Spinal cord injury increases the reactivity of rat tail artery to angiotensin II.

Hussain Al Dera,James A Brock

doi:10.3389/fnins.2014.00435

Abstract

Studies in individuals with spinal cord injury (SCI) suggest the vasculature is hyperreactive to angiotensin II (Ang II). In the present study, the effects of SCI on the reactivity of the rat tail and mesenteric arteries to Ang II have been investigated. In addition, the effects of SCI on the facilitatory action of Ang II on nerve-evoked contractions of these vessels were determined. Isometric contractions of artery segments from T11 (tail artery) or T4 (mesenteric arteries) spinal cord-transected rats and sham-operated rats were compared 6–7 weeks postoperatively. In both tail and mesenteric arteries, SCI increased nerve-evoked contractions. In tail arteries, SCI also greatly increased Ang II-evoked contractions and the facilitatory effect of Ang II on nerve-evoked contractions. By contrast, SCI did not detectably change the responses of mesenteric arteries to Ang II. These findings provide the first direct evidence that SCI increases the reactivity of arterial vessels to Ang II. In addition, in tail artery, the findings indicate that Ang II may contribute to modifying their responses following SCI.

Highlights

Angiotensin II (Ang II) plays an important role in the regulation of peripheral resistance
The main finding of this study is that chronic spinal cord injury (SCI) has differential effects on the reactivity of tail and mesenteric arteries to Ang II
But not mesenteric arteries, SCI produced a large increase in reactivity of the vascular muscle to Ang II and markedly increased the facilitation of nerve-evoked contractions produced by Ang II

Summary

Introduction

Angiotensin II (Ang II) plays an important role in the regulation of peripheral resistance. Following spinal cord injury (SCI), when supraspinal regulation of the vasculature below the lesion is lost, the renin-angiotensin system plays a greater role in regulating vascular resistance (Popa et al, 2010). In patients with cervical SCI, there was a rapid and marked rise in plasma renin levels during a head up tilt (Mathias et al, 1980). This posturally evoked renin release occurs independently of sympathetic nerve activity and most likely depends on the fall in renal perfusion pressure causing stimulation of juxtaglomerular renin secreting cells (see Mathias et al, 1980)

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Results

Conclusion