Effects of KCl infusion on potassium excretion in sheep

Abstract

To determine the quantitative relation of K excretion (UKV) to plasma K concentration (PK), three fasted, conscious, mature ewes were infused intravenously with 50 mmol KCl over 15, 30, and 60 min. Control experiments were without infusion. During KCl infusion PK was increased to 7.26 +/- 0.40 (15 min), 6.68 +/- 0.48 (30 min), and 5.59 +/- 0.3 meq/liter (60 min). During all three infusions the increase in UKV relative to the increase in PK was similar. The mean delta UKV/delta PK ratio was 160 +/- 30 (SD) mueq/min per meq/liter (range 102-203). On termination of each infusion PK decreased to control values, but UKV either remained elevated (60-min infusion) or first decreased and then increased (15- and 30-min infusions). The second, delayed kaliuresis began 30-45 min after initiation of KCl infusion and accelerated a return to the level of K balance of the control experiments. A plot of UKV against the corresponding period PK showed that, at a common value of PK, UKV was higher following KCl infusion when PK was dropping than during KCl infusion when PK was rising. The mechanisms responsible for this hysteresis phenomenon are not identified.

Gut sensing of dietary K+ intake increases renal K+ excretion

“…C and D: data from individual rats are shown with open symbols representing the 0% K ϩ diet group, and solid symbols the 1% K ϩ diet group (n ϭ 2 and 3, respectively). Rabinowitz (24,25) previously compared renal K ϩ excretion in sheep following a typical meal vs. K ϩ excretion during intravenous K ϩ infusion in the fasting state that reproduced meal-induced rises in plasma [K ϩ ]. He found that K ϩ excretion with intravenous infusion was only ¼ the amount observed with meal intake, concluding that meal-induced increases in renal K ϩ excretion cannot be explained by changes in plasma [K ϩ ].…”

“…Thus, the maintenance of K ϩ homeostasis has been traditionally understood on the basis of the concept of negative feedback control. However, Rabinowitz (21,22) challenged this traditional view when he pointed out that plasma K ϩ and aldosterone can stimulate renal K ϩ excretion only at levels above their normal ranges (3,25,31,32). In his studies in the sheep (24), meal intake over 1 h produced a pronounced kaliuresis, which occurred in the absence of a change in plasma aldosterone concentration and with only a very small (0.5 meq/l) increase in plasma [K ϩ ].…”

“…In his studies in the sheep (24), meal intake over 1 h produced a pronounced kaliuresis, which occurred in the absence of a change in plasma aldosterone concentration and with only a very small (0.5 meq/l) increase in plasma [K ϩ ]. The 0.5 meq/l rise in plasma K ϩ , when reproduced by intravenous K ϩ infusion, was too small to account for the meal-induced kaliuresis (25), leading Rabinowitz to conclude that a kaliuretic reflex arising from sensors in the splanchnic bed (i.e., gut, portal circulation, and/or liver) induced the postprandial increases in renal K ϩ excretion rather than a rise in plasma aldosterone or plasma K ϩ . According to the Rabinowitz proposal, renal K ϩ excretion is increased, without (or before) increases in extracellular [K ϩ ], by a mechanism controlled by sensing of K ϩ intake (i.e., sensing of local increase in [K ϩ ] in splanchnic areas during K ϩ intake).…”

Evidence for gut factor in K+ homeostasis

“…However, Rabinowitz (16,17) challenged this traditional view. He pointed out that plasma K ϩ and aldosterone can stimulate renal K ϩ excretion only at levels above their normal ranges (2,19,23,24). In his studies in the sheep (18), meal intake produced a pronounced kaliuresis, which was accompanied by no change in plasma aldosterone concentration.…”

Circadian rhythm of urinary potassium excretion during treatment with an angiotensin receptor blocker

“…It was reported that aldosterone can contribute to U K V only under the condition of supraphysiologic levels due to hyperkalemia. 25 In addition, recently, it was reported that dietary potassium intake was sensed in the gut, and an unidentified gut factor is activated to stimulate renal potassium. 26 Dietary potassium was constant and relatively low in this study protocol.…”