Abstract
The objective of the present cross-sectional epidemiological study from Tromsø, North Norway was to evaluate the relation between blood pressure and serum parathyroid hormone (PTH). 10419 subjects were invited to participate in the fifth Tromsø study and 8128 attended. 7954 subjects had serum PTH measured, and among these, information on blood pressure medication was available in 5841 subjects (2554 males) with serum calcium within the reference range 2.20-2.60 mmol/L. In a multiple linearregression model with age, BMI, serum calcium, serum creatinine, and smoking status as covariables, serum PTH was a significant and positive predictor of systolic and diastolic blood pressure in both genders. When dividing the cohort in PTH quartiles, and adjusting for age, BMI, serum calcium, and serum creatinine, the differences between the lowest and highest PTH quartile in systolic and diastolic blood pressure were 5.0 and 3.5 mmHg for males and 4.1 and 2.5 mmHg for females, respectively. In previous studies we have found serum PTH to be a positive predictor for future increase in blood pressure, and also that the association between serum PTH and blood pressure cannot alone be ascribed to a blood pressure induced increase in urinary calcium excretion. To further elucidate the relation between serum PTH and blood pressure, randomized clinical trials with calcium and/or vitamin D supplementation to subjects with increased serum PTH levels are needed
Highlights
Parathyroid hormone (PTH) is a peptide hormone secreted from the parathyroid glands
When the cohort was divided in PTH quartiles, there was in both genders a gradual increase in age, Body mass index (BMI), and serum creatinine with increasing PTH quartile, and a gradual decrease in serum calcium with increasing PTH quartile (Table 2)
There was in both genders a gradual and significant increase in systolic and diastolic blood pressure with increasing PTH quartile
Summary
Parathyroid hormone (PTH) is a peptide hormone secreted from the parathyroid glands. The secretion of PTH is mainly regulated by the extra-cellular ionized calcium level through a negative feed-back mechanism. PTH in turn increases the serum calcium level by increasing bone resorption and the renal tubular calcium absorption. PTH binds to specific receptors that exist on the surface of its major target organs bone and kidney cells, and on the cell membrane of a number of other organs such as the nervous system and the heart [2]. In this way, excessive PTH secretion can have a multitude of effects, and PTH has been implicated in disease states like neuropathy and left ventricular hypertrophy [2]
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