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Updated: May 1, 2026

Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
Published on: September 11, 2018
Cardiovascular responsiveness to sympathoexcitatory stress in subjects with and without mild hypertension
Elliott R Carthy1, Leigh White, Fraser D Russell
1Inflammation and Healing Research Cluster, School of Health and Sport Sciences, University of the Sunshine Coast, Maroochydore, Qld, Australia.
Purpose:
This study compared blood pressure, heart rate variability (HRV) and forearm blood flow, at rest and in response to sympathoexcitatory stressors between normotensive and mildly hypertensive participants.
Methods:
Participants aged 30-79 years with normal blood pressure (n = 49) or mild hypertension (n = 17), with no history of taking antihypertensive medication, were recruited. Participants completed a cold pressor test (CPT) followed by an ischaemic handgrip test (IHGT). Blood pressure, HRV, forearm blood flow and vascular resistance were measured at rest and in response to each test.
Results:
The CPT and IHGT evoked greater increases in mean arterial blood pressure in hypertensive participants (CPT: 10 ± 2 mmHg, IHGT: 9 ± 1 mmHg) compared with normotensive participants (CPT: 5 ± 1 mmHg, IHGT: 3 ± 1 mmHg; P < 0.05). Resting high frequency power, which is a parameter of HRV associated with parasympathetic cardiac modulation, was lower in hypertensive participants (hypertensive: 31.73 ± 4.07 nu; normotensive: 42.08 ± 2.22 nu; P = 0.026) and was negatively correlated with systolic blood pressure (r = -0.272, P = 0.03) and mean arterial pressure across all participants (r = -0.258, P < 0.05). There were no differences in HRV or forearm blood flow responses to the CPT or IHGT between groups.
Conclusion:
This study demonstrated that sympathoexcitatory stress evoked by the CPT and IHGT induces an augmented blood pressure response in individuals with mild hypertension, which supports the notion that autonomic dysfunction is likely to contribute to the pathogenesis of hypertension. It remains to be determined whether the hypertensive response is mediated through alterations in cardiac activity, peripheral vascular resistance or both.
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