Conventional peritoneal dialysis solutions (PDS) are vasoactive. This study was conducted to identify vasoactive components of PDS and to describe quantitatively such vasoactivity. Anesthetized nonheparinized rats were monitored continuously for hemodynamics while the microvasculature of the jejunum was studied with in vivo intravital microscopy. In separate experiments, vascular reactivity of rat endothelium-intact and -denuded aortic rings (2 mm) was studied ex vivo in a standard tissue bath. In both studies, suffusion of the vessels was performed with filter-sterilized isotonic and hypertonic solutions that contained glucose or mannitol as osmotic agents. PDS served as a control (Delflex 2.25%). Hypertonic glucose and mannitol solutions produced a significant vascular reactivity in aortic rings and instantaneous and sustained vascular relaxation at all levels of the intestinal microvasculature. Similarly, lactate that was dissolved in a low-pH isotonic physiologic salt solution produced significant force generation in aortic rings. Whereas isotonic glucose and mannitol solutions had no vasoactivity in aortic rings, isotonic glucose produced a selective, insidious, and time-dependent vasodilation in the intestinal premucosal arterioles ( C onventional peritoneal dialysis solutions (PDS) dilate visceral and parietal microvasculature by mechanisms possibly related to hyperosmolality, low pH, and the buffer anion system of these solutions (1,2). Studies of hyperosmolar sodium solutions perfused into the intestinal lymph produced vasodilation of submucosal arterioles through a mechanism partially mediated by a hyperosmolality-induced nitric oxide (NO) release (3). Similarly, intravenous infusion of hypertonic galactose or mannitol solutions in pigs increased the baseline hepatic blood flow by 37%, presumably by a mechanism attributed to an osmotic stress (4). Massett et al. (5) found that in vitro infusion of isolated, cannulated, and pressurized skeletal muscle arterioles with hypertonic solutions of glucose, sucrose, or mannitol at an osmolality of 330 mOsmol/kgH 2 O equally dilates these arterioles. This vascular reactivity seems to be an endothelium-dependent response, which is independent of the NO or the cyclooxygenase pathways, but can be nearly abolished by glibenclamide, an ATP-sensitive potassium channel inhibitor. Similar results were obtained with coronary arterioles perfused ex vivo with either hypertonic glucose or sucrose solutions. In these vessels, only glibenclamide caused attenuation of the hypertonic solution-mediated vascular relaxation. In addition, inhibition of inward rectifier potassium channels or calcium activated potassium channels had no effect on hyperosmolality-induced vascular reactivity (6,7). Our recent intravital videomicroscopy of the terminal ileum in rats showed that exposure of the ileum to a conventional PDS produces an instantaneous and sustained vascular relaxation at all levels of the microvasculature, which is essentially associated with doubling of blood flow in the in...