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Vol. 41, No. 6, 2004   

Free Abstract     Article (Fulltext)     Article (PDF 241 KB)     

Research Paper

The Conduction of Dilation along an Arteriole Is Diminished in the Cremaster Muscle of Hypertensive Hamsters
David T. Kurjiaka

Department of Biological Sciences, Ohio University, Athens, Ohio, USA

Address of Corresponding Author

J Vasc Res 2004;41:517-524 (DOI: 10.1159/000081808)


 goto top of page Key Words

  • Arteriole
  • Acetylcholine
  • Hypertension
  • Gap junction
  • Alpha adrenergic
  • Sympathetic nervous activity

 goto top of page Abstract

Arteriolar vasomotor responses can include a component that conducts along the vessel through gap junction channels. This study examined conducted vasomotor responses in arterioles of the hypertensive hamster. The cremaster muscle of normotensive (CHF-148) and spontaneously hypertensive (CHF-H4) hamsters was exteriorized. Micropipettes containing phenylephrine (0.1 M) or acetylcholine (ACh; 1.0 M) were positioned along second-order arterioles and diameter responses were recorded locally for every 0.4 mm upstream to 1.6 mm. Substantative local constrictions to phenylephrine(PE) were poorly conducted to the 0.4-mm site in normotensive and hypertensive hamsters. Local dilation to ACh decayed by 3 ± 1 µm/mm as it conducted along arterioles of the normotensive hamster. In contrast, conducted dilation decayed by 7 ± 1 µm/mm (p < 0.05) in the hypertensive hamster. This hypertension-induced increase in decay was reversed by alpha-adrenergic receptor blockade (phentolamine: 1 µM). However, arteriolar constriction to global alpha1- (PE) and alpha2- (clonidine) adrenergic agonists was unaffected by hypertension. Rather, sympathetic nervous activity was elevated in the hypertensive hamster as indicated by a greater reduction in arterial pressure upon sympathetic ablation (hexamethonium infusion: 30 mg/kg). This study provides the first evidence that vascular cell-cell communication is altered by the elevated sympathetic nervous activity observed in the hypertensive hamster.

Copyright © 2004 S. Karger AG, Basel


 goto top of page Author Contacts

David T. Kurjiaka, PhD
Department of Biological Sciences, Ohio University
302 Wilson Research
Athens, OH 45701 (USA)
Tel. +1 740 593 2271, Fax +1 740 593 0300, E-Mail kurjiaka@ohiou.edu


 goto top of page Article Information

This study was supported by the Ohio Valley Affiliate of the American Heart Association (Beginning Grant in Aid 9960363V) and the Ohio University Research Council.

Received: March 5, 2004
Accepted after revision: August 16, 2004
Published online: October 28, 2004
Number of Print Pages : 8
Number of Figures : 6, Number of Tables : 0, Number of References : 31

 
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