Cromakalim
Potassium Radioisotopes
Pinacidil
Minoxidil
Rubidium Radioisotopes
Nicorandil
Potassium Channels
Parasympatholytics
Diazoxide
Guanidines
Nifedipine
Guinea Pigs
Niacinamide
An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and PELLAGRA. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.
Muscle Contraction
KATP Channels
Heteromultimers of Kir6 channels (the pore portion) and sulfonylurea receptor (the regulatory portion) which affect function of the HEART; PANCREATIC BETA CELLS; and KIDNEY COLLECTING DUCTS. KATP channel blockers include GLIBENCLAMIDE and mitiglinide whereas openers include CROMAKALIM and minoxidil sulfate.
Adenosine Triphosphate
Aorta, Thoracic
Charybdotoxin
Muscle, Smooth
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
Trachea
Potassium
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
Rubidium
Microelectrodes
Nitroprusside
Vasodilation
Membrane Potentials
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
Parasympathetic Nervous System
The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.
Ureter
Nitroglycerin
Potassium Channel Blockers
Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice. (1/374)
1. Isometric tension was recorded in isolated rings of aorta, carotid, coronary and mesenteric arteries taken from endothelial nitric oxide synthase knockout mice (eNOS(-/-) mice) and the corresponding wild-type strain (eNOS(+/+) mice). The membrane potential of smooth muscle cells was measured in coronary arteries with intracellular microelectrodes. 2. In the isolated aorta, carotid and coronary arteries from the eNOS(+/+) mice, acetylcholine induced an endothelium-dependent relaxation which was inhibited by N(omega)-L-nitro-arginine. In contrast, in the mesenteric arteries, the inhibition of the cholinergic relaxation required the combination of N(omega)-L-nitro-arginine and indomethacin. 3. The isolated aorta, carotid and coronary arteries from the eNOS(-/-) mice did not relax in response to acetylcholine. However, acetylcholine produced an indomethacin-sensitive relaxation in the mesenteric artery from eNOS(-/-) mice. 4. The resting membrane potential of smooth muscle cells from isolated coronary arteries was significantly less negative in the eNOS(-/-) mice (-64.8 +/- 1.8 mV, n = 20 and -58.4 +/- 1.9 mV, n = 17, for eNOS(+/+) and eNOS(-/-) mice, respectively). In both strains, acetylcholine, bradykinin and substance P did not induce endothelium-dependent hyperpolarizations whereas cromakalim consistently produced hyperpolarizations (- 7.9 +/- 1.1 mV, n = 8 and -13.8 +/- 2.6 mV, n = 4, for eNOS(+/+) and eNOS(-/-) mice, respectively). 5. These findings demonstrate that in the blood vessels studied: (1) in the eNOS(+/+) mice, the endothelium-dependent relaxations to acetylcholine involve either NO or the combination of NO plus a product of cyclo-oxygenase but not EDHF; (2) in the eNOS(-/-) mice, NO-dependent responses and EDHF-like responses were not observed. In the mesenteric arteries acetylcholine releases a cyclo-oxygenase derivative. (+info)Differential effects of pinacidil, cromakalim, and NS 1619 on electrically evoked contractions in rat vas deferens. (2/374)
AIM: To compare the inhibitory action of electrically evoked contractions of rat epididymal vas deferens by pinacidil (Pin), cromakalim (Cro), and NS 1619. METHODS: Monophasic contractions were evoked by electric field stimulation in rat isolated epididymal half of vas deferens. RESULTS: Newly developed ATP-sensitive K+ channel openers, Pin and Cro, concentration-dependently reduced the electrically evoked (0.3 Hz, 1 ms pulse duration, 60 V) contractions and glibenclamide but not charybdotoxin antagonized the inhibitory effects of both agents. Pin shifted the concentration-response curve for norepinephrine to the right with reducing the magnitude of the maximum contraction in a glibenclamide-sensitive fashion. The large-conductance Ca(2+)-activated K+ channel opener, NS 1619, inhibited the electrically evoked contractions in a concentration-dependent manner. Charybdotoxin (100 nmol.L-1) partially reduced the effect of NS 1619 but glibenclamide (10 mumol.L-1) showed no effect. None of these 3 agents affected the basal tension. CONCLUSION: Both ATP-sensitive and Ca(2+)-activated K+ channels presented in vas deferens smooth muscles involved in regulation of muscle contractility. (+info)Role of K+ channels in A2A adenosine receptor-mediated dilation of the pressurized renal arcuate artery. (3/374)
