RESUMEN
BACKGROUND: Glucosamine is an amine-sugar that has been marketed as a natural product for the treatment of osteoarthritis. It has been popularized in the complementary section of pharmacies as a safe over-the-counter treatment for osteoarthritic pain. OBJECTIVE: We review the literature on the efficacy and safety of glucosamine in osteoarthritis. DISCUSSION: Recent research suggests that it may not only provide symptomatic pain relief, but may have a role in chondroprotection.
Asunto(s)
Glucosamina/uso terapéutico , Osteoartritis/tratamiento farmacológico , Glucosamina/química , HumanosRESUMEN
1. It has been hypothesized that the expression of angiotensin (Ang) II type 2 (AT(2)) receptors may become important in vascular disease; however, the functional existence of AT(2) receptors in normal adult humans remains to be established. 2. Vascular responses to AngII after the administration of the specific AT(2) receptor antagonist PD 123319 were determined in the forearm circulation of normal volunteers. 3. PD 123319 (8 microg/min) did not alter basal forearm blood flow, or forearm blood flow or forearm vascular resistance responses to AngII. 4. These results suggest that AT(2) receptors do not play a significant role in the regulation of forearm blood flow or forearm vascular resistance of normal volunteers, but do not preclude a role for AT(2) receptors in other vascular beds or in patients with cardiovascular disease.
Asunto(s)
Antebrazo/irrigación sanguínea , Receptores de Angiotensina/fisiología , Adulto , Angiotensina II/farmacología , Antagonistas de Receptores de Angiotensina , Estudios Cruzados , Método Doble Ciego , Humanos , Imidazoles/farmacología , Masculino , Piridinas/farmacología , Receptor de Angiotensina Tipo 2 , Flujo Sanguíneo Regional/efectos de los fármacos , Flujo Sanguíneo Regional/fisiología , Resistencia Vascular/efectos de los fármacosRESUMEN
The effects of chronic administration of candesartan, 16 mg once-daily, to normal volunteers on cardiovascular responses to angiotensin II (Ang II) and norepinephrine (NE) were examined. Fifteen healthy, non-smoking volunteers participated in a randomised, double-blind crossover study of two weeks of candesartan therapy, compared with two weeks of placebo. Blood pressure (BP) responses were measured to increasing infusion rates of intravenous Ang II and NE, along with forearm blood flow (FBF) responses into intra-brachial arterial Ang II, 2 and 24 hours after the last dose of candesartan or placebo. FBF responses to intra-brachial arterial NE were recorded approximately 2 hours following the final dose. Systolic and diastolic BP responses to intravenous infusions of Ang II during candesartan treatment were completely suppressed and significantly lower than during placebo treatment, 2 hours (candesartan 96+/-10/55+/-8 mmHg; placebo 105+/-5/64+/-8 mmHg) and 24 hours (candesartan 94+/-8/54+/-8 mmHg; placebo 103+/-7/64+/-7 mmHg) following the last dose. In contrast, FBF responses to intra-brachial arterial Ang II were significantly suppressed by candesartan compared with placebo in a subgroup of subjects 2 hours following the last dose (n=9), but not 24 hours after the last dose (n=8). FBF responses to NE were also suppressed by candesartan treatment 2 hours following the last dose, while BP responses to intravenous NE were unaltered. Chronic candesartan therapy, 16 mg once-daily effectively suppresses pressor responses to Ang II over the duration of the dosing interval.