The sympathetic nervous system in hypertension

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Abstract
To determine if the contribution of the sympathetic nervous system to blood pressure could be evidenced by low-frequency oscillations of systolic blood pressure (LFSBP), reflecting vascular sympathetic modulation, or by the decrease in blood pressure after autonomic blockade. We studied multiple system atrophy (MSA) patients, in whom supine hypertension is maintained by residual sympathetic tone (`positive controls'); pure autonomic failure (PAF) patients, in whom supine hypertension is largely independent of sympathetic tone (`negative controls'); essential hypertensive patients (HTN) and normotensive subjects (NTN). Supine systolic blood pressure (SBP) was 204 ± 8, 185 ± 6, 177 ± 9 and 130 ± 4 mmHg in MSA, PAF, HTN and NTN, respectively. LFSBP was higher in MSA and HTN (5.7 ± 1.5 and 5.8 ± 1.4 mmHg2) compared to NTN and PAF (3.3 ± 0.5 and 1.1 ± 0.5 mmHg2). Trimethaphan 2–4 mg/min induced complete autonomic blockade and lowered SBP below 125 mmHg in all NTN and all but one MSA (to 111 ± 3 and 97 ± 9 mmHg). SBP remained elevated in PAF (164 ± 7 mmHg). Responses in HTN were variable; SBP decreased below 125 mmHg in three and remained elevated in four patients. The decrease in LFSBP correlated with the reduction in SBP, with a steeper slope in MSA and HTN compared to NTN (29.0 ± 5.5, 8.4 ± 1.6 and 3.6 ± 1.2 mmHg/mmHg2, respectively). Ganglionic blockade, alone or coupled to LFSBP, discriminated between human models of sympathetic-dependent (MSA) and independent (PAF) hypertension. This approach may aid in assessing the contribution of the sympathetic nervous system in essential hypertension, in which sympathetic dependence is variably expressed.