This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dunn, W. R. Articles by Gardiner, S. M. Search for Related Content PubMed PubMed Citation Articles by Dunn, W. R. Articles by Gardiner, S. M. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information High Blood Pressure Hazardous Substances DB PAPAVERINE HYDROCHLORIDE VASOPRESSIN

(Hypertension. 1995;26:390-396.)
© 1995 American Heart Association, Inc.

Articles

Structural and Functional Properties of Isolated, Pressurized, Mesenteric Resistance Arteries From a Vasopressin-Deficient Rat Model of Genetic Hypertension

William R. Dunn; Sheila M. Gardiner

From the Department of Physiology and Pharmacology, Queen's Medical Centre, Medical School, University of Nottingham (UK).

Correspondence to William R. Dunn, Department of Physiology and Pharmacology, Queen's Medical Centre, Medical School, University of Nottingham, Clifton Boulevard, Nottingham, NG7 2UH, UK. E-mail mqzwrd@mqn1.phpharm.nottingham.ac.uk.

Abstract In this study we examined the structural and functional properties of mesenteric resistance arteries isolated from normotensive and hypertensive vasopressin-deficient rats. Hypertensive rats had a significantly higher mean arterial pressure (176±3 mm Hg) than normotensive controls (121±2 mm Hg). First- and second-order mesenteric resistance arteries were set up in a pressure myograph and pressurized to the mean arterial pressure of the rat from which they had been isolated. Vessels were fixed with glutaraldehyde, embedded in Araldite, sectioned, and examined histologically. First- and second-order mesenteric resistance arteries from hypertensive rats displayed a reduced internal diameter and increased media-to-lumen ratio compared with their normotensive controls. However, there was no evidence for an increased media content, indicating that the reduced internal diameter of hypertensive arteries was consequent to either remodeling of similar amounts of wall material or a reduced artery distensibility but not vascular growth. Pressurized arteries were also examined with respect to their responsiveness to the vasoconstrictors norepinephrine and arginine vasopressin and to the endothelium-dependent vasodilator acetylcholine and the endothelium-independent vasodilator papaverine. Both first- and second-order mesenteric arteries from hypertensive rats displayed enhanced sensitivity to norepinephrine compared with their normotensive controls. This effect was specific for norepinephrine, because responses to arginine vasopressin were similar in vessels isolated from normotensive and hypertensive rats. No evidence was found for an impaired endothelium-dependent vasodilatation in arteries from hypertensive rats. Indeed, in hypertensive vasopressin-deficient rats responses to acetylcholine were increased in first-order arteries compared with those from normotensive rats. Responses to papaverine were similar in arteries isolated from either normotensive or hypertensive rats. These observations indicate that increased blood pressure in this genetic model of hypertension may result from an altered structure of resistance arteries and/or an increased sensitivity to norepinephrine rather than from impaired endothelium-dependent vasodilatation.

Key Words: mesenteric arteries • hypertension, genetic • endothelium • vascular smooth muscle • myography • hypertrophy

This article has been cited by other articles:

				W. R. Dunn and S. M. Gardiner Differential Alteration in Vascular Structure of Resistance Arteries Isolated From the Cerebral and Mesenteric Vascular Beds of Transgenic [(mRen-2)27], Hypertensive Rats Hypertension, May 1, 1997; 29(5): 1140 - 1147. [Abstract] [Full Text]