Protoveratrine A

Protoveratrine A
Product Name Protoveratrine A
CAS No.: 143-57-7
Catalog No.: CFN98521
Molecular Formula: C41H63NO14
Molecular Weight: 793.94 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: Calcium Channel | Potassium Channel
Source: The roots of Veratrum nigrum L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Protoveratrine A has anti-hypertensive action, it has some effects on cardiovascular and respiratory systems in rats in reducing the blood pressure and heart rate,prolonging the QTc interval,decreasing the respiratory rate and increasing the respiratory width. Protoveratrine A can increase K + uptake from frog skeletal muscle and cause this tissue to release more calcium (Ca ++ ). Protoveratrine A seems to involve at least in part an inhibition of dopaminergic neuron activity, it enhances the release of acetylcholine from the nerve terminals during the resting period and at low frequency of stimulation.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    J. Pharm. Pharmacol. 1959, 11(S1):176–84.
    The effects of Protoveratrine A on the efflux of potassium ions (K+) from frog and rat skeletal muscle and the isolated electrically driven rat heart have been studied.
    No effect was seen upon the rate of efflux from skeletal muscle but that from the heart was increased. Protoveratrine A increases K+ uptake from frog skeletal muscle and causes this tissue to release more calcium (Ca++). There was no increase in Ca++ release from lobster nerve treated with Protoveratrine A. The theoretical implications of these findings are discussed.
    Toxicon. 1983;21(4):503-14.
    Potentiation by crotamine of the depolarizing effects of batrachotoxin, protoveratrine A and grayanotoxin I on the rat diaphragm.[Pubmed: 6312634]
    The interactions between crotamine and tetrodotoxin and group II sodium channel toxins, including batrachotoxin, Protoveratrine A and grayanotoxin I, were studied on the rat diaphragm muscle.
    When the diaphragm was pretreated with 0.1 micrograms crotamine/ml for 45 min (a condition known to depolarize the muscle by less than 3 mV, which is only 20% of the maximal depolarization induced by a saturating concentration of crotamine), the rate of depolarization by group II toxins was markedly enhanced and the time to reach the steady state depolarization was greatly shortened. The maximal depolarizations induced by each of the group II toxins, however, were not increased. Pretreatment with saturating concentrations of crotamine also caused no change of the steady state depolarization induced by batrachotoxin or grayanotoxin I. Moreover, pretreatment of the diaphragm with a high concentration of grayanotoxin I, whose effect is reversible, did not impede the depolarizing effect of crotamine. Tetrodotoxin restored the membrane potential, depolarized by crotamine, with 50% restoration at a concentration of 16 ng/ml, no matter whether a high (20 micrograms/ml) or a low (2 micrograms/ml) concentration of crotamine were used.
    The above results indicate that there is no competition between crotamine and group II toxins or between crotamine and tetrodotoxin. However, crotamine may affect the binding of group II toxins allosterically, increasing their affinity although the intrinsic activity may not be changed.
    J Neural Transm. 1975;37(1):43-60.
    The effects of protoveratrine and germines on the release of acetylcholine from the Auerbach plexus of the guinea-pig ileum.[Pubmed: 1159414]
    The effect of Protoveratrine A and germine-3-acetate (GMA) on the release mechanism of acetylcholine from the nerve terminals of the Auerbach plexus in the longitudinal muscle layer of the guinea-pig ileum was studied.
    Protoveratrine A, GMA and germine potentiated neuroeffector transmission in Auerbach's plexus in the longitudinal muscle preparation provided the neurons were stimulated at low frequencies (less than 10 Hz). Protoveratrine A and GMA enhanced the release of acetylcholine from the nerve terminals during the resting period and at low frequency of stimulation (less than 10 Hz). At continous stimulation with high frequency they were ineffective (greater than 10 Hz). When trains of 20 stimuli, with a pulse interval of 0.1 s (10 Hz) were repeatedly applied with intervals of 0.1 to 20 s between trains, the effect of GMA to increase ACh release depended on the length of the train interval; the longer the resting period between trains the higher was the output of ACh.
    This fact indicates that the release of ACh increased primarily during the resting periods following single stimuli or trains. The effect of GMA on ACh release proved to be highly temperature-dependent: in the presence of GMA Q10 increasing from 3.25 to 4.92. A high Ca concentration, removal of Mg or lowering of the Na concentration abolished the effect of GMA to enhance ACh release.
    Pharmacol Biochem Behav. 1980 May;12(5):735-8.
    The alpha-naphthoxyacetic acid-elicited retching involves dopaminergic inhibition in mice.[Pubmed: 7393967]

    Alpha-naphthoxyacetic acid (alpha-NOAA), one of the jumping-inducers, elicited a dose-dependent retching behavior at doses ranging from 250 to 550 mg/kg in mice and vomiting at a dose of 550 mg/kg in pigeons. Protoveratrine-A (PV-A, 0.1 mg/kg), a veratrum alkaloid, also induced retching in mice and vomiting in pigeons, while apomorphine (2 mg/kg) produced neither retching in mice nor vomiting in pigeons though it induced feeding in pigeons. The retching elicited by alpha-NOAA or PV-A was not significantly affected by scopolamine, aminooxyacetic acid and gamma-butyrolactone, but was markedly inhibited by apomorphine (2 mg/kg), this inhibitory effect being antagonized without significance by haloperidol which did not itself augment the retching.
    These results imply that the retching elicited by alpha-NOAA or PV-A seems to involve at least in part an inhibition of dopaminergic neuron activity.
    Journal of Pharmaceutical Practice, 2010, 28(5):348-51.
    Effects of Protoveratrine A on cardiovascular and respiratory system in rats.[Reference: WebLink]
    To observe the effects of Protoveratrine A(PA) on cardiovascular and respiratory system in rats.
    The experimental rats(n=40,m