1. Adenosine A2A receptor-mediated renal vasodilation was investigated by measuring the lumenal diameter of pressurized renal arcuate arteries isolated from the rabbit. 2. The selective A2A receptor agonist CGS21680 dilated the arteries with an EC50 of 130 nM. The CGS21680-induced vasodilation was, on average, 34% less in endothelium-denuded arteries. 3. The maximum response and the EC50 for CGS21680-induced vasodilation in endothelium-intact arteries were not significantly affected by incubation with the K+ channel blockers apamin (100 nM), iberiotoxin (100 nM), 3,4-diaminopyridine (1 mM), glibenclamide (1 microM) or Ba2+ (10 microM). However, a cocktail mixture of these blockers did significantly inhibit the maximum response by almost 40%, and 1 mM Ba2+ alone or 1 mM Ba2+ in addition to the cocktail inhibited the maximum CGS21680-response by 58% and about 75% respectively. 4. CGS21680-induced vasodilation was strongly inhibited when the extracellular K+ level was raised to 20 mM even though the dilator response to 1 microM levcromakalim, a K(ATP) channel opener drug, was unaffected. 5. CGS21680-induced vasodilation was inhibited by 10 microM ouabain, an inhibitor of Na+/K(+)-ATPase, but ouabain had a similar inhibitory effect on vasodilation induced by 30 nM nicardipine (a dihydropyridine Ca2+ antagonist) or 1 microM levcromakalim. 6. The data suggest that K+ channel activation does play a role in A(2A) receptor-mediated renal vasodilation. The inhibitory effect of raised extracellular K+ levels on the A(2A) response may be due to K(+)-induced stimulation of Na+/K(+)-ATPase. (+info)ATP-sensitive potassium channels regulate in vivo dopamine release in rat striatum. (4/374)
ATP-sensitive K+ channels (K(ATP)) are distributed in a variety of tissues including smooth muscle, cardiac and skeletal muscle, pancreatic beta-cells and neurons. Since K(ATP) channels are present in the nigrostriatal dopamine (DA) pathway, the effect of potassium-channel modulators on the release of DA in the striatum of conscious, freely-moving rats was investigated. The extracellular concentration of DA was significantly decreased by the K(ATP)-channel opener (-)-cromakalim but not by diazoxide. (-)-Cromakalim was effective at 100 and 1000 microM concentrations, and the maximum decrease was 54% below baseline. d-Amphetamine significantly increased extracellular DA levels at the doses of 0.75 and 1.5 mg/kg, s.c. with a 770% maximum increase. (-)-Cromakalim had no effect on d-amphetamine-induced DA release, while glyburide, a K(ATP) blocker, significantly potentiated the effects of a low dose of d-amphetamine. These data indicate that K+ channels present in the nigrostriatal dopaminergic terminals modulate basal release as well as evoked release of DA. (+info)Thiopental and propofol impair relaxation produced by ATP-sensitive potassium channel openers in the rat aorta. (5/374)
