Reference

Moxonidine in the treatment of overweight and obese patients with the metabolic syndrome: a postmarketing surveillance study

Moxonidine in the treatment of overweight and obese patients with the metabolic syndrome: a postmarketing surveillance study. Sharma, A. M.; Wagner, T.; Marsalek, P. (McMaster University, Hamilton, ON, Can.). Journal of Human Hypertension, 18(9), 669-675 (English) 2004 Nature Publishing Group. CODEN: JHHYEN. ISSN: 0950-9240. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Moxonidine is a centrally active imidazoline receptor agonist that effectively lowers blood pressure and has been shown to have beneficial effects on lipid and carbohydrate metab. We assessed the efficacy of moxonidine in a postmarketing surveillance study (CAMUS) conducted in 772 practices in Germany, documenting 4005 patients with hypertension, who were overweight and/or suffered from metabolic syndrome. Patients were treated with moxonidine (Cynt) for the first time following the baseline visit for 8 wk. Mean blood pressure decreased from 168/97 to 141/83 mmHg for all patients and from 168/96 to 141/83 mmHg for patients with metabolic syndrome. Blood pressure redn. was particularly pronounced in patients with severe hypertension at baseline. The response rate (DBP￡90 mmHg or redn. 310 mmHg) of antihypertensive treatment with moxonidine was 94.0% for all patients and 93.8% for patients with metabolic syndrome. 75438-57-2 is the cas registry number of certain chemical which is used as reagents here. The recommended targets for antihypertensive treatment of the German Diabetes Society/German Hypertension Society were reached by 30.5% of nondiabetics (goal: <140/90 mmHg) and by 3.6% of diabetics (goal: <130/80 mmHg) obsd. After 8 wk of treatment, patients achieved a mean wt. loss of 1.4 kg, which was particularly pronounced in obese patients. The rate of patients receiving antihypertensive combination therapy was 81.1% for those with metabolic syndrome, and 63.3% for all other patients. Patients with metabolic syndrome were preferentially treated with ACE inhibitors and diuretics. We conclude that moxonidine effectively reduces blood pressure in patients with metabolic syndrome while simultaneously reducing body wt. in obese patients. .

Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine

Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine. Moreira, Thiago Santos; Thomaz Takakura, Ana Carolina; Colombari, Eduardo; De Luca, Laurival Antonio; Renzi, Antonio; Menani, Jose Vanderlei (UNESP, Faculdade de Odontologia, Departamento de Fisiologia e Patologia, Universidade Estadual Paulista, Araraquara 14801-903, Brazil). Brain Research, 987(2), 155-163 (English) 2003 Elsevier Science B.V. CODEN: BRREAP. ISSN: 0006-8993. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 2 Peripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the a2-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with i.p. (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 mmol/kg of body wt.) i.p. reduced SSG vascular resistance (-50±13% vs. vehicle: 5±3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15±5% vs. vehicle: 2±3%) and MAP (16±3 mmHg, vs. vehicle: 2±3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88±12% vs. vehicle: 7±4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. 92-13-7 and 75438-57-2 are just another two chemicals used in this study. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine. .