OBJECTIVE: The renin-angiotensin system plays an important role in blood pressure control. Recently the mouse Ren-2 renin gene was introduced into the genome of rats, producing low-renin hypertensive animals. The aim of the present study was to characterize the pharmacological and morphological properties of mesenteric resistance arteries from transgenic rats. DESIGN: Segments of small arteries were taken from the mesenteric bed of 13-week-old transgenic rats and from age-matched Sprague-Dawley controls. METHODS: Vessels were mounted on an isometric myograph permitting direct measurements of vessel isometric wall tension. Vessel morphology was measured with a microscope using a water-immersion objective. RESULTS: The transgenic versus Sprague-Dawley rat comparison is similar to that seen previously for spontaneous hypertensive rats (SHR) versus Wistar-Kyoto (WKY) rats as regards active effective pressure (increased), lumen diameter (decreased) and media thickness (increased). However, in contrast to SHR vessels, where media cross-sectional area has previously been shown to be increased compared with WKY vessels, vessels from transgenic rats had the same media cross-sectional area as those from Sprague-Dawley rats. There was neither cellular hypertrophy nor hyperplasia. However, an increased number of smooth muscle layers was found, indicating a rearrangement of existing material. CONCLUSION: Although the structural changes found in transgenic rats may account for the increased pressure response, hypertension in this animal is apparently not caused by general vascular growth.
OBJECTIVE: The renin-angiotensin system plays an important role in blood pressure control. Recently the mouseRen-2renin gene was introduced into the genome of rats, producing low-reninhypertensive animals. The aim of the present study was to characterize the pharmacological and morphological properties of mesenteric resistance arteries from transgenic rats. DESIGN: Segments of small arteries were taken from the mesenteric bed of 13-week-old transgenic rats and from age-matched Sprague-Dawley controls. METHODS: Vessels were mounted on an isometric myograph permitting direct measurements of vessel isometric wall tension. Vessel morphology was measured with a microscope using a water-immersion objective. RESULTS: The transgenic versus Sprague-Dawley rat comparison is similar to that seen previously for spontaneous hypertensiverats (SHR) versus Wistar-Kyoto (WKY) rats as regards active effective pressure (increased), lumen diameter (decreased) and media thickness (increased). However, in contrast to SHR vessels, where media cross-sectional area has previously been shown to be increased compared with WKY vessels, vessels from transgenic rats had the same media cross-sectional area as those from Sprague-Dawley rats. There was neither cellular hypertrophy nor hyperplasia. However, an increased number of smooth muscle layers was found, indicating a rearrangement of existing material. CONCLUSION: Although the structural changes found in transgenic rats may account for the increased pressure response, hypertension in this animal is apparently not caused by general vascular growth.
Authors: Lenka Řezáčová; Ivana Vaněčková; Silvie Hojná; Anna Vavřínová; Pavol Valovič; Hana Rauchová; Michal Behuliak; Josef Zicha Journal: Hypertens Res Date: 2021-10-08 Impact factor: 3.872