ECE2016 Eposter Presentations Cardiovascular Endocrinology and Lipid Metabolism (51 abstracts)
Hypertension and related cardiovascular diseases: a new role for low levels of parathyroid hormone
Nadia Afzal 1 , Syed Ali Raza Kazmi 2 , Maleeha Akram 1 , Sarwat Jahan 3 , Abida Raza 4 , Ghazala Kokab Raja 5 , Saba Nazir 1 , Sidrah Nazir 5 , Afzaal Ahmed Naseem 1 , Mazhar Qayyum 1 & Syed Shakeel Raza Rizvi 1
1Department of Zoology, Pir Mehr Ali Shah Arid Agriculture University Rawalpindi, Rawalpindi, Pakistan; 2Aga Khan Health Centre, Rawalpindi, Pakistan; 3Department of Animal Sciences, Quaid-e-Azam University, Islamabad, Pakistan; 4Nuclear Medicine Oncology and Radiotherapy Institute (NORI), Islamabad, Pakistan; 5University Institute of Biochemistry and Biotechnology, Pir Mehr Ali Shah Arid Agriculture University Rawalpindi, Rawalpindi, Pakistan.
Hypertension or elevated arterial blood pressure (BP) is the most common cause of cardiovascular diseases (CVDs). The arterial BP is regulated by renin-angiotensin-aldosterone system (RAAS), whereas dysfunctional RAAS may lead to development of hypertension and associated CVDs. Parathyroid hormone (PTH) secreted by parathyroid glands regulates RAAS by directly stimulating aldosterone synthesis in zona glomerulosa cells, which leads to development of hypertension. Conversely, RAAS controls PTH secretion; in high dietary salt intake aldosterone promotes reabsorption of sodium and increases calcium excretion in renal distal tubules followed by PTH secretion. PTH is an independent cardiovascular risk factor, contributing to cardiovascular damage via binding to PTH receptors on vascular smooth muscle cells and cardiomyocytes. The present study examined the role of PTH in development of hypertension and consequent CVDs. Hundred hypertensive CVD patients of both sexes and hundred healthy age-matched controls were investigated. Blood samples were collected and plasma PTH concentrations were measured using ECLIA system. Of 15 patients treated with RAAS inhibitors (RAASi), PTH concentrations were low in 12 and within normal range in three patients. Among 26 patients under non-RAASi treatment, PTH concentrations were low in 23 and normal in three patients. Of 33 patients given combinations of RAASi and non-RAASi, PTH concentrations were low in 27 and normal in six patients. In 26 untreated patients, PTH concentrations were low in 22 and normal in four patients. Contrary to earlier reports, PTH concentrations were below normal range in 84% patients, whereas PTH concentrations were within normal range in 16% patients, irrespective of any or no treatment. The majority of patients was married, had exercise free lifestyle with no specific diet plan, belonged to low socioeconomic status, fell in the obese category and had family history of CVDs. In conclusion, our hypertensive cardiovascular patients had either low or normal values of PTH.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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