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1 eceptor antagonism, as is the case with S(-)-pindolol.
2 m (EEG) was used to assay central effects of pindolol (10 and 30 mg p.o.), a mixed beta(1/2)-adrenoce
3  depressed patients on one of two regimes of pindolol (2.5 mg t.i.d. and 5.0 mg t.i.d.) with PET and
4                                         S(-)-pindolol (3, 10, but not 1 mg/kg) produced a comparable
5 fluoxetine (20 mg/day) and either placebo or pindolol (5.0 mg b.i.d. or 2.5 mg t.i.d.), for 6 weeks,
6  (5HTP), a serotonin precursor, or with S(-) pindolol, a 5HT1A/beta adrenergic receptor antagonist or
7            The greatest effect was seen with pindolol, a partial agonist, suggesting that a H bond be
8  via the catecholamine site, whereas others (pindolol and alprenolol) can stimulate both.
9 l)-p-iodobenzamidoethyl] piperazine, (-)-(S)-pindolol, and spiperone also stimulated up-regulation of
10 ropoxy]-1,3-dihydro-2H-benzimidazol-2-o ne], pindolol, and timolol, which displayed agonistic propert
11 he 14 subjects was deemed a responder to the pindolol arm of the crossover.
12                         The effectiveness of pindolol as an adjunctive treatment to boost response to
13 zation efficiency of racemic propranolol and pindolol as model compounds in the positive ion mode und
14 th [3H]prazosin, [3H]RX21002 and [125I]-iodo-pindolol autoradiography, respectively.
15 terest as potential new antidepressants were pindolol, ciprofibrate, pioglitazone and adiphenine, as
16                                          The pindolol group, but not the placebo group, demonstrated
17 hese findings do not support the efficacy of pindolol in hastening clinical response in patients trea
18 trolled trial to assess the effectiveness of pindolol in hastening response to fluoxetine.
19 ely, are consistent with the contention that pindolol inhibits, possibly selectively, somatodendritic
20 95Q-W199Y) where secondary site CGP12177 and pindolol interaction is lost, the 3 novel secondary-site
21 ed 5-HT(1A/1B)/beta receptor antagonist S(-)-pindolol, on DA release in the NAC compared to the stria
22 eeks of treatment with fluoxetine and either pindolol or placebo were 17% (four of 23 patients) and 2
23                         Compared to placebo, pindolol produced a dose-related suppression of rapid-ey
24                  In two preliminary studies, pindolol produced robust results in hastening clinical r
25 y competitive inhibition with ritanserin and pindolol, respectively.
26                Therefore, a thorough test of pindolol's efficacy will necessitate doses higher than t
27 observed a significant increase in basal and pindolol-stimulated cAMP accumulation in COS-7 cells tra
28                                  Furthermore pindolol switched from a biphasic concentration response
29 sign was used to compare addition of 5 mg of pindolol t.i.d. or placebo for 4 weeks to a steady parox
30            The EEG power spectrum induced by pindolol tended to be opposite to what has previously be
31                                  The dose of pindolol used in clinical trials is suboptimal and may e
32 rivation, ketamine, scopolamine, GLYX-13 and pindolol used in conjunction with classical antidepressa
33 PET) was used to examine whether the dose of pindolol used to augment antidepressant medication achie
34                    The cationic beta-blocker pindolol was injected electrokinetically, and detected a
35                                              Pindolol was no more effective than placebo in augmentin
36                                              Pindolol was not significantly superior to placebo for a