Hard‐wired for hypertension? The sympathetic nervous system causing havoc to non‐responders’ blood pressure

The relationship between increasing overall health risk and increasing blood pressure (BP) is continuous, consistent and independent of other risk factors. The clinical diagnosis of high blood pressure (hypertension (HTN): >140/>90 mmHg) affects one in four adults globally and is expected to increase by 60% between 2000 and 2025 (Campbell & Chen, 2010). In attempting to understand the pathophysiology of HTN the role of the renin–angiotensin system has received much attention, owing primarily to the fact that pharmaceutical agents which inhibit this pathway have proven beneficial in lowering resting blood pressure. Despite this, it appears that no less than 50% of all cases of elevated blood pressure are caused by the syndrome of neurogenic essential hypertension (Esler, 2010). A more thorough understanding of the nervous system's response to everyday stimuli and how that response affects an individual's blood pressure, including the impact of age and sex, is necessary to expand the knowledge of the multiple pathways contributing to blood pressure control. In a recent issue of The Journal of Physiology, Donadio et al. (2012) measured physiological responses to arousal (electrical skin impulses), mental stress (timed arithmetic subtraction) and cold stress (cold water hand immersion). One of the cardiovascular responses monitored was blood pressure as it relates to sympathetic nervous activity. Their findings revealed that about one-half of study participants (classified as the responders) exhibited a brief inhibition of sympathetic nervous activity following the arousal stimuli. Interestingly, this brief inhibition corresponded to less of an increase in blood pressure during mental stress. In comparison, the non-responders did not show sympathetic nervous activity inhibition to the arousal stimuli and their blood pressure subsequently increased more during mental stress. This can be interpreted such that the responders have a nervous system that reacts to mental stress in a way that protects their vasculature, possibly reducing their susceptibility to hypertension. Classifying individuals as responders and non-responders was a cornerstone component of the research as many statistical comparisons between the groups were completed. This classification was based on whether or not an individual's sympathetic nervous system was briefly inhibited following a single arousal stimulus (electrical skin impulses). The researchers acknowledged the concern of intraindividual reproducibility by referencing one of their previous studies where reproducibility was shown over a 6 month period. It should be noted that the arousal protocol was similar between the two studies and the subjects had similar characteristics of relative age, sex and health history. Furthermore, the same pre-study controls were employed in regards to alcohol, caffeine and tobacco ingestion, and food intake (Donadio et al. 2002). Building off of this theoretically innate response of the nervous system to arousal stimuli, Donadio et al. (2012) further explored the relationship between sympathetic nervous activity and the response of the cardiovascular system. The use of muscle sympathetic nerve activity (MSNA) as a means of measuring sympathetic nervous activity was a strength of this paper. Alternative measurements of sympathetic nervous activity are heart rate variability and plasma-catecholamine assays, the latter of which includes measurements of plasma noradrenaline (NA) spillover. Plasma NA counts provide little information about the localized response of the nervous system, and can be confounded (Esler, 2010). However, it would have been beneficial to include heart rate variability as a second measure of sympathetic nervous activity as this would provide a more complete picture of sympathetic nerve activity, especially as it pertains to the cardiovascular system. The participants examined by Donadio et al. (2012), healthy males aged 33 ± 10 years with arterial BP ≤ 130/80 mmHg, exhibited no correlation between resting MSNA and resting BP values. Joyner et al. (2010) also explained that in males and females <40 years of age there is no correlation between resting MSNA and resting BP values. However, by extending the population of participants to include those >40 years of age Joyner et al. (2010) were able to explain a significant correlation between MSNA and BP in both males and females. As one ages, the nervous system's regulation of cardiovascular variables appears to change, potentially altering the nervous system's impact on vascular protection in responders. It would be valuable to the overall understanding of the nervous system's role in BP regulation for future research to use familiar distinction points such as sex (male vs. female) and age (<40 vs. >40 years of age) while also including a responder, non-responder division based on an initial arousal test. In substantiating the usefulness of an initial arousal test to classify participants, Donadio et al. (2012) have greatly contributed to the literature. The present results (Donadio et al. 2012) reinforce the importance of neural regulatory pathways in overall BP control and potential HTN development. Despite the documented importance of neural mechanisms in BP regulation, therapy specifically targeting the SNS is currently underutilized. New techniques including renal sympathetic nerve ablation, have shown promise in the reduction or control, of resting BP without the use of pharmaceuticals. Renal sympathetic nerve ablation uses a radiofrequency-emitting catheter inserted percutaneously into the femoral artery and advanced to the lumen of both left and right renal arteries. The location allows for the destruction of the sympathetic nerves entering the kidneys in the walls of the renal arteries. The average BP reduction associated with this technique has been 24/10 mmHg at 3-month follow-up and 29/16 mmHg at 12-month follow-up (Krum et al. 2009). To extend the understanding of this technique, the effect of renal ablation on the renin–angiotensin system could expose an important link between these two BP regulatory systems. An interesting extension of the primary research methods would be to analyse an acute bout of exercise as a third measure of stress. A single bout of acute exercise, in the form of aerobic movement, eccentric resistive muscular contractions, or isometric muscular contractions, has been shown to affect blood pressure for up to 24 h. Unfortunately, the response is highly variable and inconsistent. Perhaps classification of individuals as either responders or non-responders would prove valuable in deciphering response patterns. Response patterns could be useful tools for implementing long-term exercise programmes as adjunct or alternative therapy for BP reduction and control. Individuals who are non-responders to arousal stimuli (who do not display MSNA reductions) will have the largest sympathetic and BP responses to forms of stress, and may be more likely than responders to develop hypertension and cardiovascular disease later in life. In the future, classifying patients as responders or non-responders may assist in prescribing the most successful course of treatment. In conclusion Donadio et al. (2012) provided information about the sympathetic nervous system and how it responds to both arousal stimuli and bouts of mental and cold water stress. The initial separation of participants into responders and non-responders based the occurrence of MSNA inhibition was an imperative distinction as it helped extract important relationships between variables. Future research on BP management should consider using an individual's arousal response to control for the innate interindividual difference in sympathetic nervous activity.

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