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1 f nicotine was blocked by prior injection of beta-adrenergic antagonists.
2 is effect was canceled by prior injection of beta-adrenergic antagonists.
4 nd decrements are reversed by propranolol, a beta-adrenergic antagonist, and abolished by selective b
5 microl) of either propranolol (a nonspecific beta-adrenergic antagonist), atenolol (a beta1-adrenergi
9 D(2) receptor antagonist) or propranolol (a beta-adrenergic antagonist) did not alter DA-stimulated
10 de) systemic co-administration of alpha- and beta-adrenergic antagonists in young (n = 9; 26 +/- 1 ye
11 leptin-deficient and wild-type mice while a beta-adrenergic antagonist increases bone mass in wild-t
12 was completely blocked by prior injection of beta-adrenergic antagonists, indicating that beta-adrene
14 beneficial heart failure treatments, such as beta-adrenergic antagonists, involve improved contractil
15 earance was blocked by pretreatment with the beta-adrenergic antagonist, nadolol (0.5 mg/kg), but not
18 e with the nonselective alpha-adrenergic and beta-adrenergic antagonists phentolamine and propranolol
21 This effect was completely blocked by the beta-adrenergic antagonist propranolol but was not affec
23 bits (saline, 1, 3, 5 or 10 mg kg(-1) of the beta-adrenergic antagonist propranolol) were trained wit
24 abbits (saline, 1, 3, 5 or 10 mg kg-1 of the beta-adrenergic antagonist propranolol) were trained wit
25 ing in the NPE but not PE was blocked by the beta-adrenergic antagonist propranolol, the gap junction
29 Although it is the most important target for beta-adrenergic antagonists, such as beta-blockers, rela
30 d infusion of dobutamine or treatment with a beta-adrenergic antagonist, suggesting that RLC is const
33 pineal melatonin formation and is induced by beta-adrenergic antagonists, which block melatonin produ
34 taAR in the heart and is the main target for beta-adrenergic antagonists, widely used in the treatmen
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