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Remote arteriolar dilations in response to muscle contraction under capillaries
K D Cohen1, B R Berg, I H Sarelius
1Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, NY 14642, USA.
Summary
Remote muscle contraction causes upstream arteriole dilation via a novel gap junction pathway. This conducted vasodilation is insensitive to common blockers, suggesting multiple signaling mechanisms in microvascular regulation.
Area of Science:
- Physiology
- Microcirculation
- Vascular Biology
Background:
- Skeletal muscle contraction triggers remote arteriolar dilations upstream of capillaries.
- These dilations were previously hypothesized to involve gap junctions over nerves.
Purpose of the Study:
- To investigate the signaling mechanisms responsible for remote conducted vasodilation in hamster cremaster muscle arterioles.
- To differentiate between gap junction and nerve-mediated pathways, and explore the role of nitric oxide.
Main Methods:
- Used pharmacological agents including halothane, sucrose, tetrodotoxin, 18-beta-glycyrrhetinic acid, KCl, and N(omega)-nitro-L-arginine.
- Measured arteriolar diameter changes in response to selective muscle fiber contraction under stimulated conditions.
- Analyzed the effects of blockers on conducted vasodilation in module inflow and branch arterioles.
Main Results:
- Halothane and sucrose blocked dilation in module inflow and branch arterioles, respectively.
- Dilation was not blocked by tetrodotoxin or 18-beta-glycyrrhetinic acid, suggesting a non-neuronal, atypical gap junction pathway.
- Nitric oxide synthase inhibition attenuated dilation in the branch arteriole but not the module inflow arteriole.
Conclusions:
- Conducted vasodilation upstream of contracting muscle fibers involves a gap junction pathway distinct from those typically blocked by 18-beta-glycyrrhetinic acid.
- Multiple signaling pathways, potentially including nitric oxide in specific vessels, contribute to remote microvascular adjustments.
- These findings highlight the complexity of microvascular regulation during muscle activity.