[OP.7D.02] INCREASE IN PLASMA COPEPTIN CONCENTRATION IN PATIENTS WITH CONFIRMED RESISTANT ESSENTIAL HYPERTENSION. (September 2016)

• Record Type: Journal Article
• Authors: Dubourg, J.; Mendes, M.; Blanchard, A.; Frank, M.; Amar, L.; Bobrie, G.; Plouin, P.-F.; Azizi, M.
• Is Part Of: Journal of hypertension. Volume 34:(2016) Supplement 2
• Publication Date: 2016-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000491577.39539.21
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: The lack of consensus regarding the role of vasopressin in uncontrolled hypertension may be due to the use of assays with limited sensitivity. We used plasma copeptin concentration (PCop), a reliable surrogate marker for plasma vasopressin, to evaluate its role in a large population of patients with resistant (RH) and non-resistant (NRH) essential hypertension. Design and method: 166 patients with RH to > = 3 antihypertensive drugs, including a diuretic (office BP > = 140 or 90 mmHg), entered a 4-week standardized treatment with irbesartan 300 mg + HCTZ 12.5 mg + amlodipine 5 mg to confirm RH by ABPM (daytime ambulatory BP > = 135/85 mmHg). We compared PCop, plasma renin (PRC) and aldosterone concentration (PAC) and urine osmolality (Uosm) and estimated glomerular filtration rate (eGFR) after 4 weeks between patients with confirmed RH (n = 140) and NRH (n = 26). Results: Patients with RH were more frequently men, had significantly lower PRC, but similar PAC than patients with NRH. PCop was about 2-fold higher in patients with RH than in those with NRH (P = 0.001 adjusted on sex, plasma Na, daytime SBP and eGFR) even though similar plasma Na (p = 0.9). RH Uosm, 24-h and urinary output and correlation between Uosm log-PCop did not significantly differ between the two groups. Figure. No caption available. Conclusions: Patients with RH to a 4-week standardized triple therapy had a 2-fold lower PRC (indicating a persistance of volume expansion) and a 2-fold higher PCop than those of patients NRH. The increase in PCop was not explained by changes in plasma Na, nor by peripheral (renal) resistance to vasopressin. This suggests a primary central stimulation of AVP secretion in RH associated with biological signs of volume expansion.