A single 400 g NaCl pulse dose in lactating cows induced a biphasic Na+ excretion pattern with initial rapid excretion followed by a delayed second peak after ~96 h, consistent with short-term extrarenal sodium storage without concomitant changes in urinary potassium excretion.
Does a large pulse-dose of NaCl induce extrarenal sodium storage in cattle?
A large pulse-dose of NaCl in cattle resulted in a biphasic sodium excretion pattern, providing preliminary evidence of short-term extrarenal sodium storage in large mammals without corresponding urinary potassium exchange.
p-value: p=Urine Na+ excretion over time p < 0.001; Faecal Na+ excretion over time p < 0.001 (rmANOVA and GAMM)
Under conditions of dietary sodium (Na+) excess, the kidneys may fail to adequately excrete Na+, potentially compromising blood pressure homeostasis. Body tissues, such as skin, can offer sites of short-term extrarenal Na+ storage and previous research has shown that this can help guard against hypertension in small mammals (e.g., rodents). Large mammals have relatively greater Na+ storage potential, but whether extrarenal Na+ storage occurs for this group is unknown. Here, we report preliminary evidence of extrarenal Na+ storage in cattle. We provided a large pulse-dose of NaCl to four cattle (body mass: ~720 kg) and measured excretion of Na+ and potassium (K+) in urine and faeces for a period of 7-days. Following NaCl administration, Na+ excretion spiked in both urine and faeces for ~ 48 h before returning to baseline measurements. After ~ 96 h, however, Na+ excretion increased again; a consistent physiological phenomenon across all individuals studied. We did not observe a pattern in urinary K+ excretion, indicating that the mechanism of Na+ storage does not appear to involve exchange for K+. However, faecal K+ excretion was reciprocal to that of Na+, presumably reflecting exchange of Na+/K+ across the walls of the large intestine. We infer that during the initial period of Na+ stress, short-term extrarenal Na+ storage occurred and the stored Na+ was later released only when the body had returned to Na+ homeostasis. Additional experiments are required to understand how patterns of Na+ regulation changes across body sizes and the specific body compartments involved. Cattle may be a useful model system for examining the impact of high Na+ intake in mammals larger than humans.
Abraham et al. (Sat,) conducted a other in Adult lactating Original Brown Swiss cows with rumen fistulae, body mass 700–740 kg, in late lactation, free stall housing in Switzerland (n=4). Single large pulse dose of NaCl vs. Baseline measurements prior to NaCl administration was evaluated on Sodium (Na+) excretion in urine and faeces over 7 days following NaCl dose, indicating extrarenal Na+ storage mechanism (p=Urine Na+ excretion over time p < 0.001; Faecal Na+ excretion over time p < 0.001 (rmANOVA and GAMM)). A single 400 g NaCl pulse dose in lactating cows induced a biphasic Na+ excretion pattern with initial rapid excretion followed by a delayed second peak after ~96 h, consistent with short-term extrarenal sodium storage without concomitant changes in urinary potassium excretion.