ATP-sensitive potassium channel openers are used as vasodilators in the treatment of cardiovascular disorders. The effects of i.v. anaesthetics on arterial relaxation induced by ATP-sensitive potassium channel openers have not been studied. Therefore, in this study, we have examined if thiopental (thiopentone) and propofol affect the vascular response to the ATP-sensitive potassium channel openers, cromakalim and pinacidil, in the isolated rat aorta. Rings of rat thoracic aortas without endothelium were suspended for isometric force recording. Concentration-response curves were obtained in a cumulative manner. During submaximal contractions with phenylephrine 0.3 mumol litre-1, relaxation after cromakalim 0.1-30 mumol litre-1, pinacidil 0.1-30 mumol litre-1 and papaverine 0.1-300 mumol litre-1 was demonstrated. Thiopental 30-300 mumol litre-1, propofol 10-100 mumol litre-1, 10% Intralipid 45 microliters or glibenclamide 5 mumol litre-1 were applied 15 min before addition of phenylephrine. During contractions with phenylephrine, cromakalim and pinacidil induced concentration-dependent relaxation. A selective ATP-sensitive potassium channel antagonist, glibenclamide 5 mumol litre-1, abolished this relaxation, whereas it did not affect relaxation produced by papaverine. Thiopental concentrations > 30 mumol litre-1 significantly impaired relaxation produced by cromakalim or pinacidil. Propofol concentrations > 10 mumol litre-1 also significantly reduced relaxation produced by cromakalim or pinacidil, whereas Intralipid was ineffective. Thiopental 300 mumol litre-1 and propofol 100 mumol litre-1 did not alter relaxation produced by papaverine. These results suggest that the i.v. anaesthetics, thiopental and propofol, impaired vasodilatation mediated by ATP-sensitive potassium channels in vascular smooth muscle cells. (+info)Effects of nicorandil as compared to mixtures of sodium nitroprusside and levcromakalim in isolated rat aorta. (6/374)
1. The contribution of the relaxant mechanisms of nicorandil (NIC) were analysed by comparing its effects with those of sodium nitroprusside (SNP), levcromakalim (LEM) and mixtures (1:10, 1:30 and 1:100) of SNP:LEM in isolated endothelium-denuded rat aorta. 2. In rings precontracted with KCl (25 mM), the relative inhibitory potency of the soluble guanylate cyclase inhibitor ODQ and the K(ATP) channel inhibitor glibenclamide (GLI) on SNP:LEM mixtures showed a good correlation with the relative proportion of SNP and LEM in the mixtures. Furthermore, the degree of the inhibition by ODQ and GLI of the effects of the 1:30 SNP:LEM mixture varied as a function of the relative potency of SNP and LEM in KCl-, noradrenaline- (NA) or NA plus nifedipine-treated arteries. 3. The inhibitory effects of ODQ, GLI and ODQ plus GLI on NIC-induced relaxation was similar to that for the 1:30 SNP:LEM mixture in NA plus nifedipine-contracted arteries, but the inhibition of GLI or ODQ plus GLI was smaller in KCl-contracted arteries. 4. In conclusion, the relative importance of activation of the cyclic GMP pathway and K(ATP) channel opening in mixtures of SNP and LEM could be predicted by the proportion of the drugs in the mixtures and by the relative potency of SNP vs LEM in different experimental conditions. Furthermore, the present results suggest that besides these two mechanisms, a third ODQ- and GLI-insensitive mechanism, possibly involving Ca2+ channel blockade, also participates in the relaxant effects of NIC in KCl-induced contractions. (+info)Differential effects of lidocaine and mexiletine on relaxations to ATP-sensitive K+ channel openers in rat aortas. (7/374)
BACKGROUND: In cardiac myocytes, lidocaine reduces but mexiletine increases adenosine triphosphate (ATP)-sensitive K+ currents, suggesting that these class Ib antiarrhythmic drugs may differentially modify the activity of ATP-sensitive K+ channels. The effects of lidocaine and mexiletine on arterial relaxations induced by K+ channel openers have not been studied. Therefore, the current study was designed to evaluate whether lidocaine and mexiletine may produce changes in relaxations to the ATP-sensitive K+ channel openers cromakalim and pinacidil in isolated rat thoracic aortas. METHODS: Rings of rat thoracic aortas without endothelia were suspended for isometric force recording. Concentration-response curves