Indanidine
(Synonyms: 吲达尼定) 目录号 : GC32512
Indanidine是一种α-肾上腺素能激动剂。
Cas No.:85392-79-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
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Indanidine is an alpha-adrenergic agonist.
The selective alpha 1-adrenoceptor agonist, Indanidine, also behaved as a partial agonist in the aorta and produced no significant contractions of the small mesenteric artery. Since Idazoxan and Indanidine have been reported to raise blood pressure in the pithed rat via an action at vascular alpha 1-adrenoceptors, these results call into question the reliability of the small mesenteric artery assay as a predictor for alpha 1-adrenoceptor-mediated pressor activity in vivo[1].
[1]. Van der Graaf PH, et al. Analysis of the action of idazoxan calls into question the reliability of the rat isolated small mesenteric artery assay as a predictor for alpha 1-adrenoceptor-mediated pressor activity. Naunyn Schmiedebergs Arch Pharmacol. 1996 Aug-Sep;354(3):389-92.
| Cas No. | 85392-79-6 | SDF | |
| 别名 | 吲达尼定 | ||
| Canonical SMILES | CN1N=C2C=CC=C(NC3=NCCN3)C2=C1 | ||
| 分子式 | C11H13N5 | 分子量 | 215.25 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.6458 mL | 23.2288 mL | 46.4576 mL |
| 5 mM | 0.9292 mL | 4.6458 mL | 9.2915 mL |
| 10 mM | 0.4646 mL | 2.3229 mL | 4.6458 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
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动物数量 | 只 |
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DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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2.
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Systemic and regional hemodynamic characterization of alpha-1 and alpha-2 adrenoceptor agonists in pithed rats
J Pharmacol Exp Ther 1987 Mar;240(3):944-53.PMID:2882016doi
In pithed rats, blood pressure dose-response curves to i.v. cirazoline, methoxamine and phenylephrine (full alpha-1 adrenoceptor agonists) exhibited higher maxima than those to B-HT 920, M-7, UK-14,304 (full alpha-2 adrenoceptor agonists) and Indanidine (Sgd 101/75: partial alpha-1 adrenoceptor agonist). For an 80 mm Hg increase in blood pressure, full alpha-1 adrenoceptor agonists enhanced total peripheral, renal and mesenteric vascular resistances significantly more than alpha-2 adrenoceptor stimulants or Indanidine. In contrast, all compounds produced a similar degree of hindquarter vasoconstriction, suggesting that both types of alpha adrenoceptors have the same functional importance in this skeletal muscle vascular bed. Application of a multivariate discriminant analysis to the drug-induced changes in the total peripheral and mesenteric vascular resistances associated with a pressor effect of 80 mm Hg allowed their assignment to two distinct groups corresponding to the full alpha-1 and the full alpha-2 adrenoceptor agonists plus Indanidine. All investigated compounds in low doses increased cardiac output, which returned to base-line values after high doses of alpha-1 but plateaued after high doses of alpha-2 adrenoceptor agonists or Indanidine. alpha-1 adrenoceptor agonists decreased whereas alpha-2 stimulants and Indanidine successively increased and then decreased renal blood flow. Finally, all investigated compounds increased hindquarter blood flow at low doses but decreased it at high doses. The ratios of the doses of cirazoline required to produce a 100% rise in systemic and local vascular resistances in the presence or in the absence of prazosin were of similar magnitude. This was also true for M-7 when studied in the presence or in the absence of yohimbine. These findings suggest pharmacological identity within alpha-1 as well as within alpha-2 adrenoceptor populations in all investigated vascular beds. Finally, the calcium entry blocker diltiazem did not affect the increases in systemic and regional resistances evoked by cirazoline but depressed profoundly the effects of M-7 and Indanidine. In conclusion, full alpha-1 and alpha-2 adrenoceptor agonists can be discriminated easily on the basis of their systemic and regional hemodynamics in the pithed rat. That the hemodynamic effects of the partial alpha-1 adrenoceptor agonist Indanidine are similar to those of alpha-2 adrenoceptor agonists and susceptible to calcium channel blockade suggests that the alpha-1 adrenoceptors stimulated by this drug have the same coupling modality as alpha-2 adrenoceptors and share with the latter the same functional expression when stimulated.
