Study of calcium dobesilate in diabetic rats

Tejerina, Teresa; Ruiz, Emilio Muñoz; Sanz, María Jesús Mardomingo; Ganado, Patricia

doi:10.1055/s-0031-1276206

Cited by 1 publication

(2 citation statements)

References 11 publications

(15 reference statements)

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“…Dobesilate has been reported to reduce capillary permeability, to inhibit platelet aggregation and to reduce blood viscosity (Berthet et al ., 1999). In addition, DOBE is able to potentiate endothelium‐dependent relaxation in the aorta of rabbit (Ruiz et al ., 1997) and diabetic rats (Tejerina et al ., 1999). DOBE has been reported to enhance endothelial NOS activity (Suschek et al ., 1997), but it is unlikely that this mechanism is involved in the effects of DOBE in human penile arteries, since DOBE was active despite NOS inhibition with L ‐NNA.…”

Section: Discussionmentioning

confidence: 99%

“…Calcium dobesilate (DOBE) has been extensively used as an orally administered angioprotective agent, specially in the treatment of diabetic retinopathy (Berthet et al ., 1999). Although its mechanism of action is poorly understood, this compound has been shown to potentiate endothelium‐dependent relaxation of rabbit aorta (Ruiz et al ., 1997) and aorta from diabetic rats and to improve endothelial function in diabetic patients (Berthet et al ., 1999; Tejerina et al ., 1999).…”

Section: Introductionmentioning

confidence: 99%

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Calcium dobesilate potentiates endothelium‐derived hyperpolarizing factor‐mediated relaxation of human penile resistance arteries

Angulo

Cuevas

Fernández

et al. 2003

British J Pharmacology

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1 We have evaluated the participation of endothelium-derived hyperpolarizing factor (EDHF) in the endothelium-dependent relaxation of isolated human penile resistance arteries (HPRA) and human corpus cavernosum (HCC) strips. In addition, the effect of the angioprotective agent, calcium dobesilate (DOBE), on the endothelium-dependent relaxation of these tissues was investigated. 2 Combined inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX) nearly abolished the endothelium-dependent relaxation to acetylcholine (ACh) in HCC, while 60% relaxation of HPRA was observed under these conditions. Endothelium-dependent relaxation of HPRA resistant to NOS and COX inhibition was prevented by raising the extracellular concentration of K þ (35 mm) or by blocking Ca 2 þ -activated K þ channels, with apamin (APA; 100 nm) and charybdotoxin (CTX; 100 nm), suggesting the involvement of EDHF in these responses. 3 Endothelium-dependent relaxation to ACh was markedly enhanced by DOBE (10 mm) in HPRA but not in HCC. The potentiating effects of DOBE on ACh-induced responses in HPRA, remained after NOS and COX inhibition, were reduced by inhibition of cytochrome P450 oxygenase with miconazole (0.3 mm) and were abolished by high K þ or a combination of APA and CTX. 4 In vivo, DOBE (10 mg kg À1 i.v.) significantly potentiated the erectile responses to cavernosal nerve stimulation in male rats. 5 EDHF plays an important role in the endothelium-dependent relaxation of HPRA but not in HCC. DOBE significantly improves endothelium-dependent relaxation of HPRA mediated by EDHF and potentiates erectile responses in vivo. Thus, EDHF becomes a new therapeutic target for the treatment of erectile dysfunction (ED) and DOBE could be considered a candidate for oral therapy for ED.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%