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      Treatment with a Ca 2+ Channel Blocker, Barnidipine, Reduces Platelet-Derived Growth Factor B-Chain mRNA in Glomeruli of Spontaneously Hypertensive Rats

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          We investigated the effect of barnidipine hydrochloride, a Ca<sup>2+</sup> channel blocker, on the glomerular level of mRNA expression of platelet-derived growth factor (PDGF) B-chain and transforming growth factor (TGF)-β<sub>1</sub> in spontaneously hypertensive rats (SHR) with reverse transcription and polymerase chain reaction. Thirteen-week-old SHR were provided with food containing barnidipine (0.6 mg/g of food, average dose during treatment: 53 mg/kg of body mass/day) for 3 weeks. A stable reduction in systolic blood pressure relative to that of age-matched control SHR was recorded after week 1 of therapy. Although no renal histological changes were observed after 3 weeks of treatment with barnidipine, the level of expression of PDGF B-chain mRNA in glomeruli was significantly reduced relative to that in control SHR. The glomerular level of TGF-β<sub>1</sub> mRNA expression was not affected by the treatment. Treatment with barnidipine significantly reduced the excretion of urinary protein. Thus, the stable reduction in systemic blood pressure by barnidipine is associated with a reduction in PDGF B-chain mRNA expression in the glomerulus and reduction in urinary protein excretion in SHR.

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          Antihypertensive treatment of patients with proteinuric renal diseases: risks or benefits of calcium channel blockers?

          In patients with proteinuric renal diseases the rate of progression of renal insufficiency is determined by the level of blood pressure and proteinuria. It has been demonstrated that strict blood pressure control with angiotensin converting enzyme (ACE)-inhibitors or beta-blockers, aimed at reaching values below 130/80 mm Hg, attenuates the deterioration of renal function. In general, the beneficial effects of these drugs are reflected in a parallel lowering of proteinuria. Calcium channel blockers are effective antihypertensive drugs, however, their safety in patients with proteinuric renal diseases and renal insufficiency may be questioned because of reported untoward effects on urinary protein excretion. The present review discusses the potential benefits and risks of calcium channel blockers (CCBs) in the treatment of patients with renal diseases. To this end we have evaluated the effects of these drugs in animal models of progressive renal injury. In these animal models adverse effects of CCBs have been reported which are attributed to an impairment of autoregulation. In patients with proteinuria, the dihydropyridine CCBs do not lower proteinuria despite a reduction of blood pressure. Studies on the effects on the course of renal function are limited, however, the available data do suggest that this class of CCBs may be less advantageous than other antihypertensive drugs, thus arguing against the use of these agents as first-line drugs in patients with proteinuric renal diseases. Information on the effects of the non-dihydropyridine CCBs is limited to a small number of studies in patients with diabetic renal disease. Although the data suggest that these classes of CCBs might be more beneficial, more studies are needed, particularly in patients with non-diabetic renal diseases, before founded conclusions can be reached.
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            Effects of treatment with angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor antagonist (AIIRA) on renal function and glomerular injury in subtotal nephrectomized rats

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              Inhibitory effects of antihypertensive drugs on mesangial cell proliferation after anti-thymocyte serum (ATS) — induced mesangiolysis in spontaneously hypertensive rats


                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                October 1999
                26 November 1999
                : 19
                : 5
                : 615-621
                aThird Department of Medicine, Okayama University Medical School, bHealth and Medical Center and cFaculty of Education, Okayama University, Okayama, Japan
                13511 Am J Nephrol 1999;19:615–621
                © 1999 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 3, References: 34, Pages: 7
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/13511
                Laboratory Investigation


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