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- Title
Role of endogenous endothelin and nitric oxide in tubuloglomerular feedback.
- Authors
Kawabata, Masahiko; Wen-Hua Han; Ise, Takuyuki; Kobayashi, Ken-Ichi; Takabatake, Toshikazu
- Abstract
To elucidate the roles of endogenous endothelin (ET) and nitric oxide (NO) in tubuloglomerular feedback (TGF), the effects of FR139317, a specific ET-A receptor antagonist, and NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor on TGF were studied in Sprague-Dawley rats. FR139317 (1.5 mg/kg/hr i.v.) reversed the systemic pressor and renal vasoconstrictor responses induced by ET-1 (2 nmol/kg/hr i.v.), but did not alter the early proximal flow rate (EPFR) reduction in response to a loop perfusion with an artificial tubular fluid at 40 nI/mm (47 ± 3 vs. 47 ± 3% in controls). L-NNA (0.2 mg/kg + 2 µg/kg/min i.v.) had no effect on systemic blood pressure (BP), renal hemodynamics or EPFR measured at zero perfusion (31 ± 2 vs. 31 ± 2 nI/mm in controls), but enhanced the EPFR reduction during loop perfusion to 77 ± 3%. Loop perfusion with 10-3 M L-NNA in perfusate also increased the EPFR reduction to 70 ± 7%. In conclusion, inhibition of NO synthesis enhances the TGF-mediated reduction of nephron GFR. This indicates an active participation of endogenous NO in the control of afferent arteriolar tone. Endogenous ET does not influence TGF via the ET-A receptor.
- Subjects
ENDOTHELINS; NITRIC oxide; RECEPTOR antibodies; VASOCONSTRICTORS; BLOOD pressure
- Publication
Kidney International, 1996, Vol 49, pS135
- ISSN
0085-2538
- Publication type
Article