Postprandial hypotension - novel insights into pathophysiology and therapeutic implications.

Postprandial hypotension is a frequent disorder, occurring in approximately 40% of nursing-home residents, and represents a major cause of morbidity and mortality. Current approaches to management are suboptimal. While it has been generally assumed that ingestion of carbohydrate has the greatest effect, the fall in blood pressure (BP) does not appear to be mediated by the consequent elevations in blood glucose and insulin. Moreover, there is evidence that fat may decrease BP to a comparable extent to carbohydrate, although onset of the response may be slower, and that the response is affected by the type of carbohydrate. It has recently been established that the rate of nutrient delivery from the stomach into the small intestine is an important determinant of the hypotensive response to carbohydrate, so that the magnitude of the fall in BP and rise in heart rate is greater when gastric emptying is relatively more rapid. In both healthy elderly subjects and patients with type 2 diabetes, the fall in BP is attenuated when gastric emptying and small intestinal carbohydrate absorption are slowed by dietary (e.g. guar) or pharmacological (e.g. acarbose) means. Conversely, gastric distension attenuates the postprandial fall in BP. Strategies for the treatment of postprandial hypotension should, therefore, potentially be directed at (i) meal composition, particularly carbohydrate type and content, (ii) slowing gastric emptying and/or small intestinal carbohydrate absorption and/or (iii) increasing postprandial gastric distension.