AIMS: Intraglomerular pressure is one of the main drivers of progression of renal failure. Experimental data suggest that there are important differences between calcium channel blockers (CCBs) in their renal haemodynamic effects: manidipine reduces, whereas amlodipine increases intraglomerular pressure. The aim of this study was to investigate the effects of manidipine and amlodipine treatment on intragomerular pressure (P(glom)) in patients with mild to moderate essential hypertension. METHODS: In this randomized, double-blind, parallel group study, hypertensive patients were randomly assigned to receive manidipine 20 mg (n = 54) or amlodipine 10 mg (n = 50) for 4 weeks. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were determined by constant-infusion input-clearance technique with p-aminohippurate (PAH) and inulin. P(glom) and resistances of the afferent (R(A)) and efferent (R(E)) arterioles were calculated according to the model established by Gomez. RESULTS: P(glom) did not change in the manidipine group (P = 0.951), whereas a significant increase occurred in the amlodipine group (P = 0.009). There was a significant difference in the change of P(glom) by 1.2 mmHg between the manidipine and amlodipine group (P = 0.042). In both treatment arms, R(A) was reduced (manidipine P = 0.018; amlodipine P < 0.001). The reduction of R(A) was significantly more pronounced with amlodipine compared with manidipine treatment (P < 0.001). R(E) increased in both treatment arms (manidipine P = 0.012; amlodipine P = 0.002), with no difference between the treatment arms. Both CCBs significantly reduced systolic and diastolic blood pressure (BP) (both P < 0.001). However, amlodipine treatment resulted in a significantly greater decrease of BP compared with manidipine (P < 0.001). CONCLUSIONS: In accordance with experimental data after antihypertensive treatment of 4 weeks, intraglomerular pressure was significantly lower with the CCB manidipine than with amlodipine, resulting and explaining their disparate effects on albuminuria.
RCT Entities:
AIMS: Intraglomerular pressure is one of the main drivers of progression of renal failure. Experimental data suggest that there are important differences between calcium channel blockers (CCBs) in their renal haemodynamic effects: manidipine reduces, whereas amlodipine increases intraglomerular pressure. The aim of this study was to investigate the effects of manidipine and amlodipine treatment on intragomerular pressure (P(glom)) in patients with mild to moderate essential hypertension. METHODS: In this randomized, double-blind, parallel group study, hypertensivepatients were randomly assigned to receive manidipine 20 mg (n = 54) or amlodipine 10 mg (n = 50) for 4 weeks. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were determined by constant-infusion input-clearance technique with p-aminohippurate (PAH) and inulin. P(glom) and resistances of the afferent (R(A)) and efferent (R(E)) arterioles were calculated according to the model established by Gomez. RESULTS: P(glom) did not change in the manidipine group (P = 0.951), whereas a significant increase occurred in the amlodipine group (P = 0.009). There was a significant difference in the change of P(glom) by 1.2 mmHg between the manidipine and amlodipine group (P = 0.042). In both treatment arms, R(A) was reduced (manidipine P = 0.018; amlodipine P < 0.001). The reduction of R(A) was significantly more pronounced with amlodipine compared with manidipine treatment (P < 0.001). R(E) increased in both treatment arms (manidipine P = 0.012; amlodipine P = 0.002), with no difference between the treatment arms. Both CCBs significantly reduced systolic and diastolic blood pressure (BP) (both P < 0.001). However, amlodipine treatment resulted in a significantly greater decrease of BP compared with manidipine (P < 0.001). CONCLUSIONS: In accordance with experimental data after antihypertensive treatment of 4 weeks, intraglomerular pressure was significantly lower with the CCB manidipine than with amlodipine, resulting and explaining their disparate effects on albuminuria.
Authors: Giuseppe Mancia; Guy De Backer; Anna Dominiczak; Renata Cifkova; Robert Fagard; Giuseppe Germano; Guido Grassi; Anthony M Heagerty; Sverre E Kjeldsen; Stephane Laurent; Krzysztof Narkiewicz; Luis Ruilope; Andrzej Rynkiewicz; Roland E Schmieder; Harry A J Struijker Boudier; Alberto Zanchetti; Alec Vahanian; John Camm; Raffaele De Caterina; Veronica Dean; Kenneth Dickstein; Gerasimos Filippatos; Christian Funck-Brentano; Irene Hellemans; Steen Dalby Kristensen; Keith McGregor; Udo Sechtem; Sigmund Silber; Michal Tendera; Petr Widimsky; José Luis Zamorano; Serap Erdine; Wolfgang Kiowski; Enrico Agabiti-Rosei; Ettore Ambrosioni; Lars H Lindholm; Margus Viigimaa; Stamatis Adamopoulos; Enrico Agabiti-Rosei; Ettore Ambrosioni; Vicente Bertomeu; Denis Clement; Serap Erdine; Csaba Farsang; Dan Gaita; Gregory Lip; Jean-Michel Mallion; Athanasios J Manolis; Peter M Nilsson; Eoin O'Brien; Piotr Ponikowski; Josep Redon; Frank Ruschitzka; Juan Tamargo; Pieter van Zwieten; Bernard Waeber; Bryan Williams Journal: J Hypertens Date: 2007-06 Impact factor: 4.844
Authors: Marije van der Velde; Nynke Halbesma; Frank T de Charro; Stephan J L Bakker; Dick de Zeeuw; Paul E de Jong; Ronald T Gansevoort Journal: J Am Soc Nephrol Date: 2009-02-11 Impact factor: 10.121
Authors: Marko Škrtić; Yuliya Lytvyn; Petter Bjornstad; Heather N Reich; James W Scholey; Paul Yip; Etienne B Sochett; Bruce Perkins; David Z I Cherney Journal: Am J Physiol Renal Physiol Date: 2016-12-28
Authors: Jon B Rasmussen; Lovisa S Nordin; Jakúp A Thomsen; Peter Rossing; Ib C Bygbjerg; Dirk L Christensen Journal: J Clin Hypertens (Greenwich) Date: 2015-08-26 Impact factor: 3.738