Reference - Detail
| RRC ID | 108 |
|---|---|
| Author | Ozawa Y, Hayashi K, Kanda T, Homma K, Takamatsu I, Tatematsu S, Yoshioka K, Kumagai H, Wakino S, Saruta T. |
| Title | Impaired nitric oxide- and endothelium-derived hyperpolarizing factor-dependent dilation of renal afferent arteriole in Dahl salt-sensitive rats. |
| Journal | Nephrology (Carlton) |
| Abstract |
BACKGROUND AND AIMS:We previously demonstrated that acetylcholine elicited nitric oxide-dependent sustained and endothelium-derived hyperpolarizing factor (EDHF)-dependent transient dilation of afferent arterioles. The present study examined whether free radicals interacted with nitric oxide-dependent and EDHF-dependent vasodilator mechanisms in renal microvessels of salt-sensitive hypertension, using the isolated perfused hydronephrotic kidney. METHODS AND RESULTS:Following the pretreatment with indomethacin (100 micromol/L) with or without nitro- l-arginine methylester (100 micromol/L), the effect of acetylcholine on noradrenaline (0.3 micromol/L)-induced constriction was evaluated in kidneys from Dahl salt-sensitive and salt-resistant rats. Although acetylcholine (0.01-10 micromol/L) caused dose-dependent and sustained vasodilation of afferent arterioles, attenuated dilation was observed in Dahl salt-sensitive rats, compared with that in salt-resistant rats (58 +/- 4 vs 101 +/- 11% reversal at 10 micromol/L acetylcholine). In the presence of nitro- l-arginine methylester, acetylcholine elicited only transient dilation, with vasodilator response blunted in Dahl salt-sensitive rats (64 +/- 4 vs 100 +/- 9% reversal at 10 micromol/L acetylcholine). Furthermore, chronic (8-10 weeks) treatment with tempol caused partial restoration of acetylcholine (10 micromol/L)-induced sustained arteriolar dilation (71 +/- 3% reversal), but complete reversal of transient dilation (92 +/- 4% reversal). Finally, acute treatment with tempol not only improved the sustained component of the acetylcholine-induced dilation but also restored the impaired responsiveness of transient dilation in Dahl salt-sensitive rats. CONCLUSION:Both sustained (nitric oxide-mediated) and transient (EDHF-mediated) components of acetylcholine-induced afferent arteriolar dilation were attenuated in Dahl salt-sensitive rats, which was attributed, in part, to enhanced free radical activity. A reversal of the sustained and transient vasodilation by the acute tempol treatment suggests possible interaction between free radicals and EDHF as well as increased bioavailability of nitric oxide. |
| Volume | 9(5) |
| Pages | 272-7 |
| Published | 2004-10-1 |
| DOI | 10.1111/j.1440-1797.2004.00292.x |
| PII | NEP292 |
| PMID | 15504139 |
| MeSH | Acetylcholine / pharmacology Animals Arterioles / physiopathology Biological Factors / physiology* Endothelium, Vascular / physiopathology* Hypertension / physiopathology* Kidney / blood supply* Kidney / physiopathology* Male Nitric Oxide / physiology* Rats Rats, Inbred Dahl Vasodilation / drug effects |
| IF | 1.749 |
| Times Cited | 15 |
| WOS Category | UROLOGY & NEPHROLOGY |
| Resource | |
| Rats | |