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Role of transmural pressure and α‐adrenoceptors in acute mechanoadaptive remodeling in mouse tail resistance arteries
Author(s) -
Hughes Jennifer M.,
Flavahan Nicholas A.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1212-b
Subject(s) - constriction , norepinephrine , medicine , vascular resistance , chemistry , vascular smooth muscle , myogenic contraction , endocrinology , stimulation , cardiology , blood pressure , smooth muscle , dopamine
After prolonged constriction to norepinephrine, vascular smooth muscle cells (VSMs) undergo a mechanoadaptation process resulting in incomplete relaxation upon removal of the agonist. Experiments were performed to determine the role of transmural pressure (P TM ) and α‐adrenergic activation in this remodeling. Mouse tail resistance arteries were isolated and exposed to P TM s of 10 or 60 mmHg. A P TM of 60 but not 10 mmHg evoked a robust and prolonged myogenic constriction. Mechanoadaptation and remodeling of VSMs was assessed by recording pressure‐diameter relationships in Ca 2+ ‐free Krebs solution before and after interventions. Exposure of arterioles to P TM s of 10 or 60 mmHg for 5 min or 4 hrs did not alter the pressure‐diameter curves. Arterioles were constricted with norepinephrine (10 −6 M, ~50% constriction) for 5 min or 4 hrs at a P TM of 60 mmHg. Constriction to norepinephrine for 5 min did not change the pressure‐diameter curves. However, constriction to norepinephrine (10 −6 M) for 4 hrs at a P TM of 60 mmHg depressed pressure‐diameter curves, and significantly decreased arterial diameter compared with pre‐exposure controls (p<0.05). Therefore, α‐adrenoceptor stimulation but not the P TM ‐induced myogenic response causes mechanoadaptive remodeling in mouse tail resistance arteries.