Abstract
We tested the hypothesis that conduction of vasomotor responses occurs in cannulated and isolated rat cerebral penetrating arterioles. Both at the site of stimulation (local) and 500-650 μm distant from it, we observed the diameter responses and time courses thereof to pressure-ejected vasoactive stimuli. ATP locally caused an initial constriction (response onset at 0.3 s, average diameter 85% of control at 450-ms pulse with a maximum at 1.6 s after stimulation) followed by a secondary dilation (111% at 7 s). Conducted vasodilation of 111% was observed over a distance of 520 μm. Prostaglandin F(2α) (PGF(2α)) constricted the vessels locally (80%) and caused conducted vasodilation (110%). For both ATP and PGF(2α) the local constriction occurred simultaneously to the conducted vasodilation. Adenosine dilated the vessels (123%) but produced only inconsistent conducted vasodilation. Hydrogen ions initially constricted the vessels (88%) and then dilated them to 113%. Thus, although ATP and PGF(2α) are strong promoters of conduction, adenosine and hydrogen ions are not. Paradoxically, ATP and PGF(2α) caused conducted vasodilation even though the initial local response was a vasoconstriction, indicating that in cerebral arterioles conduction may be mediated through endothelial cell mechanisms rather than through smooth muscle cell communication.
Original language | English |
---|---|
Pages (from-to) | H1109-H1116 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 271 |
Issue number | 3 40-3 |
DOIs | |
State | Published - Sep 1996 |
Keywords
- adenosine
- adenosine triphosphate
- brain
- hydrogen ions
- microcirculation
- prostaglandin F(2α)
- regulation