Luminal adenosine receptors regulate amiloride-sensitive Na+ channels in A6 distal nephron cells
| Autor: | He-Ping Ma, Brian N. Ling |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
Adenosine Patch-Clamp Techniques Physiology Sodium Channels Cell Line Amiloride Adenosine A1 receptor Internal medicine Phenethylamines Purinergic P1 Receptor Agonists medicine Patch clamp Ion transporter Dose-Response Relationship Drug Reabsorption Chemistry Purinergic receptor Receptors Purinergic P1 Nephrons Adenosine receptor Endocrinology Purinergic P1 Receptor Antagonists Xanthines Theobromine medicine.drug |
| Zdroj: | American Journal of Physiology-Renal Physiology. 270:F798-F805 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.1996.270.5.f798 |
| Popis: | To investigate the effects of luminal adenosine on amiloride-sensitive Na+ channels, we applied the cell-attached patch-clamp technique to A6 distal nephron cells. Exposure to luminal 30 nM adenosine increased number of channels x open probability (NP0) from 0.38 +/- 0.08 to 0.77 +/- 0.09 (means +/- SE; P < 0.01, n = 17). Luminal exposure to an A1-receptor antagonist (30 nM 8-cyclopentyl-1,3-dipropylxanthine) abolished (P = 0.17, n = 11), whereas an A1 agonist (30 nM N6-cyclohexyladenosine) reproduced (P < 0.02, n = 6) the stimulatory effect of 30 nM adenosine. In contrast, higher concentrations of luminal adenosine (1 or 10 microM) decreased NP0 from 0.65 +/- 0.09 to 0.24 +/- 0.10 (P < 0.02, n = 11) and from 0.80 +/- 0.11 to 0.19 +/- 0.03 (P < 0.01, n = 8), respectively. Channel inhibition by high-dose luminal adenosine was abolished by an A2 antagonist (30 microM 3,7-dimethyl-1-propargylxanthine; P = 0.2, n = 10) and mimicked by an A2 agonist (100 nM CGS-21680 hydrochloride; P < 0.0005, n = 8). We conclude that 1) purinergic regulation of distal nephron Na+ channels is mediated by stimulatory apical A1 receptors and inhibitory apical A2 receptors; 2) basal urinary adenosine concentrations (in nM) would stimulate Na+ reabsorption, whereas higher urinary concentrations (in microM), e.g., renal ischemia and elevations in filtered NaCl load, would increase Na+ excretion; and 3) urinary adenosine may be involved in feedback regulation of distal nephron Na+ transport. |
| Databáze: | OpenAIRE |
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