Renal glomerular and tubular effects of antidiuretic hormone and two antidiuretic hormone analogues in house sparrows (Passer domesticus).

Abstract

We infused arginine vasotocin, the natural avian antidiuretic hormone, and two antidiuretic hormone analogues into house sparrows (Passer domesticus) to evaluate the vascular and tubular components of antidiuresis in a small (25-g) bird. During control infusion of 25 mmol L-1 NaCl (0.6 mL h-1), urine flow rate was 0.73 mL h-1, glomerular filtration rate was 10.0 mL h-1, the ratio of polyethylene glycol (PEG) in the urine relative to that in the plasma was 16.4, and urine osmolality was 279 mOsmol kg-1. Infusion of arginine vasotocin (0.4 ng kg-1 min-1) decreased urine flow rate by 50% and glomerular filtration rate by 27%, while urine osmolality and the ratio of urine PEG to plasma PEG rose to 150% and 140% of control values, respectively. A higher dose of arginine vasotocin (1.6 ng kg-1 min-1) accentuated these changes. Infusion of the antidiuretic hormone analogue dPTyr(Me)AVT, designed as an antagonist to the V1 (mammalian vascular) receptors for arginine vasopressin, by itself (4.0 ng kg-1 min-1) had no effect on any measured variable (P > or = 0.1). Infusion of the analogue along with arginine vasotocin (0.4 ng kg-1 min-1) abolished the effect of arginine vasotocin on glomerular filtration rate, which suggests that this analogue blocked vascular receptors for arginine vasotocin in house sparrows. Under these circumstances, changes in urine flow rate, the ratio of urine PEG to plasma PEG, and urine osmolality were reduced to nonsignificance. The analogue d(CH2)5[D-Ile2,Ile4,Ala-MH2]AVP, designed as an antagonist to the effects of arginine vasopressin at V2 (mammalian renal tubular) receptors, also was without effect by itself. However, in the presence of this analogue, the effects of arginine vasotocin on urine flow rate and the ratio of urine PEG to plasma PEG were significantly enhanced, and this occurred without any enhanced diminution of glomerular filtration rate. Thus, this analogue appeared to activate a tubular mechanism of antidiuresis. Overall, the data suggest that action of arginine vasotocin at renal vascular receptors plays an important role in effecting antidiuresis in house sparrows. Blockade of renal vascular actions of arginine vasotocin by a V1 antagonist suggest that these receptors may be similar to the mammalian vascular (V1) receptor. The data also suggest a separate action of arginine vasotocin at the renal tubules, but the receptors there apparently differ from the mammalian tubular (V2) receptor.