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Disturbances of extracellular potassium (K) homeostasis in calves with severe neonatal diarrhea have been studied extensively. Although total body depletion of this predominantly intracellular electrolyte is generally thought to occur in diarrheic calves, the mechanisms through which K depletion occurs are poorly understood. The aim of this study was to investigate how intracellular K homeostasis is affected by dehydration and acidemia, the 2 most important metabolic disturbances in calves with naturally occurring diarrhea. Twenty-seven calves with naturally occurring neonatal diarrhea, pronounced dehydration, and acidemia, and 2 groups of 10 healthy control calves were included in this study. Blood samples and muscle biopsies were obtained immediately before initiation of treatment (T0) and after complete rehydration and correction of acidemia (T1) from diarrheic calves. Blood samples were used to perform blood gas, blood biochemical, and hematological analyses and to determine K content in erythrocytes. Muscle biopsies were used to determine muscle tissue K content and tissue dry matter. Controls were used to determine values for erythrocyte and muscle tissue K content in healthy neonatal calves for comparison with diarrheic calves. As defined by the inclusion criteria, diarrheic calves showed pronounced acidemia and dehydration at T0. Mean muscle tissue K content and tissue dry matter remained unchanged between sampling times and did not differ from values measured in healthy control calves. Erythrocyte K content increased from 73.63 ± 13.73 to 77.64 ± 15.97 mmol/L (±standard deviation) but was associated with a concomitant decline in erythrocyte volume. Values measured at both sampling times in diarrheic calves did not differ from erythrocyte K measured in healthy control calves. The plasma K concentration (median [interquartile range]) decreased from 5.44 [4.76-6.17] to 4.16 [3.99-4.31] mmol/L between T0 and T1. Although changes in plasma [K] were associated with the degree of dehydration, neither dehydration nor acidemia was associated with changes of K content in muscle tissue or erythrocytes. In conclusion, severe dehydration and acidemia in diarrheic calves were not associated with notable changes in K content of muscle tissue or erythrocytes. These results do not support the concept of pronounced K depletion occurring in calves with neonatal diarrhea. Erythrocytes are a poor surrogate tissue in which to measure changes of intracellular K content in diarrheic calves because of concomitant changes in erythrocyte volume that complicate the interpretation of results.

Magnesium (Mg2+) is an essential mineral without known specific regulatory mechanisms. In ruminants, plasma Mg2+concentration depends primarily on the balance between Mg2+absorption and Mg2+excretion. The primary site of Mg2+absorption is the rumen, where Mg2+is apically absorbed by both potential-dependent and potential-independent uptake mechanisms, reflecting involvement of ion channels and electroneutral transporters, respectively. Transport is energised in a secondary active manner by a basolateral Na+/Mg2+exchanger. Ruminal transport of Mg2+is significantly influenced by a variety of factors such as high K+concentration, sudden increases of ammonia, pH, and the concentration of SCFA. Impaired Mg2+absorption in the rumen is not compensated for by increased transport in the small or large intestine. While renal excretion can be adjusted to compensate precisely for any surplus in Mg2+uptake, a shortage in dietary Mg2+cannot be compensated for either via skeletal mobilisation of Mg2+or via up-regulation of ruminal absorption. In such situations, hypomagnesaemia will lead to decrease of a Mg2+in the cerebrospinal fluid and clinical manifestations of tetany. Improved knowledge concerning the factors governing Mg2+homeostasis will allow reliable recommendations for an adequate Mg2+intake and for the avoidance of possible disturbances. Future research should clarify the molecular identity of the suggested Mg2+transport proteins and the regulatory mechanisms controlling renal Mg excretion as parameters influencing Mg2+homeostasis.

High-performing dairy cows require a particular composition of nutritional ingredients, adapted to their individual requirements and depending on their production status. The optimal dimensioning of minerals in the diet, one being potassium, is indispensable for the prevention of imbalances. Potassium balance in cows is the result of potassium intake, distribution in the organism, and excretion, and it is closely related to glucose and electrolyte metabolism. In this paper, we present a dynamical model for potassium balance in lactating and nonlactating dairy cows based on ordinary differential equations. Parameter values were obtained from clinical trial data and from the literature. To verify the consistency of the model, we present simulation outcomes for 3 different scenarios: potassium balance in (1) nonlactating cows with varying feed intake, (2) nonlactating cows with varying potassium fraction in the diet, and (3) lactating cows with varying milk production levels. The results give insights into the short- and long-term potassium metabolism, providing an important step toward the understanding of the potassium network, the design of prophylactic feed additives, and possible treatment strategies.

The quantitative role of different segments of the gastrointestinal tract for Ca absorption, the respective mechanisms, and their regulation are not fully identified for ruminants, that is, cattle. In different in vitro experiments the forestomach wall has been demonstrated to be a major site for active Ca absorption in sheep and goats. In order to further clarify the role of the bovine rumen for Ca transport with special attention to luminal Ca concentrations, its ionic form, and pH, electrophysiological and unidirectional flux rate measurements were performed with isolated bovine rumen epithelial tissues. For Ca flux studies (Jms, Jsm) in vitro Ussing chamber technique was applied. Standard RT-PCR method was used to characterize TRPV6 and PMCA1 as potential contributors to transepithelial active Ca transport. At Ca concentrations of 1.2 mmol L � 1 on both sides of the tissues, Jms were higher than Jsm resulting under some conditions in significant Ca net flux rates (Jnet), indicating the presence of active Ca transport. In the absence of an electrical gradient, Jnet could significantly be stimulated in the presence of luminal short-chain fatty acids (SCFAs). Increasing the luminal Ca concentrations up to 11.2 mmol L � 1 resulted in significant increases in Jms without influencing Jsm. Providing Ca in its form as respective chloride, formate, or propionate salts there was no significant effect on Jms. No transcripts specific for Ca channel TRPV6 could be demonstrated. Our results indicate different mechanisms for Ca absorption in bovine rumen as compared with those usually described for the small intestines.