Nitric oxide inhibits ADH-stimulated osmotic water permeability in cortical collecting ducts
| Autor: | Jeffrey L. Garvin, Silvia I. Pomposiello, Nestor H. Garcia |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
Osmosis medicine.medical_specialty Vasopressin Kidney Cortex Vasopressins Physiology Renal cortex medicine.medical_treatment Sodium chemistry.chemical_element In Vitro Techniques Nitric Oxide Models Biological Permeability Nitric oxide Rats Sprague-Dawley Nitroglycerin chemistry.chemical_compound Internal medicine medicine Animals Osmotic pressure Kidney Tubules Collecting Renal sodium reabsorption Reabsorption Water Diuresis Rats medicine.anatomical_structure Endocrinology chemistry Diuretic |
| Zdroj: | American Journal of Physiology-Renal Physiology. 270:F206-F210 |
| ISSN: | 1522-1466 1931-857X |
| Popis: | Nitric oxide (NO) reduces blood pressure in vivo by two mechanisms, vasodilation and increasing urinary volume: however, the exact mechanism by which it increases urinary volume is not clear. We hypothesized that NO inhibits antidiuretic hormone (ADH)-stimulated fluid reabsorption (J(r)) by the isolated rat cortical collecting duct (CCD) by decreasing water permeability (Pf) and sodium reabsorption (Jna). In the presence of 10(-11) MADH, Jv was 0.15 +/- 0.04 nl.min-1.mm-1; after 10(-6) M spermine nonoate (SPM) was added to the bath. Jv decreased to 0.06 +/- 0.03 nl.min-1.mm-1 (P < 0.03). To investigate whether the inhibition of Jv was the result of decreased Pf and/or Jna, we first tested the effect of SPM on ADH-stimulated Pf. Basal Pf was stimulated to 289.2 +/- 77.3 microns/s after 10(-11) M ADH was added to the bath (P < 0.01). SPM decreased Pf to 159.8 +/- 45.0 microns/s (P < 0.05). To ensure that this effect on Pf was due to NO release, we used another NO donor, nitroglycerin (NTG). Pf was initially -25.8 +/- 18.3 microns/s and increased to 133.9 +/- 30.5 microns/s after addition of 10(-11) M ADH (P < 0.002). NTG, 20 microM, lowered Pf to 92.4 +/- 18.4 microns/s (P < 0.02). In the presence of 10(-9) M ADH, NTG also decreased Pf(P < 0.04). Next we investigated the effect of SPM on ADH-stimulated JNa. In the presence of ADH, JNa was 37.8 +/- 7.3 pmol.min-1.mm-1. After SPM was added, it dropped to 24.3 +/- 5.1 pmol.min-1.mm-1 (P < 0.05). Time controls exhibited no change in ADH-stimulated Jv, Pf, or Jna. We concluded that 1) NO decreases ADH-stimulated water and sodium transport in the isolate CCD, and 2) water reabsorption is inhibited by a primary effect on Pf. A direct effect of NO on the CCD may explain its natriuretic and diuretic effects observed in vivo. |
| Databáze: | OpenAIRE |
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