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Structural changes during microvascular rarefaction in chronic hypertension
F Hansen-Smith1, A S Greene, A W Cowley
1Department of Biological Sciences, Oakland University, Rochester, Michigan.
Abstract:
Previous physiological studies have suggested that loss of microvessels (anatomic rarefaction) occurs in the skeletal muscle microcirculation of rats with chronic hypertension. However, little is known of the exact structural changes that occur during the process of anatomic rarefaction. The purpose of this study was to examine the muscle at the ultrastructural level to search for evidence of microvessel degeneration that would correlate with the concept of anatomic rarefaction in chronic hypertension. Cremaster muscles were removed from normal rats and from rats with chronic reduced renal mass hypertension, which was produced by a 75% reduction in kidney mass followed by salt loading (4% NaCl chow with water ad libitum) for 4 weeks. The muscles were fixed and prepared for histological examination by light and electron microscopy. Atrophy and degeneration of both endothelial cells and vascular smooth muscle cells were observed in many arterioles of the hypertensive rats. Some arterioles of hypertensive rats were degenerated to such an extent that the original identity of the cells could not be determined. The hypertensive rats also exhibited degeneration of capillaries and extravasation and uptake of red blood cells into lymphatic vessels. In contrast, age-matched control rats exhibited normal histology. The results of this study support previous physiological evidence for anatomic rarefaction in the cremaster muscle of chronically hypertensive rats.
Insights
Chronic hypertension in rats causes skeletal muscle microvessel degeneration, supporting anatomic rarefaction. Ultrastructural examination revealed significant microvascular damage in hypertensive rat cremaster muscles.
Area of Science:
- Cardiovascular Biology
- Renal Physiology
- Skeletal Muscle Research
Background:
- Physiological studies suggest microvessel loss (anatomic rarefaction) in skeletal muscle during chronic hypertension.
- The precise structural alterations underlying anatomic rarefaction remain poorly understood.
Purpose of the Study:
- To investigate ultrastructural changes in skeletal muscle microcirculation.
- To identify microvessel degeneration correlating with anatomic rarefaction in chronic hypertension.
Main Methods:
- Cremaster muscles were obtained from rats with reduced renal mass hypertension and age-matched controls.
- Histological examination using light and electron microscopy was performed.
- Hypertension was induced by 75% kidney mass reduction followed by 4 weeks of salt loading.
Main Results:
- Hypertensive rats showed atrophy and degeneration of endothelial and vascular smooth muscle cells in arterioles.
- Severe degeneration in some arterioles obscured original cell identity.
- Capillary degeneration, red blood cell extravasation, and lymphatic uptake were observed in hypertensive rats.
Conclusions:
- Ultrastructural evidence supports anatomic rarefaction in the cremaster muscle of chronically hypertensive rats.
- The study elucidates the cellular mechanisms of microvascular damage in hypertension.
- Findings correlate structural changes with previously observed physiological data.