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Intravascular pressure causes novel synchronous intercellular Ca 2+ oscillations in rat cerebral arteries
Author(s) -
Jarajapu Yagna Prasada Rao,
Christ George J,
Knot Harm J
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.a1157-b
Subject(s) - cerebral arteries , nifedipine , ryanodine receptor , depolarization , biophysics , chemistry , gap junction , vascular smooth muscle , anatomy , thapsigargin , intracellular , medicine , calcium , biology , smooth muscle , biochemistry , organic chemistry
Resistance arteries respond to intravascular pressure (Pi) by constricting, termed myogenic tone, involving membrane depolarization and Ca2+ influx resulting in a steady‐state increase in smooth muscle cytoplasmic [Ca2+] throughout the vascular wall. In the present study, utilizing high‐speed ratiometric digital imaging microscopy, we show previously undetected intercellular oscillations in the arterial wall [Ca2+] of pressurized posterior cerebral arteries. Internal diameter and arterial wall [Ca2+]/fura‐2 ratio were simultaneously monitored. Fura‐2 ratiometry (16 Hz) revealed synchronized oscillations in the arterial wall [Ca2+] at a Pi ≥ 40 mmHg. The frequency was Pi‐dependent, whereas amplitude was not. The oscillations were not affected by 10 μM ryanodine, 1μM thapsigargin and 1μM xestospongin C but reversibly inhibited by 1μM nifedipine and 20μM 18αglycerrhitinic acid. These data suggest the existence of a novel pressure‐induced oscillatory [Ca2+] signal. The oscillations depend on voltage‐gated Ca2+ channel activity and gap junctional communication and seem independent of Ca2+ release from the SR. This phenomenon may provide a mechanistic basis for the ability of resistance arteries to translate local hemodynamic forces into a conducted frequency encoded Ca2+ signal to remote arterioles contributing to an integrated response in the vascular bed.