Abstract P114: Cardiac and Renal Adrenergic Receptor Expression in Spontaneously Hypertensive Caribbean Vervets

Abstract

Sympathetic nerve activity and adrenergic receptor stimulation causes development and maintenance of hypertension in patients and experimental animal models. The Caribbean vervet ( Chlorocebus aethiops sabaeus ), an Old World non-human primate, is a translational model of human cardiovascular disease due to its recent divergence, genetic similarity, upright posture, complex social structure, and diurnal behavior. Outbred and randomly selected adult Caribbean vervets exhibit systolic blood pressures (SBP) >140 mmHg in 36% of our cohort (124 of 345 individuals). We hypothesized that gene expression of adrenergic receptor subtypes in renal and cardiac tissue would be elevated in HT Caribbean vervets, and may contribute to spontaneous hypertension. Gene expression was measured using qRT-PCR and RQs compared using the Mann-Whitney U Test. HT animals (n=18, SBP: 168.24±7.25mmHg) had increased expression of both α- and β-adrenergic receptor subtypes in renal outer medulla (a 1a : NT RQ 1 ± 0.43 vs. HT RQ 2.26 ± 0.50, p<0.05; a 1d : NT RQ 1 ± 0.34 vs. HT RQ 2.25 ± 0.32, p<0.05; a 2a : NT RQ 1 ± 0.24 vs. HT RQ 1.92 ± 0.19, p<0.05; a 2c : NT RQ 1 ± 0.15 vs HT RQ 1.65 ± 0.15, p<0.05: β 1 : NT RQ 1 ± 0.24 vs. HT RQ 1.88 ± 0.18, p<0.05; and β 2 : NT RQ 1 ± 0.21 vs. HT RQ 1.87 ± 0.24, p<0.05) compared to NT animals (n=18, SBP: 96.61±3.2 mmHg). All α- and β 1 -adrenergic receptor expression in renal cortex and inner medulla was similar between the two groups. Inner medullary β 2 adrenergic receptor expression was elevated in HT animals (NT RQ 1 ± 0.25 vs HT RQ 1.62 ± 0.10, p<0.05). In the heart, β 1 adrenergic receptor expression was upregulated in the left ventricular myocardium of HT animals (NT RQ 1 ± 0.16 vs HT RQ 1.88 ± 0.35). Together, these data suggest that the HT Caribbean vervet may exhibit an exaggerated response to sympathetic nerve activity due to increased adrenergic receptor expression in the kidney and heart, which could contribute to the spontaneous hypertension observed in this translational large animal model.