Functional evidence for an alpha 1B-adrenoceptor mediating contraction of the mouse spleen
Eur J Pharmacol 1996 Sep 12;311(2-3):187-98.PMID:8891599DOI:10.1016/0014-2999(96)00430-x.
alpha 1-Adrenoceptor agonists ((-)-adrenaline = (-)-noradrenaline > > L-phenylephrine > methoxamine > (-)-(4a R, 10a R)-3,4,4a,5,10,10a-hexahydro-6-methoxy-4-methyl-9-methylthio-2 H-naphth[2,3-b]-1,4-oxazine (SDZ NVI 085) > cirazoline) evoked contraction of isolated mouse spleen strips, whereas oxymetazoline and Indanidine were nearly inactive. Splenic contractions elicited by (-)-noradrenaline were inhibited by chloroethylclonidine (3 x 10(-6) - 6 x 10(-5) M) and partially attenuated by SZL-49 (10(-7) -10(-6) M), but remained resistant to (+/-)-isradipine (10(-9) -10(-7) M). The contractions were competitively antagonized by low concentrations of the alpha 1B-adrenoceptor-selective antagonist, spiperone (pA2 = 8.29), but by relatively high concentrations of the alpha 1A-adrenoceptor-selective receptor antagonists, tamsulosin (pA2 = 8.62), 5-methyl-urapidil (pA2 = 7.03), (+)-niguldipine (pA2 = 6.26) and the alpha 1D-adrenoceptor-selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro-[4.5]dec ane-7, 9-dione (BMY 7378) (pA2 = 6.76). Functional antagonist affinities at mouse spleen alpha 1-adrenoceptors were consistent with those at guinea-pig splenic alpha 1B-adrenoceptors, but not with those of either rat vas deferens alpha 1A- or rat aortic alpha 1D-adrenoceptors. Antagonist affinities at mouse spleen alpha 1-adrenoceptors correlated also best with published antagonist data on cloned and expressed alpha 1b-adrenoceptors but less well with those for either alpha 1a- or alpha 1d-adrenoceptors. The results provide pharmacological evidence that the alpha 1-adrenoceptor mediating smooth muscle contraction of mouse spleen is the B subtype.
Characterization of the alpha 1-adrenoceptor subtype mediating contraction of guinea-pig spleen
Eur J Pharmacol 1994 Aug 1;260(2-3):211-20.PMID:7988645DOI:10.1016/0014-2999(94)90339-5.
A series of alpha 1-adrenoceptor agonists evoked concentration-dependent contraction of isolated guinea-pig spleen strips ((-)-adrenaline > (-)-noradrenaline >> L-phenylephrine > (-)-(4aR, 10aR)-3, 4,4a,5,10,10a-hexahydro-6-methoxy-4-methyl-9-methylthio-2H-naphth [2,3-b]-1,4-oxazine (SDZ NVI 085) > cirazoline), whereas Indanidine, methoxamine, oxymetazoline and UK-14.304 were ineffective. (-)-Noradrenaline-induced contractions were inhibited by chloroethylclonidine (3 x 10(-6)-6 x 10(-5) M) and partially attenuated by SZL-49 (10(-7)-10(-6) M), but remained resistant to (+/-)-isradipine (10(-9)-10(-7) M). The contractions of the splenic strips were competitively antagonized by low concentrations of the alpha 1B-adrenoceptor-selective antagonist, spiperone (pA2 8.05), but by relatively high concentrations of the alpha 1A-adrenoceptor-selective antagonists, (+)-niguldipine (pA2 6.32) and 5-methyl-urapidil (pA2 6.95). The affinities of subtype-selective antagonists determined at guinea-pig spleen alpha-adrenoceptors significantly correlated with pKi values at rat liver alpha 1B binding sites (r = 0.96) and pA2 values at putative alpha 1B-adrenoceptors in rat aorta (r = 0.95), but differed from pKi values at rat cortical alpha 1A binding sites and pA2 values at alpha 1A-adrenoceptors in rat vas deferens. Also no correlation was obtained between antagonist affinities at guinea-pig spleen alpha-adrenoceptors and alpha 1C binding sites in rabbit liver. Thus, from the (1) potencies of agonists, (2) affinities of subtype-selective antagonists and (3) differential sensitivity of the contractions to alpha 1-adrenoceptor inactivating agents and their resistance to Ca2+ channel blockade, the alpha 1-adrenoceptor mediating smooth muscle contraction of guinea-pig spleen can be best characterized as being of the B subtype.
