Slow and incomplete sympathetic reinnervation of rat tail artery restores the amplitude of nerve-evoked contractions provided a perivascular plexus is present

Abstract

We have investigated the recovery of sympathetic control following reinnervation of denervated rat tail arteries by relating the reappearance of noradrenergic terminals to the amplitude of nerve-evoked contractions of isometrically mounted artery segments in vitro. We have also assessed reactivity to vasoconstrictor agonists. Freezing the collector nerves near the base of the tail in adult rats denervated the artery from ∼40 mm along the tail. Restoration of the perivascular plexus declined along the length of the tail, remaining incomplete for >6 mo. After 4 mo, nerve-evoked contractions were prolonged but of comparable amplitude to control at ∼60 mm along the tail; they were smaller at ∼110 mm. At ∼60 mm, facilitation of contractions to short trains of stimuli by the norepinephrine transporter blocker, desmethylimipramine, and by the α2-adrenoceptor antagonist, idazoxan, was reduced in reinnervated arteries. Blockade of nerve-evoked contractions by the α1-adrenoceptor antagonist, prazosin, was less and by idazoxan greater than control after 8 wk but similar to control after 16 wk. Sensitivity of reinnervated arteries to the α1-adrenoceptor agonist, phenylephrine, was raised in the absence but not in the presence of desmethylimipramine. Sensitivity to the α2-adrenoceptor agonist, clonidine, was maintained in 16-wk reinnervated arteries when it had declined in controls. Thus regenerating sympathetic axons have a limited capacity to reinnervate the rat tail artery, but nerve-evoked contractions match control once a relatively sparse perivascular plexus is reestablished. Functional recovery involves prolongation of contractions and deficits in both clearance of released norepinephrine and autoinhibition of norepinephrine release.

Streptozotocin-induced diabetes differentially affects sympathetic innervation and control of plantar metatarsal and mesenteric arteries in the rat

“…In rat tail arteries, a reduction in innervation density due to axon loss is associated with a decrease in the activity of neuronal NET (39). Because the effects of blocking NET on sensitivity to PE did not differ between PMAs from STZ-NI and control rats, perhaps this indicates that the changes in the perivascular plexus are produced by rearrangement of the terminal axons rather than loss of axons.…”

Purinergic Signaling and Blood Vessels in Health and Disease

“…Long-term supplementation with a high cholesterol diet decreases the release of ATP from the tail artery of aged rats (Hashimoto et al, 1998b). Both purinergic and adrenergic components are present in reinnervating sympathetic fibers after denervation of rat tail arteries (Tripovic et al, 2011). The rat tail artery is important for both balance and temperature control.…”

Prominent contribution of L-type Ca2+channels to cutaneous neurovascular transmission that is revealed after spinal cord injury augments vasoconstriction

“…Therefore a possible explanation for the changed effects of idazoxan in SCI arteries is that blockade of prejunctional ␣ 2 -adrenoceptors has a greater facilitatory effect on neurotransmitter release. Because the component of nerve-evoked contraction that is mediated by postjunctional ␣ 2 -adrenoceptors takes several seconds to develop, the peak amplitude of contractions to 10 pulses at 10 Hz is determined primarily by the activation of ␣ 1 -adrenoceptors alone (3,39). This explains why idazoxan, via its prejunctional facilitatory action, in- Percent change data are presented as means Ϯ SE.…”