Sustained response to vasopressin in isolated rat cortical collecting tubule

Abstract

The effect of arginine vasopressin (ADH) on water permeability and transepithelial voltage was examined in cortical collecting tubules from a specific pathogen-free line of male Sprague-Dawley rats (75-125 g body weight). Tubules were bathed in a medium resembling serum ultrafiltrate (310 mOsm/kg H2O) at 38 degrees C. Osmotic water permeability (Pf, micron/sec) was determined by the volume flow occurring with a hypo-osmotic perfusate (210-220 mOsm/kg H2O) and diffusional water permeability (Pd, micron/sec) was calculated from the lumen-to-bath flux of tritiated water using an isosmotic perfusate. In the absence of ADH, both Pf and Pd were low, 17 +/- 6 and 9.0 +/- 0.6 (SEM), respectively. ADH added to the bath at concentrations above 0.5 microunits/ml increased Pf, with a maximal response at 40 microunits/ml or greater. With 100 microunits/ml ADH, Pf and Pd were, respectively, 994 +/- 117 and 37.0 +/- 2.4. Without ADH, the transepithelial voltage was variable (range, -5.4 to +2.5 mV; mean, -1.9 +/- 0.4); however, with 100 microU/ml ADH, it hyperpolarized (lumen-negative) by 4.2 +/- 0.8 mV. In contrast to findings in the rabbit, both the hyperpolarization and the increased water permeability persisted for at least 3 hr. The higher water permeabilities are consistent with the shorter length of the cortical collecting tubule in the rat, and may reflect the importance of attaining osmotic equilibration within the cortex during maximal antidiuresis.

Control of sodium and potassium transport in the cortical collecting duct of the rat. Effects of bradykinin, vasopressin, and deoxycorticosterone.

“…Arginine vasopressin added to the bath caused a sustained increase in both the transepithelial potential difference and the rate of net sodium absorption, which is consistent with prior observations (15,18). These results contrast with observations in rabbit cortical collecting ducts in which there is only a transient stimulation of potential difference and sodium transport (19,22).…”

“…This increase in sodium absorption was associated with the appearance of a significant rate of spontaneous fluid absorption (P < 0.005 vs. control), which was undoubtedly facilitated by the marked increase in osmotic water permeability caused by vasopressin in this segment (15). Vasopressin also caused a marked enhancement of the lumen-negative potential difference, from a control level of -10.7±3.4 mV to -26.6±5.8 mV (P < 0.01), and caused a marked increase in net potassium secretion from a control level of -5.1±2.5 pmol/mm per min to -16.6±6.2 (P < 0.05).…”

Effects of vasopressin and bradykinin on anion transport by the rat cortical collecting duct. Evidence for an electroneutral sodium chloride transport pathway.

“…1, right) was lumen-negative (-6.1±0.8 mV) in the absence of AVP. As in previous studies ( 1,9,10) 2. In initial control measurements, total CO2 was secreted (-7.3±1.8 pmol/min per mm).…”

“…In our experiments, the chloride concentration in the reabsorbed fluid (calculated as the rate of chloride absorption divided by the rate of fluid absorption) was 150-160 mM with vasopressin present, compared with 1 8 mM in the perfusate and bath. The luminal chloride concentration fell only [8][9][10] meq/liter below the perfusate despite the absorption of 20% or more of the perfused chloride.…”

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

“…Vasopressin binding to V2 receptors in principal cells of the CD not only increases the permeability to water of the luminal membrane through its action on AQP2 but also increases sodium reabsorption by stimulating the activity of the epithelial sodium channel ENaC (5,28). Thus, it is logical to assume that V2 actions of vasopressin on the CD should reduce sodium excretion by a direct effect, as is discussed further below.…”