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Differential Ca2+ Coupling of Alpha‐Adrenoreceptors in Murine Mesenteric Arteries and Veins
Author(s) -
Hlavacova Alexandra,
Xu Hui,
Galligan James J.
Publication year - 2008
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.22.1_supplement.912.8
Subject(s) - thapsigargin , mesenteric arteries , ouabain , contraction (grammar) , chemistry , medicine , anatomy , blood vessel , extracellular , artery , endocrinology , calcium , biochemistry , sodium , organic chemistry
Mesenteric veins are more sensitive to adrenergic stimulation than arteries and this could be due to different Ca 2+ handling mechanisms in arteries and veins. We studied Ca 2+ handling in pressurized arteries (60 mmHg) and veins (8 mmHg). Veins were more sensitive to the constrictor effects of norepinephrine (NE) than arteries; EC 50 values were 50 and 300 nM respectively. CdCl 2 (100 μM), but not nifedipine (1 μM) or GdCl 3 (10 μM), blocked NE responses in arteries and veins. Thapsigargin (1 μM) caused a strong contraction in veins that recovered slowly (~30 min). Thapsigargin did not contract arteries. NE responses in arteries and veins were blocked by thapsigargin. In the presence of ouabain (0.1 mM), thapsigargin produced a small arterial contraction. NE responses after in the presence of thapsigargin and ouabain were reduced in arteries but abolished in veins. We conclude that veins are more reactive to NE than arteries. Both vessels use extracellular Ca 2+ to support NE‐induced contraction but capacitive Ca 2+ entry and L‐type Ca 2+ do not contribute to Ca 2+ entry in arteries or veins. Facilitation of Ca 2+ influx and inhibition of Ca 2+ removal by ouabain after intracellular Ca 2+ depletion is sufficient for NE to contract arteries, but not veins. Veins have larger Ca 2+ stores and more efficient store refilling than arteries; this may account for increased reactivity of veins to NE.