The workout pump isn’t just for show – it provides a valuable effect to your training. The increased bloodflow helps supply the muscles with oxygen and nutrients and remove waste products like lactic acid. The temporary swelling of the muscles results in stretching of the muscle fascia which allows for continued muscle growth. The pump is also a powerful motivating factor, by acting as positive feedback on your workout, rewarding your efforts by making you look your best. Antaeus Labs Thunderbolt isn’t your run-of-the-mill “pump supp”. We’ve only included those things we think will make the biggest difference to your workouts and your progress in the gym. The new and improved Thunderbolt formula also introduces two new bioavailability-enhanced ingredients for maximum pump.
Kallidinogenase is a naturally-occurring vasodilatory human enzyme. The kallidinogenase, also known as kallikrein, found in Thunderbolt is a natural human enzyme in recombinant form. We use enteric coated acid-resistant capsules for maximum bioavailability and absorption from the GI tract. Kallikrein is a serine protease which cleaves kininogen to release the potent vasoactive kinin peptides bradykinin (BK) or kallidin. Within skeletal muscle, bradykinin promotes glucose uptake and improves blood flow. [1] Kinins have a very short half-life, as they are destroyed in less than 20secs by through the action of kininases (aminopeptidases) present in the tissues and blood. Hence, kinins are unsuitable for use as exogenously administered agents. In plasma, kininogen is in excess, leaving kallikrein as the limiting factor in kinin formation. Therefore, kallikrein is a far better choice for activating the kinin–kallikrein system. Kallidinogenase is stable for 28 months at room temperature, and about five years if kept refrigerated. [2]
Primary effects:
Kallidinogenase increases peripheral and cerebral bloodflow via Bradykinin B1 and B2 receptors. It is a peripheral vasodilator. [3]
Other beneficial effects:
Kallidinogenase strongly increases prostaglandin levels, which may increase the anabolic response to exercise. [4,5]
It also has significant pro-fertility effects, [6,7,8] is nephroprotective, has diuretic effects via activation of the Bradykinin B2 receptor, and increases bloodflow to the brain. [9] B2 receptor activation also increases vascular permeability and allows the blood brain barrier to be crossed more easily.
Arginine Butyrate
Arginine Butyrate activates the nitric oxide pathway and inhibits histone deacetylase to increase follistatin and reduce myostatin.
Primary effects:
HDAC inhibitors have potential as anabolic agents as they increase follistatin and reduce myostatin levels. [10,11] In mouse models of muscular dystrophy arginine butyrate demonstrated beneficial effects including increased muscle strength and increased utrophin expression. [12] Exposure of myoblasts to HDAC inhibitors results in upregulation of follistatin expression. In turn, follistatin binds to and suppresses the activity of myostatin, a TGF-β family member that negatively regulates muscle mass. [13]
Other beneficial effects:
Arginine’s NO-mediated functions are fairly well known. L-arginine is converted into NO by the enzyme NO synthase (eNOS). Nitric oxide causes relaxation vascular smooth muscle by binding to and activating guanylate cyclase and increasing intracellular levels of cyclic-guanosine 3’,5’-monophosphate, causing vasodilation which lowers arterial pressure. [14] This improves blood flow which increases the “pump”. Nitric oxide also inhibits platelet aggregation and adhesion. [15] Arginine is also a precursor of creatine, and plays a role in accelerating tissue repair following injuries. [16]
Copper
Copper is a trace element required for human health. It is included here to prevent diet-related deficiency, which may impair vasodilation.
Primary effects:
Copper deficiency has been shown to block acetylcholine-mediated vascular smooth muscle relaxation. [17,18]
Other beneficial effects:
Copper potentiates the vasodilatory and antiplatelet actions of endogenous nitrosothiols: Copper ions are important catalysts in the decomposition of low molecular weight nitrosothiols (like GSNO) by superoxide dismutase (Cu/Zn SOD). [19]. Copper also enables many metabolic functions, the absorption of iron and formation of red blood cells, and the function of the immune system.
Quercetin-Niacinamide Cocrystals
Quercetin is a hydrophobic and lipophilic aglycone flavonol present in a wide variety of fruits and vegetables. Niacinamide is a form of Vitamin B3. As cocrystals the two compounds form a solid-state crystalline lattice structure, stabilized by hydrogen bonds.
Primary effects:
Quercetin induces vasodilatory effects in humans in both in vivo and ex vivo experiments. [20] Quercetin achieves this vasodilation by inducing phosphorylation of endothelial nitric oxide synthase (eNOS) in endothelial cells, [21] and also by the production of endogenous vasodilatory prostanoids through cyclooxygenase enzyme inhibition. [22] In vitro experiments suggest quercetin is capable of increasing blow flow in blood vessels by up to 50%. [23] Quercetin-Niacinamide cocrystals have improved solubility and oral bioavailability profiles compared to free quercetin, with much faster time to maximum concentration (Tmax). [24]
Other beneficial effects:
Quercetin has many potential beneficial effects, which have been studied to varying degrees of scientific rigour. Research has suggested anti-inflammatory properties (through the inhibition of histamine release from mast cells), inhibition of platelet aggregation, blood pressure-lowering effects (which may be dependent on an individual’s genetics), while evidence of improvements in human endurance has been equivocal. [25] Niacinamide and quercetin are both SIRT1 activators. [26] Though the exact function of the sirtuin family of enzymes in mammals is not fully understood, SIRT1 facilitates longevity in “lower” organisms, and has been implicated in human aging and metabolic- and age-related conditions. [27,28]
Visnadine-Cyclodextrin Complex
Visnadine is a component of the plant Ammi visnaga (Bishop’s Weed), a member of the carrot family which has been used as a folk remedy around the Mediterranean since the time of the ancient Egyptians. Bishop’s Weed contains several compounds with vasodilatory properties including visnadine, visnagin, and khellin, of which visnadine is the most potent. [29] It is used in Thunderbolt complexed with cyclodextrins, for improved bioavailability.
Primary effects:
Visnadine is a peripheral and coronary vasodilator. It is believed to be vasodilatory through inhibition of calcium entry through voltage-gated L-type channels, and not through the release of endothelium-derived relaxing factors. [29][30]
Get maximum pump with new Antaeus Labs Thunderbolt. Look and perform your best with Antaeus Labs.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
References:
1. Wicklmayr M, Dietze G, Brunnbauer H, Rett K, Mehnert H. Dose-dependent effect of bradykinin on muscular blood flow and glucose uptake in man. Hoppe-Seyler’s Z Physiol Chem. 1983 Jul;364(7):831–3. 2. Tanimoto T, Fukuda H, Kimura T. [Long-term stability of Kallidinogenase Reference Standard]. Eisei Shikenjo Hokoku. 1989;(107):119–20. 3. Ogawa K, Ito T, Ban M, Motizuki M, Satake T. Effects of kallidinogenase on urinary kallikrein excretion and plasma prostanoid concentrations in patients with essential hypertension. Experientia. 1986 Sep 15;42(9):1014–5. 4. Honda M, Nagashima Y, Hatano M, Nishino T, Awaya J, Washino N, et al. Effects of purified hog pancreatic kallikrein on the kinin-prostaglandin system and renin-angiotensin-aldosterone system. Nephron. 1985;41(1):34–8. 5. Ogawa K, Ito T, Ban M, Motizuki M, Satake T. Effects of kallidinogenase on urinary kallikrein excretion and plasma prostanoid concentrations in patients with essential hypertension. Experientia. 1986 Sep 15;42(9):1014–5. 6. Kamidono S, Hazama M, Matsumoto O, Takada KI, Tomioka O, Ishigami J. