Abstract 219: Altered Renal and Cardiac Morphology in a Non-Human Primate Model of Spontaneous Essential Hypertension

Abstract

Current models of essential hypertension are limited in comparisons to human pathophysiology due to distinct differences in postural positioning, circadian rhythmicity, and genetic variation. We have identified a unique non-human primate model of spontaneous, essential hypertension in Chlorocebus aethiops sabaeus , the African Green, or vervet, monkey. Using forearm plethysmography under light ketamine sedation (~15mg/kg), adult vervets were categorized as hypertensive (HT; SBP >140mmHg), borderline hypertensive (BHT; 120mmHg < SBP < 140mmHg), or normotensive (NT; SBP < 120 mmHg). Of the 168 males phenotyped, 32% (53 of 168) were HT (average SBP = 168.79±3.29mmHg), 27% (45 of 168) were BHT (average SBP = 129.58±0.88mmHg), and 41% (70 of 168) were NT (average SBP = 100.21±1.65mmHg). In a smaller study of 18 adult females, 1 was found to be HT (SBP = 156mmHg), 2 were BHT (average SBP = 134±2.0mmHg), and 15 were NT (average SBP = 98.06±4.32mmHg). Fixed paraffin-embedded histological sections of vervet cardiac (H&E) and renal (periodic acid Schiff) tissues were digitized and analyzed. Wall/lumen ratios of renal arterioles (average diameter 33.01±0.5μm) were greater in HT (0.33±0.03) compared to NT (0.24±0.01) male monkeys. Bowman’s capsule space was increased in HT (43.14±3.98% area) glomeruli compared to NT (29.92±2.42% area) glomeruli (p<0.05). Indicative of left ventricular hypertrophy, left ventricular cells were decreased in HT (1833.33±65.48 cells/mm 2 ) compared to NT monkeys (2223.61±59.72 cells/mm 2 ; p<0.05). The increased wall/lumen ratios and Bowman’s capsular spaces indicate that renal vascular hypertrophy and glomerular damage occur in this non-human primate model of essential hypertension. Left ventricular hypertrophy combined with renal glomerular and vascular dysfunction provides strong evidence for using this non-human primate model as a translational experimental species.