Blockade by nifedipine of responses to intravenous bolus injection or infusion of alpha 1- and alpha 2-adrenoceptor agonists in the pithed rat
Br J Pharmacol 1987 Jun;91(2):355-65.PMID:2886168DOI:10.1111/j.1476-5381.1987.tb10290.x.
Nifedipine was tested against pressor responses in the pithed rat to ten agonists with varying selectivity for alpha 1- and alpha 2-adrenoceptors, injected as a bolus or infused intravenously: i.e. amidephrine, azepexole, cirazoline, Indanidine, M7, methoxamine, noradrenaline (NA), oxymetazoline, phenylephrine and xylazine. Nifedipine, administered before the agonists, inhibited responses initiated by all agonists, usually for both the bolus and infusion responses. With a bolus, blockade was significantly greater against the more prolonged, secondary components of the pressor responses. This demonstrates that calcium-entry occurs during the secondary component of the alpha-adrenoceptor-mediated response and can be initiated by either alpha 1- or alpha 2-adrenoceptor subtypes. The time courses of responses to infusion varied. Selective alpha 1-adrenoceptor agonists, with the exception of Indanidine, did not produce a stable pressor response during the 20 min infusion time but alpha 2-adrenoceptor agonists did. Nifedipine reduced responses to infusion with no preference for alpha 1- or alpha 2-agonists. Phenylephrine and NA produced pressor responses which reached a peak and then declined during the remainder of the infusion. The levels of NA in arterial and venous plasma were measured by h.p.l.c. during the infusion of NA. Arterial NA levels rose throughout the infusion whereas venous levels remained relatively unaffected. The absolute levels of plasma NA suggest that a large proportion of intravenously administered NA is removed in the pulmonary circulation and the remainder is removed in the systemic circulation with negligible recirculation. The consequences of these results, for assessment of the mechanisms of action of adrenoceptor agonists and calcium entry blockers, are discussed.
[3H]idazoxan and some other alpha 2-adrenergic drugs also bind with high affinity to a nonadrenergic site
Mol Pharmacol 1989 Mar;35(3):324-30.PMID:2564631doi
We compared the pharmacological properties of the alpha 2-adrenergic radioligand [3H]idazoxan with those of [3H]rauwolscine in rat and [3H]yohimbine in human renal cortical membranes. The density of "specific" [3H]idazoxan binding sites (defined by 100 microM tolazoline) was twice as high as that of [3H]rauwolscine in rat kidney and four times as high as that of [3H]yohimbine in human kidney. A variety of structurally different drugs fully competed for specific [3H]rauwolscine and [3H]yohimbine binding, with affinities appropriate for the interaction with alpha 2-adrenergic receptors. Specific [3H]idazoxan binding, however, was only partially competed for by the catecholamines epinephrine and norepinephrine in both tissues. Thus, [3H]idazoxan labels both alpha 2-adrenergic receptors and a nonadrenergic site. Clonidine, B-HT 920, moxonidine, phentolamine, prazosin, yohimbine, dopamine, and serotonin also could not compete for this site. However, UK 14,304, guanabenz, Indanidine, tolazoline, oxymetazoline, and SK&F 104,078 competed for the additional [3H]idazoxan sites with affinities similar to those at alpha 2-adrenergic receptors. [3H]idazoxan binding substantially in excess of [3H]rauwolscine or [3H]yohimbine binding was also found in human platelets, myometrium, and erythroleukemia (HEL) cells but not in three cell lines lacking alpha 2-receptors (MDCK, BC3H1, and Jurkat cells). Although we have been unsuccessful thus far in defining the precise nature of the additional [3H]idazoxan binding sites, we hypothesize that these sites may be closely affiliated with alpha 2-adrenergic receptors but clearly distinct from the catecholamine binding site of the receptor. The results indicate that care must be taken in the use of [3H]idazoxan or drugs that are recognized at its nonadrenergic site when studying alpha 2-adrenergic effects and receptor subtypes.