Endothelium-derived relaxing factors in the kidney of spontaneously hypertensive rats.
Acetylcholine (ACh)-induced vasodilation is mainly due to endothelium-derived nitric oxide (EDNO) and hyperpolarizing factor (EDHF). To explore the mechanisms underlying attenuated endothelium-dependent vasodilation in hypertensive arteries, we measured the EDNO released from isolated kidneys of spontaneously hypertensive rats (SHR) using a sensitive chemiluminescence assay system of NO. ACh-induced renal vasodilation was significantly smaller in SHR than in the normotensive control, Wistar-Kyoto rats (WKY). However, ACh-induced NO release did not differ between SHR and WKY (10(-7) M: SHR +37 +/- 2 [SE] vs. WKY +32 +/- 4 fmol/min/g kidney). Perfusion with a 20 mEq/L high-K+ buffer, which is reported to inhibit action of EDHF, significantly reduced ACh-induced vasorelaxation in WKY but not in SHR, resulting in identical renal perfusion pressure in SHR and wKY under these conditions. These results indicate that attenuated ACh-induced vasorelaxation in the SHR kidney may be attributed to a decrease in EDHF rather than that in EDNO.
Hayakawa
H
H
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Hirata
Y
Y
Suzuki
E
E
Kakoki
M
M
Kikuchi
K
K
Nagano
T
T
Hirobe
M
M
Omata
M
M
D000109:Acetylcholine / Q000008:administration & dosage; D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000031:analogs & derivatives; D007668:Kidney / Q000098:blood supply*; D008163:Luminescent Measurements; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D019323:omega-N-Methylarginine
D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D001120:Arginine; D000109:Acetylcholine