Impact of Type 2 Diabetes Mellitus on Sympathetic Neural Mechanisms in Hypertension

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Abstract

Background-Essential hypertension (EHT) is a major cardiovascular risk factor, and the additional presence of type 2 diabetes mellitus (DM2) increases this risk. However, although the sympathetic nerve hyperactivity of EHT is known to play a role in cardiovascular risk, the level of sympathetic nerve activity is known neither in DM2 nor in hypertensive type 2 diabetic patients (EHT+DM2). Therefore, we planned to quantify the vasoconstrictor sympathetic nerve activity in patients with EHT+DM2 and with DM2 relative to that in matched groups with EHT and normal blood pressure (NT). Methods and Results-In 68 closely matched subjects with EHT+DM2 (n = 17), DM2 (n = 17), EHT (n = 17), and NT (n = 17), we measured resting muscle sympathetic nerve activity as the mean frequency of multiunit bursts (MSNA) and of single units (s-MSNA) with defined vasoconstrictor properties. The s-MSNA in EHT+DM2 (97±3.8 impulses/100 beats) was greater (at least P<0.001) than in EHT (69±3. 4 impulses/100 beats) and DM2 (78±4.1 impulses/100 beats), and all these were significantly greater (at least P<0.01) than in NT (53±3.3 impulses/100 beats) despite similar age and body mass index. The MSNA followed a similar trend. In addition, the level of insulin was also raised in EHT+DM2 (20.4±3.6 μU/mL) and DM2 (18.1±3.1 μU/mL; at least P<0.05) compared with HT or NT. Conclusions-Patients with EHT+DM2, EHT, or DM2 had central sympathetic hyperactivity, although plasma insulin levels were raised only in EHT+DM2 and DM2. The combination of EHT and DM2 resulted in the greatest sympathetic hyperactivity and level of plasma insulin, and this hyperactivity could constitute a mechanism for the increased risks of this condition.

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APA

Huggett, R. J., Scott, E. M., Gilbey, S. G., Stoker, J. B., Mackintosh, A. F., & Mary, D. A. S. G. (2003). Impact of Type 2 Diabetes Mellitus on Sympathetic Neural Mechanisms in Hypertension. Circulation, 108(25), 3097–3101. https://doi.org/10.1161/01.CIR.0000103123.66264.FE

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