Impaired baroreflex sensitivity (BRS) is associated with hypertension and cardiovascular risk. Lipid abnormalities accompanying insulin resistance may impair BRS. To test this, nine obese, dyslipidemic hypertensive and seven healthy normotensive individuals were studied. The BRS was measured during a phenylephrine infusion before and after nonesterified fatty acids (NEFAs) and triglycerides were raised for 1 h with an Intralipid and heparin infusion, ie, acute dyslipidemia. The obese group had higher values than lean controls for several components of the insulin resistance syndrome including blood pressure (BP) and heart rate, as well as fasting insulin, triglycerides, and NEFA. The BRS was lower in obese hypertensive subjects than healthy controls at baseline (P < .0001); BRS declined from 8.3 +/- 0.4 to 5.2 +/- 0.3 (P < .001) in obese hypertensive subjects and from 15.9 +/- 2.2 to 7.5 +/- 0.7 msec/mm Hg (P = .04) in controls with acute dyslipidemia. The reduction in BRS correlated with the rise in NEFAs (r = -0.59, P = .02) but not triglycerides (r = -0.07, P = NS). These observations indicate that elevating NEFAs acutely impairs BRS. The findings suggest that lipid abnormalities in obese hypertensives may contribute to elevated BP and increased cardiovascular events by impairing BRS.
Numerous challenges confront the development of a strong dental public health presence in US dental schools. These challenges include, among others, insufficient numbers of academic dental public health specialists and insufficient motivations to encourage promising candidates to pursue specialty status.
These nondiplomate teachers of predoctoral DPH desire training, but appear to have barriers and perceive few benefits to achieving DPH board certification.
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We have shown that lipid abnormalities present in obese hypertensives could contribute to their enhanced α
1
-adrenoceptor sensitivity. In this study, we examined if changing lipids with an intralipid/heparin infusion could contribute to impaired baroreflex sensitivity (BRS). To test this hypothesis, we compared the dose of the α
1
-adrenoceptor agonist, phenylephrine, to raise MAP 20 mmHg (PD
20
) before and after an infusion of intralipid/heparin. Also, we determined BRS by the ratio of the change in heart rate recorded in msec over the change in systolic BP in mmHg. We studied six obese hypertensive subjects with a mean age of 40.6 ± 2 and % body fat by DEXA of 30 ± 4%. Raising plasma NEFA levels lowered the PD
20
from a baseline of 1.21 to 0.8 μg/m
2
/min (p=0.05). With raising NEFAs, BRS was decreased from 6.3 ± 0.55 to 3.6 ± 0.42 msec/mmHg (p=0.02)(Δ = baseline measurements, ♦ = intralipid/heparin measurments). These data suggest that acute increases in plasma NEFAs enhance α
1
-adrenoceptor vascular reactivity and reduce BRS which may contribute to the maintenance of elevated BP in patients with obesity hypertension.
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