Comparison of the frequency dependence of venous and arterial responses to sympathetic nerve stimulation in guinea‐pigs.

Abstract

SUMMARY1. 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'S5-Hz) of lumbar colonic nerve trunks produced frequency-dependent slow depolarizations in all venous and in 92 % ofarterial 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 az-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.

Differential contributions of alpha-1 and alpha-2 adrenoceptors to vasoconstriction in mesenteric arteries and veins of normal and hypertensive mice

“…Veins are more sensitive than arteries to the constrictor effects of sympathetic nerve stimulation (Hottenstein and Kreulen, 1987;Luo et al, 2003). In the present studies we confirmed that are more sensitive than arteries to the contractile effects of NE (Luo et al, 2003).…”

An electrophysiological study of excitatory purinergic neuromuscular transmission in longitudinal smooth muscle of chicken anterior mesenteric artery

“…It seems that the longitudinal smooth muscle activity together with the circular one would be well adapted to perform a peristaltic-like action or autonomous pulsation, which would help in increasing the rate of blood flow in distal branches supplying all viscera. Unlike mammalian circular arterial smooth muscle cells in which EFS evoked fast excitatory junctional potentials (EJPs) with short latencies, 10-20 ms and total durations of 0.3-1 s (Burnstock & Holman, 1961;Bell, 1969b;Bennett, 1972;Hirst, 1977;Itoh et al, 1983;Hottenstein & Kreulen, 1987), EFS to mesenteric arterial longitudinal smooth muscle cells did not produce fast EJPs but depolarizations that were relatively slowly developing (380 ms latency; 4.5 s time to peak) and long lasting (24 s total duration), similar to those recorded from the guinea-pig mesenteric vein (Hirst & Jobling, 1989;Hottenstein & Kreulen, 1987;Suzuki, 1981). Such long latency of EFSevoked depolarization recorded from chicken mesenteric arterial longitudinal smooth muscle cells might relate to the EFS-evoked depolarization being mediated via metabotropic receptor rather than the ionotropic one.…”

Purinergic receptors in the splanchnic circulation

“…In contrast, in the guinea-pig mesenteric vein a slow depolarization [166] that is resistant to purinoceptor desensitization with α,β-meATP [65,67] is observed rather than fast EJPs. This has led to the conclusion that ATP is not involved in these junctional events [65,67] and, hence, is not released during nerve stimulation. However, a study on guinea-pig mesenteric vessels [155] revealed that arterial contractile response to sympathetic nerve stimulation is due exclusively to noradrenaline, whereas at least three different neurotransmitters (noradrenaline, ATP and neuropeptide Y) appear to contribute to the venous neural response.…”

“…For instance, in the guinea-pig mesenteric artery, sympathetic nerve stimulation gives rise to rapidly rising excitatory junction potentials of brief duration that are resistant to prazosin, but are blocked by α,β-meATP [67,82]. In contrast, in the guinea-pig mesenteric vein a slow depolarization [166] that is resistant to purinoceptor desensitization with α,β-meATP [65,67] is observed rather than fast EJPs. This has led to the conclusion that ATP is not involved in these junctional events [65,67] and, hence, is not released during nerve stimulation.…”

“…The difference in the contribution of ATP to the neural response in artery and vein was suggested to be related to the presence of different populations of ATP receptors, i.e., in artery, rapidly desensitizing P2X 1 receptors predominate whereas in vein, non-desensitizing P2Y receptors predominate [116]. However, the apparent contradictory results between these different studies [67,82,155] may also be ascribed to differences in the methodological approaches (evaluation of membrane potentials by electrophysiology vs contractile and [ 3 H]-noradrenaline release studies) or to the size of the vessels studied (the studies of Kreulen [82] involved a broader range of internal diameters of the vessels). Besides, there might be differences in the postjunctional effects of prejunctionally released neurotransmitters, as it is suggested to occur in the human saphenous vein [147], where ATP is co-released with noradrenaline but did not appear to generate the non-adrenergic component of contraction.…”