Recurrent dehydration and heat stress cause chronic kidney damage in experimental animals. The injury is exacerbated by rehydration with fructose-containing beverages. Fructose may amplify dehydration-induced injury by directly stimulating vasopressin release and also by acting as a substrate for the aldose reductase-fructokinase pathway, as both of these systems are active during dehydration. The role of vasopressin in heat stress associated injury has not to date been explored. Here we show that the amplification of renal damage mediated by fructose in thermal dehydration is mediated by vasopressin. Fructose rehydration markedly enhanced vasopressin (copeptin) levels and activation of the aldose reductase-fructokinase pathway in the kidney. Moreover, the amplification of the renal functional changes (decreased creatinine clearance and tubular injury with systemic inflammation, renal oxidative stress, and mitochondrial dysfunction) were prevented by the blockade of V1a and V2 vasopressin receptors with conivaptan. On the other hand, there are also other operative mechanisms when water is used as rehydration fluid that produce milder renal damage that is not fully corrected by vasopressin blockade. Therefore, we clearly showed evidence of the cross-talk between fructose, even at small doses, and vasopressin that interact to amplify the renal damage induced by dehydration. These data may be relevant for heat stress nephropathy as well as for other renal pathologies due to the current generalized consumption of fructose and deficient hydration habits.

In this article, we examine the inflammatory response and redox dysregulation induced by acute myocardial IRI, and highlight potential therapeutic options for targeting redox dysregulation, in order to attenuate the detrimental effects of the inflammatory response following an AMI, so as to reduce MI size and prevent heart failure.

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The entry of calcium ions from the nixtamalization solution into maize kernels over time was followed in model experiments using radiolabeled calcium ions, with autoradiographic evaluation of the kernels after different cooking and steeping times. Calcium ions immediately entered the pericarp and were rapidly fixed at the outer boundary of the endosperm, especially at the external surface of the germ. Entry of calcium into the endosperm occurred gradually after long steeping times, except in the case of broken kernels, for which massive invasion by calcium was observed. After extended steeping times, a moderate amount of calcium‐45 was evident in the germ. Specific perforation of the outer layers of the grains provided a defined route of facilitated entry of calcium into the endosperm. No fundamental difference with respect to penetrability by calcium ion was seen in a comparison between flint‐type grains and grains containing only floury endosperm.