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Blood lipids may detrimentally affect autonomic and circulatory control. We tested the hypotheses that acute elevations in free fatty acids and triglycerides (acute hyperlipidemia) impair baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA: sympathetic BRS), increase MSNA at rest, and augment physiological responses to exercise. Eighteen young adults were examined in this randomized, double-blinded, and placebo-controlled study. BRS was determined using the modified Oxford technique before (pre) and 60 min (post) after initiating infusion of Intralipid (0.8 ml x m(-2) x min(-1)) and heparin (1,000 U/h) (experimental; n = 12) to induce acute hyperlipidemia, or saline (0.8 ml x m(-2) x min(-1)) and heparin (1,000 U/h) (control; n = 6). Responses to isometric handgrip to fatigue (IHG) were also determined. Blood pressure increased more (P < 0.05) in experimental than control subjects during the infusion. MSNA at rest (14 +/- 2 vs. 11 +/- 1 bursts/min), cardiovagal (19.8 +/- 1.8 vs. 19.1 +/- 2.4 ms/mmHg pre and post, respectively) and sympathetic BRS (-5.5 +/- 0.6 vs. -5.2 +/- 0.4 au x beat(-1) x mmHg(-1)), and the neural and cardiovascular responses to IHG were unchanged by acute hyperlipidemia (pre vs. post) in experimental subjects. Similarly, MSNA at rest (10 +/- 2 vs. 12 +/- 2 bursts/min), cardiovagal (22.1 +/- 4.0 vs. 21.0 +/- 4.6 ms/mmHg) and sympathetic BRS (-5.8 +/- 0.5 vs. -5.5 +/- 0.5 au x beat(-1) x mmHg(-1)), and the neural and cardiovascular responses to IHG were unchanged by the infusion in control subjects. These data do not provide experimental support for the concept that acute hyperlipidemia impairs reflex cardiovagal or sympathetic regulation in humans.

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Section: Discussioncontrasting

confidence: 99%

mentioning

confidence: 93%

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Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans

Monahan¹,

Dyckman²,

Ray³

2007

Journal of Applied Physiology

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“…Two studies have presented conflicting evidence regarding acute baroreflex resetting and reduced baroreflex sensitivity in response to 1-h lipid infusion [14,44]. Although our present study was not designed to assess baroreflex function, the concomitant increase in BP, HR and MSNA supports the concept of resetting of the arterial baroreflexes to defend higher pressures.…”

Section: Baroreflex Modulationsupporting

confidence: 70%

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

Florian

Pawelczyk

2009

Clinical Science

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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 Q (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 (Q/mean arterial pressure; P<0.001) compared with baseline, without a change in Q. MSNA burst frequency increased during Intralipid infusion compared with baseline (+4.9+/-1.3 bursts/min; P<0.05), and total MSNA (frequencyxamplitude) 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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“…Cholylglycine is one of the components of bile acid, and bile acid can consume the fat. The increased cholylglycine resulted from the rise of fat, which could lead to the rapid arterial baroreceptor resetting, baroreflex sensitivity reduction, and increased blood pressure 19, 20. Cholylglycine reduction observed after the treatment of Ping Gan prescription suggested that abnormal fat metabolism may be involved in the pathway of hypertension.…”

Section: Resultsmentioning

confidence: 99%

Application of ultra‐performance liquid chromatography coupled with mass spectrometry to metabonomic study on spontaneously hypertensive rats and intervention effects of Ping Gan prescription

Jiang

Xie

2012

J of Separation Science

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This study describes the metabonomic characters of the spontaneously hypertensive rats (SHR) and intervention effects of Ping Gan prescription. Ultra performance LC coupled with Q-TOF MS (UPLC/MS-Q-TOF) was employed to develop a metabonomic method of the plasma of SHR. There was a significant difference in metabolic profiling observed between predose group of Wistar Kyoto rats and model group (SHR) by using the principal components analysis (PCA). Some significant changes in metabolites such as LysoPC(22:6), LysoPC(20:4), LysoPC(18:1), cholylglycine, PE(P-16:0e/0:0), sphingosine-1-phosphate, and 2-oxo-4-methylthio butanoic acid were identified. These biochemical changes were associated with the disturbance in sphingolipid metabolism and fat metabolism, which would be helpful to further understand the essence of hypertension and the therapeutic mechanism of Ping Gan prescription. This study suggests that the metabonomic method may be a valuable and feasible tool to explore the therapeutic effect and mechanism of traditional Chinese medicine (TCM).

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Mechanism of lipid enhancement of α1-adrenoceptor pressor sensitivity in hypertension

Abstract: These findings suggest that in hypertensive patients, the primary mechanism for short-term alpha1-pressor hypersensitivity in response to hyperlipidemia is via the acute impairment of BRS.

Cited by 9 publications

References 37 publications

Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans

Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans

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

Application of ultra‐performance liquid chromatography coupled with mass spectrometry to metabonomic study on spontaneously hypertensive rats and intervention effects of Ping Gan prescription

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