were obtained in a cumulative fashion. During submaximal contractions to phenylephrine (3 x 10(-7) M), relaxations to cromakalim (10(-7) to 3 x 10(-5) M), pinacidil (10(-7) to 3 x 10(-5) M), or diltiazem (10(-7) to 3 x 10(-4) M) were obtained. Lidocaine (10(-5) to 3 x 10(-4) M), mexiletine (10(-5) to 10(-4) M) or glibenclamide (5 x 10(-6) M) was applied 15 min before addition of phenylephrine. RESULTS: During contractions to phenylephrine, cromakalim and pinacidil induced concentration-dependent relaxations. A selective ATP-sensitive K+ channel antagonist, glibenclamide (5 x 10(-6) M), abolished these relaxations, whereas it did not alter relaxations to a voltage-dependent Ca2+ channel inhibitor, diltiazem (10(-7) to 3 x 10(-4) M). Lidocaine (more than 10(-5) M) significantly reduced relaxations to cromakalim or pinacidil in a concentration-dependent fashion, whereas lidocaine (3 x 10(-4) M) did not affect relaxations to diltiazem. In contrast, mexiletine (more than 10(-5) M) significantly augmented relaxations to cromakalim or pinacidil. Glibenclamide (5 x 10(-6) M) abolished relaxations to cromakalim or pinacidil in arteries treated with mexiletine (10(-4) M). CONCLUSIONS: These results suggest that lidocaine impairs but mexiletine augments vasodilation mediated by ATP-sensitive K+ channels in smooth muscle cells. (+info)Inhibitory effect of 4-aminopyridine on responses of the basilar artery to nitric oxide. (8/374)
1. Voltage-dependent K+ channels are present in cerebral arteries and may modulate vascular tone. We used 200 microM 4-aminopyridine (4-AP), thought to be a relatively selective inhibitor of voltage-dependent K+ channels at this concentration, to test whether activation of these channels may influence baseline diameter of the basilar artery and dilator responses to nitric oxide (NO) and cyclic GMP in vivo. 2. Using a cranial window in anaesthetized rats, topical application of 4-AP to the basilar artery (baseline diameter = 240+/-5 microm, mean +/- s.e.mean) produced 10+/-1% constriction. Sodium nitroprusside (a NO donor), acetylcholine (which stimulates endothelial release of NO), 8-bromo cyclic GMP (a cyclic GMP analogue), cromakalim (an activator of ATP-sensitive K+ channels) and papaverine (a non-NO, non-K+ channel-related vasodilator) produced concentration-dependent vasodilator responses that were reproducible. 3. Responses to 10 and 100 nM nitroprusside were inhibited by 4-AP (20+/-4 vs 8+/-2% and 51+/-5 vs 33+/-5%, respectively, n=10; P<0.05). Responses to acetylcholine and 8-bromo cyclic GMP were also partially inhibited by 4-AP. In contrast, 4-AP had no effect on vasodilator responses to cromakalim or papaverine. These findings suggest that NO/cyclic GMP-induced dilator responses of the basilar artery are selectively inhibited by 4-aminopyridine. 4. Responses to nitroprusside were also markedly inhibited by 10 microM 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (an inhibitor of soluble guanylate cyclase; 16+/-4 vs 1+/-1% and 44+/-7 vs 7+/-1%; n=10; P<0.05). 5. Thus, dilator responses of the rat basilar artery to NO appear to be mediated by activation of soluble guanylate cyclase and partially by activation of a 4-aminopyridine-sensitive mechanism. The most likely mechanism would appear to be activation of voltage-dependent K+ channels by NO/cyclic GMP. (+info)Cromakalim and cicletanine against pacing-induced myocardial ischemia in conscious rabbits<...
Cromakalim
- Levcromakalim
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A novel potassium channel gene, KCNQ2, is mutated in an inherited epilepsy of newborns
The role of oxygen-derived free radicals in augmented relaxations to levcromakalim in the aorta from hypertensive rats. -...
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Cromakalim
... (INN) is a potassium channel-opening vasodilator. The active isomer is levcromakalim. It acts on ATP-sensitive ...
