A Comparison of the Effect of Hypothyroidism on Pressure Natriuresis in Male Wistar Kyoto (WKY) Rats and Spontaneously Hypertensive Rats (SHR)

Almost 1 billion people worldwide suffer from hypertension, or high blood pressure. Studies indicate hypothyroidism, starting at weaning, is associated with a decrease in systolic pressure in the Spontaneously Hypertensive Rat (SHR). Additionally, it has been determined that thyroid hormones are critical in the synthesis of nitric oxide. Nitric oxide (NO) is required for normal urinary sodium elimination in response to a rise in blood pressure (pressure natriuresis). The production of nitric oxide is impaired in patients with hypertension, a condition referred to as endothelial dysfunction. Nitric oxide inhibition results in a marked decrease in pressure natriuresis in male rats. Impaired pressure natriuresis, is observed in all instances of hypertension. However, past studies found no impact of hypothyroidism on the pressure natriuresis response. This study sought to determine the relationship between developmental hypothyroidism and changes in pressure natriuresis in Spontaneously Hypertensive Rats (SHRs) and their parent strain, the normotensive (normal blood pressure) Wistar Kyoto Rat (WKY). This was accomplished through monitoring acute changes in urinary sodium excretion in response to a rise in blood pressure in control and hypothyroid, SHR and WKY male rats. All experimental groups exhibited a comparable resting mean arterial pressure (MAP) and a comparable increase in mean arterial pressure resulting from artery ligation. Interestingly, only hypothyroid WKYs exhibited a significantly greater increase in sodium excretion with an increase in MAP compared to their control counterparts. Comparable urine volume excretion was observed in all groups. These results indicate a strain specific response in pressure natriuresis to hypothyroidism