INTERMITTENT PARATHYROID HORMONE ADMINISTRATION ATTENUATES ENDOTHELIAL DYSFUNCTION IN OLD RATS

Aging is an independent risk factor for cardiovascular disease and is characterized by a decline in endothelial function. Parathyroid hormone (PTH) administration has been shown to increase endothelial nitric oxide synthase (eNOS) expression. The purpose of this investigation was to determine the effect of intermittent PTH administration on aortic endothelial function in old rodents. We hypothesized that intermittent PTH administration would improve endothelial function in older rodents. Old (24 mo) and young (4 mo) Fischer-344 rats were given 10 injections of PTH (1-34) (43 μg/kg/day) or phosphate buffered saline (100 μl/day) over 15 days. Endothelium-dependent relaxation of aortic rings in response to acetylcholine (10^-9-10^-5 M) was significantly impaired in old control (OC) compared to young control (YC) as indicated by a reduced area under the curve (AUC, 100 ± 6.28 vs. 54.08 ± 8.3%; P < 0.05) and impaired maximal relaxation (E_max, 70.1 ± 4.48 vs. 92.9 ± 4.38%; P < 0.05). E_max was improved in old animals treated with PTH (OPTH) (OC, 70.1 ± 4.48 vs. OPTH, 85 ± 7.48%; P < 0.05) as well as AUC (OC, 54.08 ± 8.3 vs. OPTH 82.5 ± 5.7%; P < 0.05) while LogEC₅₀ was not different. Endothelial-independent relaxation in response to sodium nitroprusside was not different among groups. Aortic eNOS protein expression was significantly decreased in OC compared to YC (P < 0.05). PTH treatment restored eNOS expression in OPTH animals (P < 0.05). These data suggest PTH may play a role in attenuating age-related impairments in aortic endothelial function.

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