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STEREOLOGICAL STUDIES ON MESENTERIC RESISTANCE ARTERY STRUCTURE IN NEW ZEALAND GENETICALLY HYPERTENSIVE AND CONTROL RATS
Author(s) -
Ledingham J. M.,
Millar J. A.
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb01705.x
Subject(s) - lumen (anatomy) , hyperplasia , blood pressure , medicine , perfusion , muscle hypertrophy , stereology , artery , anatomy , blood vessel , vascular smooth muscle , endocrinology , smooth muscle
SUMMARY 1. Stereological methods were used to quantitate and compare the structure of mesenteric resistance arteries (MRA) in New Zealand genetically hypertensive (GH) rats aged 4, 10 and 16 weeks and their normotensive control strain (N). 2. Blood pressure (BP) (tail‐cuff and intra‐arterial) were recorded before the vessels were fixed by perfusion and embedded in Technovit Kulzer GmbH D‐6393, Wehrheim, Germany). 3. Media and lumen volumes were measured on transverse sections (TS), by the Cavalieri method, and numbers of smooth muscle (SM) cells were estimated by the optical disector method. 4. There were no significant differences in lumen volume per unit vessel length between GH and age‐matched N groups at any age. However, at 10 and 16 weeks volume in GH groups was 9–10% lower than their respective N groups. 5. Media volume per unit vessel length increased in GH rats at all ages. The media/lumen ratio also increased in GH at all ages. 6. Smooth muscle cell density (SM cell number per unit volume of media) decreased in GH rats at all ages, i.e. there was no evidence of hyperplasia. 7. Blood pressure (tail‐cuff and intra‐arterial) significantly increased in GH rats at 4 weeks of age and also at 10 and 16 weeks. 8. These results show that media volume is increased in GH early in life, is not due to hyperplasia, but may be due to hypertrophy of the SM cells, an increase in the amount of extracellular matrix or a combination of both. However, since hypertension is also present at an early age, structural abnormalities cannot be said to be a primary cause of GH hypertension.