TY - JOUR
T1 - Mediator role of prostaglandins in acetylcholine-induced vasodilation and control of resting vascular diameter in the hamster cremaster microcirculation in vivo
AU - De Wit, Cor
AU - Von Bismarck, Philipp
AU - Pohl, Ulrich
N1 - Copyright:
Copyright 2015 Elsevier B.V., All rights reserved.
PY - 1993
Y1 - 1993
N2 - Acetylcholine (ACh) is widely used as a standard test substance for nitric oxide (NO)-mediated vasodilation. However, it also augments the release of prostaglandins, a group of other endothelium-derived smooth muscle relaxants. Using intravital microscopy in the cremaster muscle of anesthetized hamsters, we studied the relative roles of NO and prostaglandins in mediating ACh- induced dilation and in the control of basal vessel tone (253 arterioles in 31 experiments). Nω-nitro-L.-arginine (L-NNA), a competitive inhibitor of NO synthase, significantly reduced ACh-induced vasodilation (by 42-73%), irrespective of whether it was applied intravenously (30 mg/kg) or topically (30 μM). Additional indomethacin (3 μM, topical) nearly abolished the dilator response. In contrast, the vascular responses to the endothelium-independent dilator sodium nitroprusside were not affected. The resting diameters (range; 6-114 μm) were significantly (p < 0.05) reduced after L-NNA or indomethacin by 10.2 and 16.6% of control diameter, respectively. The constriction induced by L-NNA was stronger in larger (>50 μm) than in smaller (<50 μm) vessels, whereas indomethacin was equipotent in both groups. Thus, in addition to NO, dilating prostaglandins are important mediators of the ACh- induced dilation and contribute to the control of resting arteriolar diameter in the hamster cremaster microcirculation in vivo.
AB - Acetylcholine (ACh) is widely used as a standard test substance for nitric oxide (NO)-mediated vasodilation. However, it also augments the release of prostaglandins, a group of other endothelium-derived smooth muscle relaxants. Using intravital microscopy in the cremaster muscle of anesthetized hamsters, we studied the relative roles of NO and prostaglandins in mediating ACh- induced dilation and in the control of basal vessel tone (253 arterioles in 31 experiments). Nω-nitro-L.-arginine (L-NNA), a competitive inhibitor of NO synthase, significantly reduced ACh-induced vasodilation (by 42-73%), irrespective of whether it was applied intravenously (30 mg/kg) or topically (30 μM). Additional indomethacin (3 μM, topical) nearly abolished the dilator response. In contrast, the vascular responses to the endothelium-independent dilator sodium nitroprusside were not affected. The resting diameters (range; 6-114 μm) were significantly (p < 0.05) reduced after L-NNA or indomethacin by 10.2 and 16.6% of control diameter, respectively. The constriction induced by L-NNA was stronger in larger (>50 μm) than in smaller (<50 μm) vessels, whereas indomethacin was equipotent in both groups. Thus, in addition to NO, dilating prostaglandins are important mediators of the ACh- induced dilation and contribute to the control of resting arteriolar diameter in the hamster cremaster microcirculation in vivo.
UR - http://www.scopus.com/inward/record.url?scp=0027214511&partnerID=8YFLogxK
U2 - 10.1159/000159006
DO - 10.1159/000159006
M3 - Journal articles
C2 - 8399988
AN - SCOPUS:0027214511
SN - 1018-1172
VL - 30
SP - 272
EP - 278
JO - Journal of Vascular Research
JF - Journal of Vascular Research
IS - 5
ER -