Hypertension and triglyceride catabolism: implications for the hemodynamic model of the metabolic syndrome.

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Abstract
Objective: We sought to determine if hypertensive adults have a blunted triglyceride catabolic rate (TG K2) and if related hemodynamic and vascular alterations are determinants of TG K2. Methods: Fasting levels of insulin, glucose, lipoproteins and plasma catecholamines were measured in 10 normotensive and 10 hypertensive adults. TG K2 was determined by an intravenous fat tolerance test. Forearm blood flow, maximum forearm blood flow and minimal forearm vascular resistance were determined by strain gauge plethysmography. Vascular compliance and systemic hemodynamics were measured by computerized arterial pulse waveform analysis. Results: Compared to normotensives, hypertensives had a significantly elevated blood pressure (145 ± 8/94 ± 11 versus 111 ± 15/74 ± 14 mm Hg, p < 0.001), systemic vascular resistance (1695 ± 441 versus 1172 ± 430 dynes × sec × cm−5, p = 0.02) and reduced large vessel compliance (11.7 ± 3.6 versus 15.1 ± 3.1 ml/mm Hg × 100, p = 0.04). There were no significant group differences in TG K2 (3.07 ± 2.01 versus 2.88 ± 2.12 mg/dL/min, p = 0.85) or other metabolic and anthropometric variables. TG K2 was not predicted by the forearm vascular measures or the hemodynamic variables, but was correlated to waist/hip ratio (r = −0.71, p = 0.001), fasting triglycerides (r = −0.64, p = 0.003), and male gender (r = 0.56, p = 0.012). An enhanced TG K2 was independently predicted by a reduced small vessel compliance (r = −0.61, p = 0.006). Conclusions: Elevated blood pressure per se and hypertension-related hemodynamic and vascular alterations are not associated with reduced TG K2 or other metabolic abnormalities. Rather, aspects of the insulin resistance syndrome are closely related to abdominal adiposity. The independent association between small vessel compliance and TG K2 deserves further investigation.