Functional differences in activation between mesenteric veins and arteries during sympathetic stimulation are likely a result of differences in neuromuscular transmission.
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Differential venous depolarizations suggest vessel-specific sympathetic transmission; leaves open translation to human vascular control or alpha-blockade.
Intracellular potentials and measurements of contractions were recorded in adjacent veins and arteries in the colonic mesentery of the guinea-pig in vitro during stimulation of post-ganglionic nerve trunks. 2. Repetitive stimulation (0.5-5 Hz) of lumbar colonic nerve trunks produced frequency-dependent slow depolarizations in all venous and in 92% of arterial smooth muscle cells. Excitatory junction potentials were observed for each nerve shock in arteries, but not in veins. 3. Low-frequency stimulations produced slow depolarizations of greater amplitude and longer duration in veins than in arteries. The frequencies at which half-maximal depolarizations and contractions occurred were always lower for veins than for arteries. 4. The alpha 1-adrenergic antagonist prazosin (5 X 10(-7) M) reduced the mean arterial slow depolarizations by 82% and reduced mean venous slow depolarizations by 58% for 5 Hz stimulations. Arterial contractions were completely inhibited by prazosin but venous contractions were incompletely reduced in a frequency-dependent manner. 5. These findings suggest that functional differences in activation between mesenteric veins and arteries during sympathetic stimulation are a result of differences in neuromuscular transmission.
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Hottenstein et al. (1987) studied this question.
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