Beta-2 adrenergic receptor
"Response of guinea pig smooth and striated urethral sphincter to cromakalim, prazosin, nifedipine, nitroprusside, and ...
Symplocos paniculata
Traditional Bangladeshi healers use the bark as an antidiarrhoeal as it contains an antispasmodic similar to cromakalim. The ...
List of MeSH codes (D03)
... cromakalim MeSH D03.438.150.500 - ellagic acid MeSH D03.438.150.600 - hematoxylin MeSH D03.438.150.909 - vitamin e MeSH D03.438 ... cromakalim MeSH D03.830.219.500 - ellagic acid MeSH D03.830.219.600 - hematoxylin MeSH D03.830.219.909 - vitamin e MeSH D03.830 ... cromakalim MeSH D03.383.129.578.399 - maleimides MeSH D03.383.129.578.399.418 - ethylmaleimide MeSH D03.383.129.578.617 - ...
List of drugs: Cp-Cz
Crolom Cromolyn cromakalim (INN) cromitrile (INN) cromoglicate lisetil (INN) cromoglicic acid (INN) Cromoptic cronidipine (INN ...
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Ma, H., Folmes, C. D. L., Wu, J., Morey, R., Mora-Castilla, S., Ocampo, A., Ma, L., Poulton, J., Wang, X., Ahmed, R., Kang, E., Lee, Y., Hayama, T., Li, Y., Van Dyken, C., Gutierrez, N. M., Tippner-Hedges, R., Koski, A., Mitalipov, N., Amato, P., & 6 othersWolf, D. P., Huang, T., Terzic, A., Laurent, L. C., Belmonte, J. C. I. & Mitalipov, S., Aug 13 2015, In: Nature. 524, 7564, p. 234-238 5 p.. Research output: Contribution to journal › Article › peer-review ...
Plus it
... whereas cromakalim showed little selectivity. In addition to increasing the time to the onset of contracture, BMS-191095 ... which is comparable to 4.7 μM and 3.0 μM for cromakalim and BMS-180448, respectively. Comparisons of cardioprotective and ... which retain the cardioprotective activity of agents such as cromakalim while being significantly less potent as vasodilators. ...
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Effects of cromakalim (BRL 34915) on mechanical responses of rat vas deferens to noradrenaline and naphazoline. Grana, E., ... Inhibition by glibenclamide of the effects of cromakalim on responses of rat vas deferens to naphazoline. Grana, E., Barbieri, ... Cromakalim has been shown to inhibit naphazoline-induced contractions and spontaneous activity induced by exposure to ...
PMID- 21949453
Activation of IK-ATP with cromakalim resulted in uncoupling at 23.3(1.9) min (p < 0.002 v control). Glibenclamide without ... APD80 during ischaemia was significantly shorter in the preconditioning and cromakalim groups than in the control group from 5 ... cromakalim (BRL 34915), an opener of IK-ATP; (5) sustained ischaemia after 10 min perfusion with 20 microM glibenclamide ...
DeCS
Cromakalim, (3R-cis)-Isomer. Cromakalim, (3R-trans)-Isomer. Cromakalim, (3S-cis)-Isomer. Cromakalim, (3S-trans)-Isomer. ... Cromakalim - Preferred Concept UI. M0029396. Scope note. A potassium-channel opening vasodilator that has been investigated in ... Cromakalim, (trans)-Isomer. Lemakalim. Levcromakalim. Tree number(s):. D03.383.129.578.150. D03.383.663.283.455. D03.633. ... Cromakalim Entry term(s):. BRL 38226. BRL 38227. BRL-34915. BRL-38226. BRL-38227. BRL38226. BRL38227. ...
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Potassium channels in nervous tissue. - Centre for Evidence-Based Medicine (CEBM), University of Oxford
New windows on the mechanism of action of K(ATP) channel openers. - Department of Physiology, Anatomy and Genetics (DPAG)
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TBI - Theoretical Biochemistry Group - Publications - 1999-1990
Role of Adenosine Triphosphate-sensitive Potassium Channels in Coronary Vasodilation by Halothane, Isoflurane, and Enflurane |...
