Hyperinnervation of Mesenteric Arteries in Spontaneously Hypertensive Rats by Sympathetic but Not Primary Afferent Axons

Vol. 42, No. 4, 2005

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Research Paper

Hyperinnervation of Mesenteric Arteries in Spontaneously Hypertensive Rats by Sympathetic but Not Primary Afferent Axons
Susan E. Luff^a, Simone B. Young^a, Elspeth M. McLachlan^b

^aMonash Micro Imaging, School of Biomedical Science, Monash University, Clayton, and
^bPrince of Wales Medical Research Institute and University of New South Wales, Randwick, Australia

Address of Corresponding Author

J Vasc Res 2005;42:348-358 (DOI: 10.1159/000086886)

Key Words

Nerve growth factor
Neuromuscular junctions
Substance P
Vascular innervation

Abstract

Hypertrophy of the perivascular plexus is thought to play a role in the development of hypertension in spontaneously hypertensive rats (SHR). However, it is not known whether the sympathetic varicosities are more numerous or larger, or form more neurovascular junctions. Further, a parallel hypertrophy of primary afferent terminals around the vessels might modulate any effects of hypertrophied sympathetic terminals. We have investigated the perivascular plexus around second-order mesenteric arteries of SHR and Wistar-Kyoto (WKY) rats by electron microscopy. Noradrenergic terminals were identified by the presence of small granular vesicles after chromaffin fixation, and substance P (SP+) afferent axons were identified by immunohistochemistry. The numbers of noradrenergic axon and varicosity profiles were higher (48 and 25%, respectively) in SHR than in WKY rats, and the majority lay closer to the medio-adventitial border. In contrast, there was no difference in the numbers of SP+ axons. Sympathetic and SP+ varicosities were indistinguishable in size, shape, vesicle content and mitochondrion content between each other and between the strains. However, both the number of neuromuscular junctions and the proportion of varicosities that formed them in SHR arteries were more than double those in WKY vessels. The data clearly show that hyperinnervation in SHR is specific for noradrenergic axons.

Author Contacts

Dr. Susan E. Luff
Monash Micro Imaging, School of Biomedical Science
Monash University, PO Box 13F
Clayton, Vic. 3800 (Australia)
Tel. +61 3 9905 2746, Fax +61 3 9905 2733, E-Mail susan.luff@med.monash.edu.au

Article Information

This work was supported by the National Heart Foundation of Australia and the National Health and Medical Research Council.

Received: August 6, 2004
Accepted after revision: April 23, 2005
Published online: July 6, 2005
Number of Print Pages : 11
Number of Figures : 5, Number of Tables : 3, Number of References : 39

Medline Abstract (ID 16015033)

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