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Does our fat tell our brain what to do? A ‘sympathetic’ appraisal

The prevalence of essential hypertension is much higher in humans with excessive stored fat (obese) than in individuals with normal habitus. Nevertheless, this is not an invariable association. Obesity does not strictly speaking ‘cause’ hypertension, but rather produces a strong predisposition for hypertension development. Not all fat depots are equal in producing this predisposition. Fat in the abdominal viscera has a particularly strong effect on blood pressure. 
 
Plausible mechanisms have been proposed linking fat accumulation to the development of hypertension. These include: reductions in renal sodium and water excretion; altered function and structure of large and small arteries; and increased activity of the renin–angiotensin–aldosterone system. In addition, compelling evidence indicates that increased sympathetic nervous system activity (SNA) is a critical connection between visceral adiposity and high blood pressure (Davy & Orr, 2009; da Silva et al. 2009). This conclusion was once contentious, in part because SNA is only moderately elevated in obese subjects. Also, the increase in SNA occurs in some organs (i.e. kidney and skeletal muscle) but not others (heart and splanchnic bed). A further complication is that obese individuals often exhibit high SNA but normal blood pressure. Nevertheless, increased SNA appears to be a necessary precondition for hypertension development in many obese subjects. 
 
It is therefore important to understand exactly how amassing of visceral fat leads to an elevation in SNA. Multiple factors may play a role: elevated circulating levels of leptin, insulin, non-esterified fatty acids and angiotensin II, reduced circulating concentrations of adiponectin or ghrelin, and sleep apnoea all occur in obesity; each has been shown to increase SNA. Tonic baroreflex-mediated inhibition, however, is by far the most powerful physiological controller of SNA, at least acutely. Sympathoexcitation related to a reduction in baroreflex inhibition has been documented in animal models of obesity and in overweight humans, although not uniformly (Davy & Orr, 2009). Nevertheless, there is general agreement that the declines in SNA and blood pressure that occur with weight loss in obese subjects are associated with augmented baroreflex sensitivity (Straznicky et al. 2010). 
 
How does obesity cause reduced baroreflex function? In this issue of The Journal of PhysiologyHuber and Schreihofer (2010) report experiments designed to examine that question. Their studies were conducted in Zucker rats – a well-characterized genetic model of obesity caused by a defect in leptin receptor function. They showed earlier that these rats have impaired baroreflex-mediated sympathoinhibition, so the current study concentrated on identifying mechanism(s). Proper baroreflex function depends on (1) reproducible transduction of arterial pressure into neural sensory information relayed to the brain, and (2) integration of that sensory information by specific neural networks in the brain to produce appropriate changes in SNA. Obesity is associated with both stiffening of large arteries and with major changes in the quantity and nature of chemical signals sent from adipose tissue to the brain (primarily to facilitate regulation of energy balance). Therefore, these investigators logically chose to explore both sensory coding of arterial pressure information, and central (brain) processing of those sensory signals, in their effort to identify the mechanism of impaired baroreflex function. 
 
The results were unambiguous. Transduction of arterial pressure into sensory afferent information was completely normal in the obese Zucker rats, whereas the ability of baroreceptor-derived sensory input entering the brain to cause sympathoinhibition was significantly attenuated. The first outcome is a bit surprising. Both obesity and hypertension lead to reduced compliance of large arteries and therefore would be expected to limit pressure-induced distension of the arterial wall where baroreceptor sensory endings are located. This mechanism, while not operating in the rats studied here, could contribute to baroreflex dysfunction later in life as arterial structural changes become more prominent. 
 
While the results clearly point to impaired processing of baroreceptor inputs by the brain as a cause for baroreflex dysfunction in obese rats, the data shed little light on the specific mechanism(s) responsible. However, the authors discuss some very reasonable possibilities. Fortunately, we know a great deal about the organization, function and neurochemistry of brain pathways subserving the baroreflex. This will allow the authors and others to design additional detailed experiments to test specific hypotheses about how obesity affects baroreflex function. 
 
The paper encourages additional interesting questions about the relationships between obesity, SNA and hypertension. First, the authors showed that SNA is increased to the splanchnic region in Zucker rats. This appears to make sense given the close link between visceral adiposity and SNA. However, hepatomesenteric SNA was reported to be normal in obese normotensive humans, whereas renal and muscle SNA is increased (Davy & Orr, 2009). It seems important now to determine if splanchnic SNA is elevated in obese hypertensive humans. Second, the long-term impact of baroreflexes on SNA has been rightly questioned based on evidence that baroreflexes ‘reset’ in response to sustained changes in blood pressure. However, recent findings show that chronic, direct activation of the carotid baroreflex with an implantable device produces well-maintained reductions in SNA and blood pressure in human hypertensives (Heusser et al. 2010). Similar findings were reported in obesity-related hypertension in dogs (Lohmeier et al. 2007). We may have been too hasty in discounting the baroreflex as an important factor in the long-term regulation of SNA and blood pressure.