Key result
Sympathetic neuroeffector mechanisms differ fundamentally between rat mesenteric arteries and veins, with veins showing left-shifted frequency-response curves for noradrenaline overflow.
There are fundamental differences in sympathetic neuroeffector mechanisms between mesenteric arteries and veins, which likely contribute to their distinct hemodynamic functions.
Does not support clinical translation; leaves open whether sympathetic differences between arteries and veins affect human hemodynamics.
As arteries are resistance blood vessels while veins perform a capacitance function, it might be expected that sympathetic neural control of arteries and veins would differ. The function of sympathetic nerves supplying mesenteric arteries (MA) and veins (MV) in rats was investigated using in vitro continuous amperometry with a carbon fibre microelectrode and video imaging. We simultaneously measured noradrenaline (NA) overflow at the blood vessel adventitial surface and vasoconstriction evoked by electrical stimulation of perivascular sympathetic nerves. Sympathetic nerve arrangement was studied using glyoxylic acid-induced fluorescence of NA. We found that: (i) there were significant differences between MA and MV in the arrangement of sympathetic nerves; (ii) frequency-response curves for NA overflow and vasoconstriction for MV were left-shifted compared to MA; (iii) the P2X receptor antagonist, pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microm), reduced constrictions in MA but not in MV while the alpha(1)-adrenergic receptor antagonist, prazosin (0.1 microm), blocked constrictions in MV but not in MA; (iv) NA overflow for MA was enhanced by the alpha(2)-adrenergic receptor antagonist, yohimbine (1.0 microm), and attenuated by the alpha(2)-adrenergic receptor agonist, UK 14,304 (1.0 microm), while yohimbine and UK 14,304 had little effect in MV; (v) cocaine (10 microm) produced larger increases in NA overflow in MA than in MV; (vi) UK 14,304 constricted MV but not MA while yohimbine reduced constrictions in MV but not MA. We conclude that there are fundamental differences in sympathetic neuroeffector mechanisms in MA and MV, which are likely to contribute to their different haemodynamic functions.
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Park et al. (2007) studied this question. Electrical stimulation and pharmacological agents vs. Mesenteric arteries vs veins was evaluated on Noradrenaline overflow and vasoconstriction. Sympathetic neuroeffector mechanisms differ fundamentally between rat mesenteric arteries and veins, with veins showing left-shifted frequency-response curves for noradrenaline overflow.
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