Unraveling the Complex Molecular Interplay and Vascular Adaptive Changes in Hypertension-Induced Kidney Disease
Lyubomir Gaydarski,
Iva N. Dimitrova,
Stancho Stanchev,
Alexandar Iliev,
Georgi Kotov,
Vidin Kirkov,
Nikola Stamenov,
Tihomir Dikov,
Georgi P. Georgiev,
Boycho Landzhov
Affiliations
Lyubomir Gaydarski
Department of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria
Iva N. Dimitrova
Department of Cardiology, University Hospital “St. Ekaterina”, Medical University of Sofia, 1431 Sofia, Bulgaria
Stancho Stanchev
Department of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria
Alexandar Iliev
Department of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria
Georgi Kotov
Department of Rheumatology, Clinic of Rheumatology, University Hospital “St. Ivan Rilski”, Medical Faculty, Medical University of Sofia, 1612 Sofia, Bulgaria
Vidin Kirkov
Department of Health Policy and Management, Faculty of Public Health “Prof. Dr. Tzekomir Vodenicharov”, Medical University of Sofia, 1431 Sofia, Bulgaria
Nikola Stamenov
Department of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria
Tihomir Dikov
Department of General and Clinical Pathology, Medical University of Sofia, 1431 Sofia, Bulgaria
Georgi P. Georgiev
Department of Orthopedics and Traumatology, University Hospital Queen Giovanna-ISUL, Medical University of Sofia, 1527 Sofia, Bulgaria
Boycho Landzhov
Department of Anatomy, Histology and Embryology, Medical University of Sofia, 1431 Sofia, Bulgaria
Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate the role of the apelin receptor (APLNR), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF) in hypertension-induced renal damage. We used two groups of spontaneously hypertensive rats aged 6 and 12 months, representing different stages of AH, and compared them to age-matched normotensive controls. The kidney tissue samples were prepared through a well-established protocol. All data analysis was conducted with a dedicated software program. APLNR was localized in tubular epithelial cells and the endothelial cells of the glomeruli, with higher expression in older SHRs. The localization of nNOS and VEGF was similar. The expression of APLNR and nNOS increased with AH progression, while VEGF levels decreased. CD was lower in young SHRs compared to controls and decreased significantly in older SHRs in comparison to age-matched controls. Our statistical analysis revealed significant differences in molecule expression between age groups and varying correlations between the expression of the three molecules and CD.
