saline: 2 ± 1%) [F (3, 17) = 53,07; p < 0 05], without changing h

saline: 2 ± 1%) [F (3, 17) = 53,07; p < 0.05], without changing hindlimb vascular resistance or blood flow ( Fig. 2, Fig. 3 and Fig. 4). Prior injection of Dasatinib in vitro moxonidine (20 nmol/1 μl) i.c.v. alone or combined with yohimbine (320 nmol/2 μl) did not modify the pressor response (18 ± 4 and 16 ± 3 mmHg, respectively), the tachycardia (12 ± 4 and 13 ± 3 bpm, respectively), the increase in SM vascular resistance

(20 ± 4% and 19 ± 4%, respectively) and the reduction of blood flow (−10 ± 4% and −12 ± 3%, respectively) produced by i.c.v. pilocarpine (Fig. 2 and Fig. 3). The baseline MAP and HR immediately before yohimbine or vehicle injections in each group of rats are presented in Table 1. The present results show that central injections of pilocarpine reduce SSG vascular resistance and the increase MAP, HR and mesenteric vascular resistance. Contrary to the reduction in the salivary gland vascular resistance, the combination of moxonidine and pilocarpine injected i.c.v. increased SSG vascular resistance, an effect abolished by the previous injection

of yohimbine i.c.v. The changes in mesenteric vascular resistance, MAP and HR produced by pilocarpine i.c.v. were not altered by the central injection of moxonidine. Hindlimb vascular resistance was not affected by either treatment. These results suggest that the activation this website of central α2-adrenoceptors may oppose to the effects of central cholinergic receptor activation in the SSG vascular resistance. The effects produced by i.c.v. injection of pilocarpine on MAP, HR and on SSG and mesenteric resistances were similar to those produced by peripheral injections of pilocarpine, which reinforces the suggestion that pilocarpine injected peripherally may act centrally to reduce SSG vascular resistance and to increase MAP, HR and mesenteric vascular resistance.6 and 10 In addition to the central effects, pilocarpine injected

peripherally may also produce SSG vasodilation by acting Tenofovir nmr directly in the salivary glands. In spite of this direct effect on salivary glands, moxonidine injected i.c.v. combined with pilocarpine injected intravenously also increased SSG vascular resistance,10 similar to the effects of moxonidine combined with pilocarpine i.c.v. (present results). Moxonidine injected i.c.v. alone also increases SSG vascular resistance,10 which suggests that the activation of central α2-adrenoceptors overcomes the effects central cholinergic activation resulting in increased SSG vascular resistance when pilocarpine is combined with moxonidine both injected i.c.v. The importance and the involvement of the central α2-adrenoceptors in the inhibition of salivation were shown previously by injecting clonidine intracisternally in cats that received electrical stimulation of brainstem parasympathetic nuclei.19 The effect of clonidine was inhibited by prior intracisternal injection of yohimbine.

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