Abstract
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 (Jv, nanoliters per minute per millimeter) was 1.14±0.12 and osmotic water permeability coefficient (Pf, 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 Jv and Pf 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 Jv and Pf 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), Jv and Pf 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 Jv to 1.07±0.19 (P < 0.001) and Pf to 193.3±35.9 (P < 0.005). PH (10-5 M) alone did not significantly affect Jv and Pf in the presence of AVP (100 μU/ml) nor in the presence of 8-bromo adenosine 3',5' cyclic monophosphate (8-BrcAMP). Jv and Pf 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 Jv and Pf in the presence of AVP. Jv and Pf 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 (10μU/ml). However, in the presence of AVP in a concentration of 2.5 μU/ml, Jv was 0.60±0.07 and Pf 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 Jv was 0.01±0.12 and Pf was 4.6±11.0. The addition of ISO at 25 or 37°C did not result in any significant change in Jv or Pf.
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.
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Selected References
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