G Simon1, B Csiky. 1. Department of Medicine, Veterans Administration Medical Center and University of Minnesota, Minneapolis 55417, USA.
Abstract
BACKGROUND: In a previous study, we found that neonatal sympathectomy prevented the development of angiotensin II (ANG II)-induced hypertension but not the development of structural changes in small mesenteric arteries. OBJECTIVES: To investigate further the dissociation between hypertension and structural vascular changes in sympathectomized ANG II-treated rats by extending morphometric measurements to include all segments of the mesenteric arterial tree. METHODS: Neonatally sympathectomized and sham-sympathectomized male Sprague-Dawley rats, aged 34 months, were administered 200 ng/kg per min ANG II subcutaneously for 4 weeks. Sham-operated sympathectomized and sham-sympathectomized rats were controls. At the end of the treatment period the mesenteric circulation of rats was perfusion-fixed for morphometric measurements. RESULTS: Tail systolic blood pressure in ANG II-treated sham-sympathectomized rats increased by 47 mmHg (P < 0.001); the increase of systolic blood pressure (11 mmHg) in ANG II-treated sympathectomized rats did not attain statistical significance. Sympathectomy alone increased the lumen and reduced the wall : lumen ratio of first- and second-order branches of the superior mesenteric artery (hypotrophic outward remodeling). ANG II treatment increased the dimensions, wall thickness, and wall area of first- and second-order arteries (hypertrophic outward remodeling) and the wall : lumen ratio of small resistance arteries in sham-sympathectomized rats. Neonatal sympathectomy attenuated the development of structural changes in large arteries but had no effect on the development of structural changes in small arteries of ANG II-treated rats. CONCLUSION: Hypertension and sympathetic innervation appear to be contributing to the development of structural changes in large arteries of ANG II-treated rats because sympathectomy attenuated these changes. Structural changes in small arteries, on the other hand, appear to be due to a direct trophic effect of ANG II.
BACKGROUND: In a previous study, we found that neonatal sympathectomy prevented the development of angiotensin II (ANG II)-induced hypertension but not the development of structural changes in small mesenteric arteries. OBJECTIVES: To investigate further the dissociation between hypertension and structural vascular changes in sympathectomized ANG II-treated rats by extending morphometric measurements to include all segments of the mesenteric arterial tree. METHODS: Neonatally sympathectomized and sham-sympathectomized male Sprague-Dawley rats, aged 34 months, were administered 200 ng/kg per min ANG II subcutaneously for 4 weeks. Sham-operated sympathectomized and sham-sympathectomized rats were controls. At the end of the treatment period the mesenteric circulation of rats was perfusion-fixed for morphometric measurements. RESULTS: Tail systolic blood pressure in ANG II-treated sham-sympathectomized rats increased by 47 mmHg (P < 0.001); the increase of systolic blood pressure (11 mmHg) in ANG II-treated sympathectomized rats did not attain statistical significance. Sympathectomy alone increased the lumen and reduced the wall : lumen ratio of first- and second-order branches of the superior mesenteric artery (hypotrophic outward remodeling). ANG II treatment increased the dimensions, wall thickness, and wall area of first- and second-order arteries (hypertrophic outward remodeling) and the wall : lumen ratio of small resistance arteries in sham-sympathectomized rats. Neonatal sympathectomy attenuated the development of structural changes in large arteries but had no effect on the development of structural changes in small arteries of ANG II-treated rats. CONCLUSION:Hypertension and sympathetic innervation appear to be contributing to the development of structural changes in large arteries of ANG II-treated rats because sympathectomy attenuated these changes. Structural changes in small arteries, on the other hand, appear to be due to a direct trophic effect of ANG II.