Modulation of the hydro-osmotic effect of vasopressin on the rabbit cortical collecting tubule by adrenergic agents

The effects of catecholamines on antidiuretic hormone ([Arg⁸]-vasopressin [AVP])-induced water absorption were evaluated in cortical collecting tubules isolated from the rabbit kidney and perfused in vitro. In the presence of AVP (100 μU/ml), net fluid volume absorption (J(v), nanoliters per minute per millimeter) was 1.14 ± 0.12 and osmotic water permeability coefficient (P(f) x 10^-4 centimeters per second) was 217.3 ± 39.9. The addition of the alpha-adrenergic agonist, phenylephrine (PE), in a concentration of 10^-6 M resulted in a significant decrease in J(v) and P(f) to 0.83 ± 0.13 (P < 0.001) and 148.8 ± 41.8 (P < 0.02), respectively. Increasing the concentration of PE to 10^-5 M resulted in a further decrease in J(v) and P(f) to 0.53 ± 0.05 (P < 0.05 vs PE 10^-6 M) and 88.5 ± 9.0 (P < 0.05 vs. PE 10^-6 M), respectively. In a separate group of tubules, in the presence of AVP (100 μU/ml) and PE (10^-5 M), J(v) and P(f) were 0.35 ± 0.07 and 66.0 ± 17.3, respectively. The addition of the alpha-adrenergic antagonist, phentolamine (PH), in a concentration of 10^-6 M resulted in a significant increase in J(v) to 1.07 ± 0.19 (P < 0.001) and P(f) to 193.3 ± 35.9 (P < 0.005). PH (10^-5 M) alone did not significantly affect J(v) and P(f) in the presence of AVP (100 μU/ml) nor in the presence of 8-bromo adenosine 3',5' cyclic monphosphate (8-BrcAMP). J(v) and P(f) were 1.20 ± 0.21 and 174.0 ± 25.8, respectively, in the presence of 8-BrcAMP (10^-4 M). We next examined the effect of the beta-adrenergic agonist, isoproterenol (ISO), on J(v) and P(f) in the presence of AVP. J(v) and P(f) were 1.04 ± 0.10 and 202.6 ± 17.2, respectively, in the presence of AVP (100 μU/ml) and 1.06 ± 0.18 and 193.4 ± 27.7, respectively, in the presence of AVP (10 μU/ml). However, in the presence of AVP in a concentration of 2.5 μU/ml, J(v) was 0.60 ± 0.07 and P(f) was 100.7 ± 24.7. ISO (10^-6 and 10^-5 M) did not have any significant effect in the presence of the above maximal and submaximal concentrations of AVP. In the absence of AVP, control J(v) was 0.01 ± 0.12 and P(f) was 4.6 ± 11.0. The addition of ISO at 25 or 37°C did not result in any significant change in J(v) or P(f). These studies indicate that alpha-adrenergic agonists directly inhibit AVP-mediated water absorption at the level of the tubule, an effect that can be blocked by a specific alpha-adrenergic antagonist. This effect appears to be exerted at the level of activation of adenylate cyclase since it is absent in the presence of cAMP. The beta-adrenergic agonists do not directly inhibit or enhance AVP-mediated water absorption at the level of the renal tubule.