Functional and Structural Postglomerular Alterations in the Kidney of Prehypertensive Spontaneously Hypertensive Rats

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Abstract
The kidney plays a major role in the development of hypertension. Following the Borst‐Guyton theory of an altered set‐point for fluid and electrolyte homeostasis we aim to investigate functional and structural renal parameter during the development of hypertension. Therefore we focus on counter current exchange related factors. We compared 4 and 8 weeks old Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) concerning basic renal parameters as creatinine and phosphorus clearance and urinary osmolality. Mean arterial pressure (MAP) was measured intra‐arterially. Vasa recta were investigated using immunohistochemistry for α‐smooth‐muscle actin (ASMA) and plastification for geometric analyses. Blood pressure was not yet significantly elevated in SHR at 4 weeks but at 8 weeks it was higher in SHR (116 ± 7 vs. 102 ± 4 mm Hg; p < 0.01). Kidney weight/body weight ratio was lower in SHR at both ages. In 4 weeks old SHR, phosphorus clearance and urinary osmolality were decreased compared to WKY [0.02 ± 0.01 vs. 0.05 ± 0.02 (ml/min*100 g BW) p < 0.03; 14.2 ± 2.2 vs. 18.9 ± 2.9 (osmol/kg*24 h urine) p < 0.05] indicating reduced tubular reabsorption. At 8 weeks phosphorus clearance and urinary osmolality were comparable to WKY. α‐Actin was found in vasa recta in a 4‐times higher degree in SHR with a predominant location in the outer medulla. Radii of vasa recta in the outer medulla decreased during development. In plastificated sections vasa recta of SHR revealed sphincter‐like pattern. Functional and structural alterations related to the counter current exchanger are already evident in prehypertensive SHR. During development of hypertension both factors get adapted to higher blood pressure level. Sphincter‐like structures in vasa recta suggest contractility of pericytes/vascular smooth muscle cells (vSMC). As these were just seen in SHR that might allude to a higher potential to contract. We conclude that differences in postglomerular structure and function may contribute to the development of hypertension in SHR.