Differential Ca2+ Coupling of Alpha‐Adrenoreceptors in Murine Mesenteric Arteries and Veins

Abstract

Mesenteric veins are more sensitive to adrenergic stimulation than arteries and this could be due to different Ca2+ handling mechanisms in arteries and veins. We studied Ca2+ handling in pressurized arteries (60 mmHg) and veins (8 mmHg). Veins were more sensitive to the constrictor effects of norepinephrine (NE) than arteries; EC50 values were 50 and 300 nM respectively. CdCl2 (100 μM), but not nifedipine (1 μM) or GdCl3 (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 Ca2+ to support NE‐induced contraction but capacitive Ca2+ entry and L‐type Ca2+ do not contribute to Ca2+ entry in arteries or veins. Facilitation of Ca2+ influx and inhibition of Ca2+ removal by ouabain after intracellular Ca2+ depletion is sufficient for NE to contract arteries, but not veins. Veins have larger Ca2+ stores and more efficient store refilling than arteries; this may account for increased reactivity of veins to NE.