| Name | angiotensin II |
|---|---|
| Synonyms | AGT; ANG II; ANHU; Angiotensin I; Angiotensin II; Angiotensinogen; Angiotensinogen precursor; SERPINA 8… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16543267 | Ma X, Bielefeldt K, Tan ZY, Whiteis CA, Snitsarev V, Abboud FM, Chapleau MW: Dual mechanisms of angiotensin-induced activation of mouse sympathetic neurones. J Physiol. 2006 May 15;573(Pt 1):45-63. Epub 2006 Mar 16. The IA channel blocker 4-aminopyridine triggered AP generation in TNs and prevented the Ang II-induced APs but not the depolarization. Ang II directly activates neurones in sympathetic ganglia. |
6(0,0,0,6) | Details |
| 15694920 | Kubo T, Hagiwara Y: Protein kinase C activation-induced increases of neural activity are enhanced in the hypothalamus of spontaneously hypertensive rats. Brain Res. 2005 Feb 8;1033(2):157-63. Pressure application of 4-aminopyridine, a blocker of the transient current, onto angiotensin II-sensitive neurons increased their firing rate and the increase of unit firing rate was almost the same in WKY and SHR. We have previously reported that some neurons in the anterior hypothalamic area (AHA) are tonically activated by endogenous angiotensins in rats and that activities of these angiotensin II-sensitive neurons in the AHA are enhanced in spontaneously hypertensive rats (SHR). |
5(0,0,0,5) | Details |
| 10847588 | Czirjak G, Fischer T, Spat A, Lesage F, Enyedi P: TASK (TWIK-related acid-sensitive K+ channel) is expressed in glomerulosa cells of rat adrenal cortex and inhibited by angiotensin II. Mol Endocrinol. 2000 Jun;14(6):863-74. In Xenopus oocytes injected with mRNA prepared from glomerulosa tissue the expressed K+ current at -100 mV was virtually insensitive to tetraethylammonium (3 mM) and 4-aminopyridine (3 mM). |
3(0,0,0,3) | Details |
| 16123110 | Ono K, Toyono T, Honda E, Inenaga K: Transient outward K+ currents in rat dissociated subfornical organ neurones and angiotensin II effects. J Physiol. 2005 Nov 1;568(Pt 3):979-91. Epub 2005 Aug 25. Tetraethylammonium at 1 mm, which blocks Kv3 channel-derived currents, and blood-depressing substance-I, a Kv3.4-specific blocker, at 2 microm suppressed the I (A)-like component of whole-cell outward currents in some neurones. 4-Aminopyridine at 5 mm inhibited I (A) s in the presence of tetraethylammonium at 1 mm. |
4(0,0,0,4) | Details |
| 20051248 | Jin H, Hadri L, Palomeque J, Morel C, Karakikes I, Kaprielian R, Hajjar R, Lebeche D: KChIP2 attenuates cardiac hypertrophy through regulation of I (to) and intracellular signaling. J Mol Cell Cardiol. 2010 Jan 4. In neonatal myocytes, KChIP2 notably reversed Ang II-induced hypertrophic changes in protein synthesis and MAP-kinase activation. Interestingly, blocking I (to) with 4-aminopyridine in KChIP2-overexpressing adult cardiomyocytes significantly increased the Ca (2+) transients to control levels. |
1(0,0,0,1) | Details |
| 20044444 | Gao L, Li Y, Schultz HD, Wang WZ, Wang W, Finch M, Smith LM, Zucker IH: Downregulated Kv4.3 expression in the RVLM as a potential mechanism for sympathoexcitation in rats with chronic heart failure. Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H945-55. Epub 2009 Dec 31. Elevated central angiotensin II (ANG II) plays a critical role in the sympathoexcitation of chronic heart failure (CHF) by stimulating upregulated ANG II type 1 receptors (AT (1) R) in the rostral ventrolateral medulla (RVLM). In intact animals, we found that microinjection of the voltage-gated potassium channel blocker, 4-aminopyridine, into the RVLM evoked a sympathoexcitation and hypertension in both normal and CHF rats. |
1(0,0,0,1) | Details |
| 18156198 | Walsh KB, Zhang J: Neonatal rat cardiac fibroblasts express three types of voltage-gated K+ channels: regulation of a transient outward current by protein kinase C. Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H1010-7. Epub 2007 Dec 21. Finally, pretreatment of the cells with 4-AP inhibited angiotensin II-induced intracellular Ca (2+) mobilization. I (to) was inhibited by the antiarrhythmic agent flecainide (100 microM) and BaCl (2) (1 mM) but was unaffected by 4-aminopyridine (4-AP; 0.5 and 1 mM). |
