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Symposium Report |
Department of Physiology & Institute for Biomedical Research, University of Sydney, Australia
The following papers were presented at a symposium on neural mechanisms in obesity-related hypertension, at the 25th Annual Meeting of the Australian Neuroscience Society in Perth in February, 2005. As discussed by Eikelis and Esler in the first of these papers (Eikelis & Esler, 2005), obesity is a major nutritional disorder, particularly in the industrialized world. Early studies suggested that obesity is associated with reduced activity of the sympathetic nervous system, but more recently direct measurements of sympathetic activity in humans has demonstrated clearly that the opposite is the case, i.e. obesity is associated with overactivity of the sympathetic nervous system, rather than suppression (Eikelis & Esler, 2005). Thus, it has been proposed that obesity-associated hypertension is due to sympathetic overactivation. What causes sympathetic overactivation in obesity? In humans, obesity is associated with increased release of the hormone leptin from adipocytes and this has led to the hypothesis that increased levels of circulating leptin may increase sympathetic activity via an action in the brain, particularly in the hypothalamus (Haynes, 2005; Montanaro et al. 2005). One difficulty with this hypothesis, however, is that obesity is generally associated with leptin resistance, but as pointed out by Haynes (2005) this resistance may be restricted to the weight-reducing effects of leptin (i.e. reduced appetite and increased thermogenesis), while the pressor and sympathoexcitatory effects of leptin are preserved. The mechanisms that may cause such selective leptin resistance are discussed by Haynes (2005). A further factor that may also be of crucial importance is that, apart from adipose tissue, leptin is also released from the brain itself (Eikelis & Esler, 2005). Thus, brain-derived leptin is also likely to contribute to the central effects of the hormone.
The paper by Montanaro et al. (2005) discusses in some detail the organization of the pathways within the brain that mediate the sympathoexcitatory effects of leptin. First, they describe the distribution of neurones within the hypothalamus that have direct and indirect descending projections to the spinal sympathetic outflow to the heart, kidney and skeletal muscle vasculature, and the relationship between such neurones and leptin receptors in the hypothalamus. Next, they describe functional experiments in which leptin was microinjected into discrete hypothalamic nuclei. In the final paper in this series, Morris et al. (2005) discuss the relationship between nutrition in early life and the risk of obesity and hypertension in later life, based on studies in rats. These studies show that overnourishment in early life leads to marked increases in leptin and insulin levels, and also increases in blood pressure. In addition, there were changes in the level of neurotransmitters such as neuropeptide Y in the hypothalamus, which also contribute to sympathetic overactivation associated with overnourishment and increased body weight. Collectively, the four papers in this symposium provide an excellent summary of our current understanding of the mechanisms that link obesity to sympathetic overactivation and hypertension.
References
Eikelis
N
&
Esler
MD (2005). The neurobiology of human obesity. Exp Physiol
90, 673–682.
Haynes
WG (2005). Role of leptin in obesity-related hypertension. Exp Physiol
90, 683–688.
Montanaro
MS, Allen
AM
&
Oldfield
BJ (2005). Structural and functional evidence supporting a role for leptin in central neural pathways influencing blood pressure. Exp Physiol
90, 689–696.
Morris
MH, Velkoska
E
&
Cole
TJ (2005). Central and peripheral contributions to obesity associated hypertension: impact of early overnourishment. Exp Physiol
90, 697–702.
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