The sympathetic nervous system and blood pressure in humans: implications for hypertension

Abstract

A neurogenic component to primary hypertension (hypertension) is now well established. Along with raised vasomotor tone and increased cardiac output, the chronic activation of the sympathetic nervous system in hypertension has a diverse range of pathophysiological consequences independent of any increase in blood pressure. This review provides a perspective on the actions and interactions of angiotensin II, inflammation and vascular dysfunction/brain hypoperfusion in the pathogenesis and progression of neurogenic hypertension. The optimisation of current treatment strategies and the exciting recent developments in the therapeutic targeting of the sympathetic nervous system to control hypertension (for example, catheter-based renal denervation and carotid baroreceptor stimulation) will be outlined. Keywords: sympathetic nerve activity; neurogenic hypertension; immune-to-brain signalling The sympathetic renaissancePrimary (or essential) hypertension (termed hypertension from here on) accounts for the vast majority of hypertensive cases (B95%).1 Although the aetiology of this condition is incompletely understood, it appears that along with genetic factors, several environmental and behavioural 'hypertensiogenic' factors have been identified, such as obesity, insulin resistance, high-salt intake, low physical activity levels and stress.1 Given the elevated risk of stroke, renal failure, myocardial infarction and coronary heart disease in those afflicted with high blood pressure, the elucidation of the key pathogenic features and optimisation of effective therapeutic strategies are critical.The most common form of hypertension is neurogenic hypertension, defined as high blood pressure with sympathetic overdrive, loss of parasympathetically mediated cardiac variability and excessive angiotensin II (Ang II) activity.2 The importance of the sympathetic nervous system in the short-term regulation of blood pressure via the modulation of peripheral vascular tone and cardiac output is well established, while the role of the sympathetic nerve activity (SNA) in long-term blood pressure control is more controversial. [3][4][5] Although the concept of a potential neurogenic component to hypertension is not new, 4 it has perhaps received less attention than the renin-angiotensin system (RAS), which has been a prominent therapeutic and research target in hypertension over the past few decades. Nevertheless, the activation of the sympathetic nervous system and the RAS in hypertension appears inextricably, and reciprocally, linked. Evidence from studies in both patients and animal models of hypertension strongly implicate the chronic sympathetic neural activation in the aetiology and progression of hypertension (Figure 1). 2,[6][7][8][9] The use of regional surgical sympathectomy to treat hypertension over 50 years ago before the availability of antihypertensive medications that lower sympathetic activity provides an early indication of the clinical appreciation for a significant neurogenic component to hypertension.10 Recent clini...

Truly Refractory Hypertension

“…16 Although 2 device-related therapies that putatively function by reducing sympathetic tone 12,17 did not help our patient, we still have reason to believe that abnormal autonomic function is contributing to her problem. 18 Through the Internet, our patient became aware of a third novel device-related therapy to address sympathetic tone. She traveled to Bristol, UK, and was evaluated for a deep-brain stimulator to lower her blood pressure.…”

The carotid body as a putative therapeutic target for the treatment of neurogenic hypertension

“…It is established that in many patients, sympathetic nerve activity increases proportionately as hypertension develops and this may be a causative factor [1][2][3][4][5] , but it is unclear what triggers heightened sympathetic traffic (reviewed in ref. 6). Despite good pharmacological control of arterial pressure in most patients with essential hypertension, a significant proportion remain drug resistant or intolerant to medication 7,8 , and this has been highlighted as a growing problem 9,10 .…”

Influence of additional risk factors on the antihypertensive efficacy of eprosartan and telmisartan in patients with essential hypertension

“…За даними J. P. Fisher et al (2012), препарат опти-мізує вегетативний профіль у хворих з АГ завдяки зниженню добового коефіцієнта симпато-вагальної рів-новаги на 18 % від початкового, при цьому абсолютна величина зниження ІММ ЛШ корелювала зі ступенем збільшення потужності високочастотного компонента спектра [10,28].…”