1(0,0,0,1) | Details |
| 12505875 | Littler CM, Morris KG Jr, Fagan KA, McMurtry IF, Messing RO, Dempsey EC: Protein kinase C-epsilon-null mice have decreased hypoxic pulmonary vasoconstriction. Am J Physiol Heart Circ Physiol. 2003 Apr;284(4):H1321-31. Epub 2002 Dec 27. In contrast, the voltage-gated K (+) channel (K (V)) antagonist 4-aminopyridine increased the response of -/- mice beyond that of +/+ mice. In isolated, salt solution-perfused lung, reactivity to acute hypoxic challenges (0% and 3% O (2)) was compared with responses to angiotensin II (ANG II) and KCl. |
1(0,0,0,1) | Details |
| 11041555 | Kurtz A, Hamann M, Gotz K: Role of channels in the control of renin secretion from isolated perfused rat kidneys. Pflugers Arch. 2000 Oct;440(6):889-95. Whilst all four K+ channel blockers increased renal vascular resistance, only 4-aminopyridine and barium attenuated isoproterenol-stimulated renin secretion in an additive fashion and augmented the inhibitory effect of angiotensin II. |
112(1,2,2,2) | Details |
| 15654262 | Fukada SY, Tirapelli CR, de Godoy MA, de Oliveira AM: Mechanisms underlying the endothelium-independent relaxation induced by angiotensin II in rat aorta. J Cardiovasc Pharmacol. 2005 Feb;45(2):136-43. The combination of L-NAME, indomethacin, and TEA completely abolished the relaxation induced by angiotensin II. 4-Aminopyridine (4-AP) as well as charybdotoxin reduced angiotensin II-induced relaxation. |
88(1,1,1,8) | Details |
| 11692027 | Bains JS, Follwell MJ, Latchford KJ, Anderson JW, Ferguson AV: Slowly inactivating conductance (I (D)): a potential target for stroke therapy. Stroke. 2001 Nov;32(11):2624-34. Manipulations that inhibit this current (4-aminopyridine or angiotensin II) increase neuronal excitability and augment cell death after NMDA receptor activation. |
31(0,1,1,1) | Details |
| 10710133 | Satake N, Imanishi M, Keto Y, Ishikawa M, Yamada H, Shibata S, Tomiyama A: The inhibitory effect of KT3-671, a nonpeptide angiotensin-receptor antagonist, on rabbit and rat isolate vascular smooth muscles: a possible involvement of K (ATP) channels. J Cardiovasc Pharmacol. 2000 Mar;35(3):457-67. ODQ (3 x 10 (-6) M), N (G)-nitro- (3 x 10 (-4) M), 4-aminopyridine (3 x 10 (-3) M), tetraethylammonium (TEA; 10 (-3) M), or iberiotoxin (10 (-7) M) did not affect the inhibitory action of KT3-671 or CV-11974. The vasoinhibitory effect of KT3-671, a recently synthesized nonpeptide angiotensin II (Ang II), AT1-receptor antagonist, and the factors affecting insurmountable antagonism of Ang II were examined in rabbit and rat isolated vascular smooth muscle preparations. |
7(0,0,0,7) | Details |
| 17287434 | Chen Q, Pan HL: Signaling mechanisms of angiotensin II-induced attenuation of GABAergic input to hypothalamic presympathetic neurons. J Neurophysiol. 2007 May;97(5):3279-87. Epub 2007 Feb 7. However, Ang II-induced inhibition of mIPSCs persisted in the presence of either CdCl (2), a voltage-gated Ca (2+) channel blocker, or 4-aminopyridine, a blocker of voltage-gated K (+) channels. |
7(0,0,0,7) | Details |
| 14757704 | Soares de Moura R, Resende AC, Emiliano AF, Tano T, Mendes-Ribeiro AC, Correia ML, de Carvalho LC: The role of bradykinin, AT2 and angiotensin 1-7 receptors in the EDRF-dependent vasodilator effect of angiotensin II on the isolated mesenteric vascular bed of the rat. Br J Pharmacol. 2004 Mar;141(5):860-6. Epub 2004 Feb 2. However, this effect is not affected by ATP and voltage-dependent K (+) channel blockers (glybenclamide and 4-aminopyridine). 5. |
7(0,0,0,7) | Details |
| 18692643 | Zulli A, Ye B, Wookey PJ, Buxton BF, Hare DL: Calcitonin gene-related peptide inhibits angiotensin II-mediated vasoconstriction in human radial arteries: role of the Kir channel. J Thorac Cardiovasc Surg. 2008 Aug;136(2):370-5. Epub 2008 Jun 19. N-nitro- methyl ester, 4-aminopyridine, charybdotoxin, and apamin had no effect on calcitonin gene-related peptide relaxation, but Ba (2+) impaired the effects of alpha-calcitonin gene-related peptide. |
6(0,0,0,6) | Details |