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Responses to endothelium‐derived factors and their interaction in mesenteric arteries from Wistar‐Kyoto and stroke‐prone spontaneously hypertensive rats
Author(s) -
Sekiguchi Fumiko,
Nakahira Tomohiro,
Kawata Kyoko,
Sunano Satoru
Publication year - 2002
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2002.03778.x
Subject(s) - apamin , endothelium derived hyperpolarizing factor , nitric oxide , vasodilation , endothelium , mesenteric arteries , chemistry , pharmacology , medicine , endocrinology , hyperpolarization (physics) , charybdotoxin , potassium channel , artery , stereochemistry , nuclear magnetic resonance spectroscopy
Summary 1. Responses to endothelium‐derived nitric oxide (EDNO), indomethacin‐sensitive endothelium‐derived contracting factor (EDCF) and hyperpolarization by endothelium‐derived hyperpolarizing factor (EDHF) and the interaction among these factors in mesenteric arteries from 16‐week‐old Wistar Kyoto (WKY) rats and age‐matched stroke‐prone spontaneously hypertensive rats (SHRSP) were studied, observing the time‐course of the response to 10 −5 mol/L acetylcholine (ACh). 2. The effects of EDNO, EDCF and EDHF were blocked by N ω ‐nitro‐ l ‐arginine (10 −4 mol/L), indomethacin (10 −5 mol/L) and a combination of apamin (5 × 10 −6 mol/L) and charybdotoxin (10 −7 mol/L), respectively. 3. The response to EDNO observed in the absence of EDCF and EDHF was not different between preparations from WKY rats and SHRSP. The response to EDCF observed in the absence of EDNO and EDHF was slightly greater in preparations from SHRSP. The response to EDHF in the absence of EDNO and EDCF was much greater in preparations from WKY rats. 4. Endothelium‐derived contracting factor attenuated the relaxation in response to EDNO, the attenuation being greater in preparations from SHRSP. Relaxation in response to EDNO was blocked by EDHF in preparations from WKY rats, but not in preparations from SHRSP. 5. The response to EDCF was augmented by both EDNO and EDHF. The augmentation was greater in preparations from SHRSP. 6. The response to EDHF was attenuated by EDNO in preparations from WKY rats, but not in preparations from SHRSP. The response to EDHF was attenuated by EDCF in preparations from both WKY rats and SHRSP, the attenuation being greater in preparations from SHRSP. 7. These results suggest that there are interactions among these factors in terms of their release or the response to ACh in mesenteric arteries that differ between preparations from WKY rats and SHRSP. In addition, involvement of factors other than these three factors, which also differs between preparations from WKY rats and SHRSP, is suggested.