The increases in CBF by cromakalim were dose dependent. Glibenclamide blunted the increases in CBF caused by cromakalim and ... Cromakalim caused modest, dose-dependent decreases in SS, although MVO2did not change consistently (Table 5). Glibenclamide ... Furthermore, it has been shown that various drugs, such as cromakalim, may modulate the opening of the KATPchannels. [8,9] ... Table 5. Effect of Intracoronary Infusion of Cromakalim at 2.5 and 5.0 micro gram/min (CROM-2.5 and CROM-5.0, respectively) on ...
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
NEW (2008) DeCS DESCRIPTORS WITH SCOPE NOTES (UNIT RECORD FORMAT; 21/02/2008
Vasodilator1
- The effectiveness of glibenclamide was verified from inhibition of coronary vasodilator responses to the KATP channel opener cromakalim without effect on those to the KATP channel-independent vasodilators, sodium nitroprusside and acetylcholine. (silverchair.com)
Opener1
- This study was attempted to investigate the effects of cromakalim (CRK), $K^{+}$ channel opener, and glibenclamide (GLY), $K^{+}$ channel blocker, on intestinal function of rabbit. (koreascience.kr)
Smooth1
- Comparisons of cardioprotective and vasorelaxant potencies in vitro and in vivo showed BMS-191095 to be significantly more selective for cardioprotection with virtually no effect on peripheral smooth muscle, whereas cromakalim showed little selectivity. (aspetjournals.org)
Minoxidil3
- KATP channel blockers include GLIBENCLAMIDE and mitiglinide whereas openers include CROMAKALIM and minoxidil sulfate. (jefferson.edu)
- 1. The effect of intracerebroventricular (i.c.v.) administration of different potassium channel blockers (tetraethylammonium, apamin, charybdotoxin, gliquidone), potassium channel openers (pinacidil, minoxidil, cromakalim) and aODN to mKv1.1 on immobility time was evaluated in the mouse forced swimming test, an animal model of depression. (epfl.ch)
- By contrast pinacidil (10-20 microg per mouse i.c.v.), minoxidil (10-20 microg per mouse i.c.v.) and cromakalim (20-30 microg per mouse i.c.v.) increased immobility time when administered in the same experimental conditions. (epfl.ch)
Diazoxide1
- Feleder E.C, Adler-Graschinsky E. Endothelium-mediated and N omega-nitro-L-arginine methyl ester-sensitive responses to cromakalim and diazoxide in the rat mesenteric bed. (kiev.ua)
Pinacidil2
- The K ATP COs typified by pinacidil are sensitive to L-arginine analogues whereas the K ATP COs typified by cromakalim are insensitive to L-arginine analogues. (shu.ac.uk)
- This sensitivity appears to be independent of nitric oxide synthase (NOS) action as the vasorelaxant and Rb efflux responses to pinacidil are insensitive to the NOS inhibitor L-N5-(1-iminoethyl) ornithine (L-NIO).Pinacidil and cromakalim are believed to have a degree of commonality in how they interact with the K ATP CO binding site on SUR2B. (shu.ac.uk)
Explains1
- In contrast, cromakalim is not believed to interact with this particular region of the K ATP CO binding site, which explains the insensitivity of cromakalim to L-NAME. (shu.ac.uk)
Mouse1
- Michael Fautsch, Ph.D. , and others tested cromakalim in mouse and human models alone and in combination with latanoprost-free acid. (mayoclinic.org)
Channel1
- Mayo researchers have shown that the K-ATP channel opener cromakalim has potential as a hypotensive agent to lower intraocular pressure. (mayoclinic.org)
Human1
- 6. A novel cromakalim analogue induces cell cycle arrest and apoptosis in human cervical carcinoma HeLa cells through the caspase- and mitochondria-dependent pathway. (nih.gov)