High-normal blood pressure is associated with increased resting sympathetic activity but normal responses to stress tests

Abstract Objective. High-normal blood pressure (BP) increases the risk of cardiovascular (CV) disease. The mechanisms underlying this increased risk are not clear. Sympathetic activation appears to be a potential mechanism linking high-normal BP to CV disease. This study examined whether high-normal BP compared with optimal BP is linked to sympathoexcitation at rest and/or during laboratory stressors. Methods. Heart rate (HR), BP and muscle sympathetic nerve activity (MSNA) were obtained at rest and during stress tests (sustained handgrip and mental stress) in 18 subjects (15 males and three females) with high-normal BP (systolic BP of 130–139 mmHg, diastolic BP of 85–89 mmHg, or both) and in 12 subjects (10 males and two females) with optimal BP (< 120/80 mmHg) matched for age (34 ± 3 years in both groups) and body mass index (25 ± 2 kg/m2 in both groups). Results. Despite the higher resting BP levels, MSNA was higher in subjects with high-normal BP than in the optimal BP group (26 ± 3 vs 18 ± 2 bursts/min, p< 0.05). During sustained handgrip, MSNA increased by 37 ± 14% in high-normal BP group compared with an increase of 49 ± 15% in optimal BP group (p = 0.55). Changes during mental stress were 50 ± 28% and 37 ± 12%, respectively (p = 0.73). There were no significant differences in SBP responses to handgrip and mental stress between the high-normal and optimal BP groups. Baseline HR and chronotropic responses to stress tests were comparable between the two groups. Conclusion. In comparison with optimal BP, high-normal BP is associated with increased resting MSNA, but normal neural and circulatory responses to stress tests. These findings suggest that tonic activation of the sympathetic nervous system may precede overt arterial hypertension and contribute to an excess risk of CV disease in subjects with high-normal BP.

[1]  B. Wallin,et al.  Vascular adrenergic responsiveness is inversely related to tonic activity of sympathetic vasoconstrictor nerves in humans , 2006, The Journal of physiology.

[2]  G. Jennings,et al.  CHRONIC MENTAL STRESS IS A CAUSE OF ESSENTIAL HYPERTENSION: PRESENCE OF BIOLOGICAL MARKERS OF STRESS , 2008, Clinical and Experimental Pharmacology and Physiology.

[3]  G. Jennings,et al.  Contribution of individual organs to total noradrenaline release in humans. , 1984, Acta physiologica Scandinavica. Supplementum.

[4]  Leiv Sandvik,et al.  Long-Term Stability of Cardiovascular and Catecholamine Responses to Stress Tests: An 18-Year Follow-Up Study , 2010, Hypertension.

[5]  D. Levy,et al.  Impact of high-normal blood pressure on the risk of cardiovascular disease. , 2002, The New England journal of medicine.

[6]  M. Esler,et al.  Sympathetic nerve activity and neurotransmitter release in humans: translation from pathophysiology into clinical practice. , 2003, Acta physiologica Scandinavica.

[7]  E. Lambert,et al.  Reduced sympathoneural responses to the cold pressor test in individuals with essential hypertension and in those genetically predisposed to hypertension. No support for the "pressor reactor" hypothesis of hypertension development. , 2004, American journal of hypertension.

[8]  D. Levy,et al.  Impact of High-Normal Blood Pressure on the Risk of Cardiovascular Disease , 2001 .

[9]  G. Lambert,et al.  Stress and Its Role in Sympathetic Nervous System Activation in Hypertension and the Metabolic Syndrome , 2011, Current hypertension reports.

[10]  G. Mancia,et al.  Comparison between reproducibility and sensitivity of muscle sympathetic nerve traffic and plasma noradrenaline in man. , 1997, Clinical science.

[11]  Paolo Palatini,et al.  Role of elevated heart rate in the development of cardiovascular disease in hypertension. , 2011, Hypertension.

[12]  O. Tochikubo,et al.  Augmented sympathetic nerve activity in response to stressors in young borderline hypertensive men. , 1991, Acta physiologica Scandinavica.

[13]  S. Kjeldsen,et al.  High screening blood pressure is related to sympathetic nervous system activity and insulin resistance in healthy young men , 2004, Blood pressure.

[14]  J P Greenwood,et al.  Single-unit sympathetic discharge : quantitative assessment in human hypertensive disease. , 1999, Circulation.

[15]  R. Rea,et al.  Baroreflex control of muscle sympathetic nerve activity in borderline hypertension. , 1990, Circulation.

[16]  E A Anderson,et al.  Elevated Sympathetic Nerve Activity in Borderline Hypertensive Humans Evidence From Direct Intraneural Recordings , 1989, Hypertension.

[17]  Sc Prospective,et al.  Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies , 2002 .

[18]  J. Floras,et al.  Absence of post exercise hypotension and sympathoinhibition in normal subjects: additional evidence for increased sympathetic outflow in borderline hypertension. , 1991, The Canadian journal of cardiology.

[19]  S. Kjeldsen,et al.  Sympathoadrenal Stress Reactivity Is a Predictor of Future Blood Pressure: An 18-Year Follow-Up Study , 2008, Hypertension.

[20]  Guido Grassi,et al.  Assessment of Sympathetic Cardiovascular Drive in Human Hypertension: Achievements and Perspectives , 2009, Hypertension.

[21]  G. Grassi,et al.  How to assess sympathetic activity in humans. , 1999, Journal of hypertension.

[22]  Floras Js,et al.  Absence of post exercise hypotension and sympathoinhibition in normal subjects: additional evidence for increased sympathetic outflow in borderline hypertension. , 1991 .

[23]  R. Schmieder,et al.  Evidence against elevated sympathetic vasoconstrictor activity in borderline hypertension. , 1998, Journal of the American Society of Nephrology : JASN.

[24]  Paul A. Smith,et al.  Relationship between central sympathetic activity and stages of human hypertension. , 2004, American journal of hypertension.

[25]  B. Wallin,et al.  Renal noradrenaline spillover correlates with muscle sympathetic activity in humans. , 1996, The Journal of physiology.

[26]  F. Abboud,et al.  Potentiation of Sympathetic Nerve Responses to Hypoxia in Borderline Hypertensive Subjects , 1988, Hypertension.