The role of the nervous system in hypertension

Abstract

The central nervous system plays an important role in the minute-to-minute regulation of arterial pressure, but its contribution to chronic regulation of arterial pressure is less clear. A nervous system role in essential hypertension in humans has been postulated for decades, but conclusive data on the relationship has been lacking. However, several lines of evidence in animal models and in humans suggest that the sympathetic nervous system is a primary contributor to the development and maintenance of some forms of essential hypertension. The primary final common pathway for the nervous system's contribution to hypertension is the sympathetic nervous system. Sympathetic nervous system overactivity may result from either inappropriately elevated sympathetic drive from brain centers, an increase in synaptically released neurotransmitters in the periphery, or amplification of the neurotransmitter signal at the target tissue. This review examines recent evidence for the central and peripheral nervous systems' roles in hypertension, and considers recent findings in this area that suggest that sex steroids and circadian rhythms are important considerations in the nervous system's regulation of arterial pressure.

Long-term modulation of tyrosine hydroxylase activity and expression by endothelin-1 and -3 in the rat anterior and posterior hypothalamus

“…In the hypothalamus, the ET system is highly expressed, suggesting that these peptides participate in the regulation of diverse biological functions controlled at this level (4,30). The hypothalamus coordinates endocrine, neuroendocrine, and autonomic signals involved in the control of the cardiovascular activity, water, and sodium homeostasis, as well as hormone release (18,21,37,55). Among the different areas and nuclei that form the hypothalamus, the anterior and posterior hypothalamic regions play a major role in the regulation of the cardiovascular activity (37,55).…”

“…The hypothalamus coordinates endocrine, neuroendocrine, and autonomic signals involved in the control of the cardiovascular activity, water, and sodium homeostasis, as well as hormone release (18,21,37,55). Among the different areas and nuclei that form the hypothalamus, the anterior and posterior hypothalamic regions play a major role in the regulation of the cardiovascular activity (37,55). The anterior hypothalamic region (AHR) is a sympathoinhibitory area, whereas the posterior region (PHR) behaves as a sympathoexcitatory area (37).…”

“…The anterior hypothalamic region (AHR) is a sympathoinhibitory area, whereas the posterior region (PHR) behaves as a sympathoexcitatory area (37). Functional impairment of these areas has been associated with hypertension (37,55). In addition, ETs through ET A receptors in the spinal cord also regulate cardiovascular and sympathetic activity (42).…”

“…Catecholamines [dopamine, norepinephrine (NE), and epinephrine] are widely distributed in the brain, NE being a major neurotransmitter in diverse neuronal circuits, including the hypothalamus (37,55). Tyrosine hydroxylase (TH), the key enzyme in the biosynthesis of catecholamines, is a specific marker of catecholaminergic neurons (13,14,29).…”

Brain cyclooxygenase and prostanoid TP receptors are involved in centrally administered epibatidine-induced secretion of noradrenaline and adrenaline from the adrenal medulla in rats

“…Nicotine administered into the rostral ventrolateral medulla increases blood pressure and renal sympathetic nerve activity (Tseng et al, 1993(Tseng et al, , 1994, whereas nicotine administration into the nucleus tractus solitarius induces hypotension, probably by an enhancement of inhibitory baroreflex (Tseng et al, 1993(Tseng et al, , 1994Ashworth-Preece et al, 1998). Chronic treatment of nicotine is able to intensify and accelerate the development of hypertension in spontaneously hypertensive rats (Bui et al, 1994;Ferrari and Fior-Chadi, 2007), in which the central dysregulation of sympatho-adrenomedullary outflow has been suggested to be involved (Barron and Van Loon, 1989;Wyss and Carlson, 2001;Guyenet, 2006). However, the precise mechanisms of this alkaloid-induced central modulation of the sympathoadrenomedullary outflow are largely undefined.…”