Hypokalemic cattle are often treated orally with potassium salts such as KCl. However, as postulated by Rabinowitz (1988), surplus potassium might induce renal kaliuresis by means of specific receptors located in the gastrointestinal tract. This mechanism might circumvent blood potassium levels, causing the therapy to be ineffective.
A study was therefore conducted to measure the K balance of six lactating dairy cows. All ex-cretions of the animals (feces, urine and milk) were collected over the course of five consecu-tive days. Samples were taken in short intervals and analyzed for K, along with samples of diet components. On two control days, basic K excretion via the different pathways was measured. On three treatment days, either 80 g KCl in 4 l of water were applied directly into the rumen via fistulae, or 1.49 g KCl in 100 ml of water, or an equimolar amount of NaCl (volume control) were applied via duodenal cannulae. The amount of K applied to the duo-denum was chosen to induce an equal concentration difference in rumen and duoduo-denum.
After application of KCl into the rumen, the amount of K excreted with the urine increased
significantly (by 24 % on average). This increase was not observed after application into the duodenum. An immediate significant rise of K excretion after feeding (postprandial kaliu-resis) was observed only after ruminal addition of K. The amount of urine excreted approximately paralleled K excretion, but only 13 % of the variance in urine K concentrations depended on urine volume. Calculating the [K]/[Krea] ratio in the urine to estimate fractional excretion proved to be rather unreliable. K excretion with milk remained relatively constant, independent of treatment. With rations containing 0.8 % potassium in total, all six cows showed a negative K balance overall; this was somewhat alleviated when adding K to the rumen, but remained negative. This may have been caused by relatively high temperatures during the experiment period (in mid August), which could have led to increased K turnover rates. As K excreted with milk did not show any variation with treatment, high K losses with milk might plausibly strain K balance. Usual recommendations for K content in dairy cow rations might promote the development of K deficiencies. Dividing therapeutic doses into several smaller portions might help increase K retention. Stimulation of kaliuresis by means of K sensors in the gastrointestinal tract seems plausible. These might be located proximally to the duodenum, or possibly extraintestinally, and seem to respond to the overall amount of K, rather than to K concentration in chyme.
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