Abstract
Increased sympathetic activity is one cause of obesity-induced hypertension. Over-activity of an adrenergic system in mesenteric perivascular adipose tissue (MPVAT) could contribute to high BP given its close proximity to splanchnic arteries and veins. We tested the hypothesis that high fat (HF) fed models of obesity-induced hypertension have elevated norepinephrine (NE) in MPVAT, increasing exposure of arteries to NE. Male Dahl S and Sprague-Dawley (SD) rats were fed a HF (60% fat, 0.3% NaCl; kcal) or a normal fat diet (NF; 10% fat, 0.25% NaCl; kcal) from weaning age (n=5). At 20-29 weeks of age, rats were sacrificed and tissues collected (all results shown in the table). HF increased the body weight of Dahl but not SD. Total fat mass was increased in the HF vs NF rats of both models. Mean arterial BP measured by radiotelemetry was elevated in the Dahl S HF vs NF and slightly elevated in the SD HF vs NF rats. Plasma NE was not elevated in either model. Surprisingly, MPVAT had significantly less NE in the Dahl S HF vs NF but was not altered in the SD. Expression of genes involved in NE synthesis, uptake and metabolism was measured by PCR to determine whether the MPVAT’s adrenergic system was altered in HF rats. Tyrosine hydroxylase ( Th ) mRNA was not detected in the Dahl S (SD not measured). Expression for the NE metabolizing enzymes monoamine oxidase-A (MAO-A) and catechol-o-methyl transferase ( Comt ) was not different. However, S lc22a3 mRNA (organic cation transporter 3) was reduced in the SD HF vs NF rat. These data reveal that the elevation in BP in Dahl S and SD rats fed a HF diet may be due to a mechanism that is independent of elevated NE in PVAT.Funding: NIHP01HL70687, F31 HL12803501
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