Bradykinin-induced growth inhibition of normal rat kidney (NRK) cells is paralleled by a decrease in epidermal-growth-factor receptor expression

Zoelen, E.J.J. van; Peters, P.H.J.; Afink, Gijs B.; Genesen, Siebe van; Roos, Albert de; Rotterdam, Walter van; Theuvenet, A.P.R.

doi:10.1042/bj2980335

Cited by 23 publications

(15 citation statements)

References 40 publications

(21 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since ACE is the same as kininase II (the primary bradykinin-degrading enzyme), these additional effects of its inhibition must also be considered: bradykinin is mitogenic and modulates TGF-β1 stimulation of renal fibroblasts (30). Although many of the effects of Ang II are mediated by AT 1 receptors, there is increasing evidence that other receptors are involved.…”

Section: Discussionmentioning

confidence: 99%

Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice

et al. 1999

View full text Add to dashboard Cite

A novel approach was employed to assess the contribution of the renin-angiotensin system (RAS) to obstructive nephropathy in neonatal mice having zero to four functional copies of the angiotensinogen gene (Agt). Two-day-old mice underwent unilateral ureteral obstruction (UUO) or sham operation; 28 days later, renal interstitial fibrosis and tubular atrophy were quantitated. In all Agt genotypes, UUO reduced ipsilateral renal mass and increased that of the opposite kidney. Renal interstitial collagen increased after UUO linearly with Agt expression, from a fractional area of 25% in zero-copy mice to 54% in two-copy mice. Renal expression of transforming growth factor-β1 was increased by ipsilateral UUO in mice expressing Agt, but not in zero-copy mice. However, the prevalence of atrophic tubules due to UUO did not vary with Agt expression. Blood pressure was not different in all groups, except for a reduction in sham zero-copy mice. We conclude that a functional RAS is not necessary for compensatory renal growth. This study demonstrates conclusively that angiotensin regulates at least 50% of the renal interstitial fibrotic response in obstructive nephropathy, an effect independent of systemic hemodynamic changes. Angiotensininduced fibrosis likely is a mechanism common to the progression of many forms of renal disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice

et al. 1999

View full text Add to dashboard Cite

show abstract

“…32 Bradykinin has a strong inhibitory effect on growth stimulation of normal rat kidney fibroblasts induced by growth factors. 33 Thus it remains unclear that bradykinin is involved in the antitrophic effect of ACE inhibitors in the kidney. A pronounced reduction in the residual kidney weight by enalapril compared to candesartan cilexetil may be caused by a mechanism other than the potentiation of bradykinin by enalapril.…”

Section: S69mentioning

confidence: 99%

Effects of candesartan cilexetil on oxidative state and renal function in 5/6 nephrectomized rats

et al. 1999

View full text Add to dashboard Cite

We have investigated the influence of a novel angiotensin II type 1 receptor antagonist, candesartan cilexetil, on the oxidative state of renal tissue and renal function in 5/6 nephrectomized rats, and compared its effects with those of an angiotensin-converting enzyme inhibitor, enalapril. Candesartan cilexetil (1 and 5 mg/kg per day), enalapril (5 mg/kg per day) and vehicle were orally administered once daily for 16 weeks after 5/6 nephrectomy. There was a marked degree of proteinuria evident prior to treatment, an average of 5.69 mg/mg creatinine in the nephrectomized rats, vs 1 to 2 mg/mg creatinine in the control group matched for species and body weight. Inhibition of development of proteinuria by candesartan cilexetil was dose dependent. Enalapril also significantly blunted the rise in urinary protein. Malondialdehyde content in the homogenate from the renal cor-

show abstract

“…BK has been described to facilitate or inhibit cell proliferation depending on the cell phenotype [112][113][114][115][116]. To our knowledge, only one study has been performed to investigate this aspect on chondrocytes and failed to measure an increase on the rate of DNA synthesis as measured by [ 3 H]thymidine uptake experiments [102].…”

Section: Kinins Effects On Chondrocytesmentioning

confidence: 84%

Knee osteoarthritis: a role for bradykinin?

Meini

Maggi

2008

Inflamm. res.

View full text Add to dashboard Cite

Osteoarthritis (OA) is a painful and degenerating progressive disease of the joints which affects millions of patients worldwide. The cause of OA is largely unknown. Among the potential therapies for the symptomatic treatment of OA, the intra-articular administration of a specific bradykinin (BK) B2 receptor antagonist has been reported to produce a long lasting analgesic effect in patients affected by knee OA. BK is a vasodilator and inflammatory nonapeptide which is generated in OA synovium. It contributes to the initiation and maintenance of inflammation, to exciting and sensitizing sensory nerve fibres, thus producing pain, and to activating synoviocytes and chondrocytes which are the main cells involved in the homeostasis of synovial fluid and cartilage, respectively. Moreover, BK synergistically potentiates the effects produced by pro-inflammatory cytokines. Biochemical and preclinical evidence supporting the therapeutic relevance of B2 receptor blockade in OA pathophysiology are reviewed in this publication.

show abstract

Bradykinin-induced growth inhibition of normal rat kidney (NRK) cells is paralleled by a decrease in epidermal-growth-factor receptor expression

Cited by 23 publications

References 40 publications

Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice

Reduced angiotensinogen expression attenuates renal interstitial fibrosis in obstructive nephropathy in mice

Effects of candesartan cilexetil on oxidative state and renal function in 5/6 nephrectomized rats

Knee osteoarthritis: a role for bradykinin?

Contact Info

Product

Resources

About