Sympathoinhibitory signals from the gut and obesity-related hypertension

Abstract

Several gastrointestinal hormones are commonly associated with satiety and digestion, but recent studies suggest they are also involved in regulating hemodynamic demand after a meal. These hormones released from the gut postprandially play a role in short-term cardiovascular regulation via a vagally mediated sympathoinhibitory reflex mechanism, similar to that of the arterial baroreflex. It has been hypothesized that activation of this reflex may promote greater blood flow to the splanchnic and renal vasculature that have increased haemodynamic demand after a meal, while simultaneously inducing vasoconstriction to the skeletomuscular vasculature where it is needed less. Together, the renal and splanchnic circulations can command over 50 % of cardiac output so that the role of gut hormones in controlling sympathetic vasomotor tone to these vascular beds may be more important in cardiovascular regulation than previously thought. The exact aetiology of obesity-related hypertension remains to be determined and is likely to be multifactorial, although the involvement of gut hormone signalling in the development of this disease has not previously been considered. Diets rich in fats and increased food intake are amongst the leading causes of obesity and precipitate significant changes such as inflammation in the gastrointestinal environment that can lead to blunted vagal afferent signalling. In obesity, these changes may disrupt sympathoinhibitory mechanisms and subsequently lead to increased vascular resistance in the gastrointestinal and renal vascular beds, contributing to the development of hypertension.