Hypertension-induced peripheral neuropathy and the combined effects of
hypertension and diabetes on nerve structure and function in rats.
Authors Gregory JA, Jolivalt CG, Goor J, Mizisin AP, Calcutt NA
Submitted By Nigel Calcutt on 1/30/2013
Status Published
Journal Acta Neuropathologica
Year 2012
Date Published 10/1/2012
Volume : Pages 124 : 561 - 573
PubMed Reference 22791295
Abstract Diabetic neuropathy includes damage to neurons, Schwann cells and blood vessels.
Rodent models of diabetes do not adequately replicate all pathological features
of diabetic neuropathy, particularly Schwann cell damage. We, therefore, tested
the hypothesis that combining hypertension, a risk factor for neuropathy in
diabetic patients, with insulin-deficient diabetes produces a more pertinent
model of peripheral neuropathy. Behavioral, physiological and structural indices
of neuropathy were measured for up to 6 months in spontaneously hypertensive and
age-matched normotensive rats with or without concurrent streptozotocin-induced
diabetes. Hypertensive rats developed nerve ischemia, thermal hyperalgesia,
nerve conduction slowing and axonal atrophy. Thinly myelinated fibers with
supernumerary Schwann cells indicative of cycles of demyelination and
remyelination were also identified along with reduced nerve levels of myelin
basic protein. Similar disorders were noted in streptozotocin-diabetic rats,
except that thinly myelinated fibers were not observed and expression of myelin
basic protein was normal. Superimposing diabetes on hypertension compounded
disorders of nerve blood flow, conduction slowing and axonal atrophy and
increased the incidence of thinly myelinated fibers. Rats with combined
insulinopenia, hyperglycemia and hypertension provide a model for diabetic
neuropathy that offers an opportunity to study mechanisms of Schwann cell
pathology and suggests that hypertension may contribute to the etiology of
diabetic neuropathy.

Investigators with authorship
Nigel CalcuttUniversity of California San Diego

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