From the Institute of Physiology and Pathophysiology,
Johannes-Gutenberg-Universität, Mainz, Germany.
Correspondence to Dr Cor de Wit, Institute of Physiology and Pathophysiology, Johannes-Gutenberg-Universität Mainz, Duesbergweg 6, D-55099 Mainz, Germany. E-mail dewit{at}mailvms.zdv.uni-mainz.de
Abstract—A myogenic vasoconstriction
may amplify the effects of circulating vasoconstrictors. In cremaster
arterioles, the contribution of a myogenic component to the
constriction on intravenous infusion of
norepinephrine (NE) or angiotensin II (Ang II)
was studied. Second, the role of endothelium-derived
nitric oxide (NO) in the control of these myogenic constrictions and
its site of action in the resistance vascular bed was investigated. In
30 anesthetized (pentobarbital) hamsters, the cremaster was
prepared for intravital microscopy, and a pneumatic vessel occluder was
placed around the aorta to vary blood pressure in the hindquarter of
the animal. Intravenous infusion of NE (0.5 nmol/min)
increased the systemic blood pressure by 52±2 mm Hg.
Simultaneously, constrictions of up to 33±6% were
observed in the small arterioles (SAs; maximal inner diameter, 36 to
65 µm). The constrictions were not significantly altered by a
local adrenergic blockade but were abolished when the pressure
elevation in the cremaster arterioles was blocked by partial occlusion
of the abdominal aorta. Diameters in large arterioles (LAs; maximal
inner diameter, 65 to 127 µm), however, did not change
significantly on NE infusion. Similar responses in the arterioles were
observed when the local pressure was increased stepwise from 60 to
120 mm Hg by partial opening of the aortic occluder. However,
after treatment of the cremaster tissue with the inhibitor
of the NO synthase,
NG-nitro-L-arginine (L-NNA,
30 µmol/L), a significant pressure-induced constriction of up to
16±3% occurred in LAs, whereas the magnitude of the constriction in
SAs remained unchanged. L-NNA also abolished the increases in blood
flow that were observed with increments in pressure in control animals.
Similar results were obtained when Ang II was used to increase blood
pressure. We conclude that a myogenic constriction of SAs contributes
markedly to the overall response of cremaster arterioles to circulating
vasoconstrictors. NO effectively opposes the myogenic response in LAs,
thus preventing myogenic constrictions in a vascular region where
constriction cannot be fully controlled by metabolic
dilation. If this attenuating effect of NO on myogenic constriction
also takes place in other organs, it might be a decisive mechanism in
controlling changes of total peripheral vascular resistance
elicited by vasoconstrictors.
© 1998 American Heart Association, Inc.
Scientific Contributions
Nitric Oxide Opposes Myogenic Pressure Responses Predominantly in Large Arterioles In Vivo
Key Words: endothelium • angiotensin II • norepinephrine • arterioles • blood pressure • microscopy
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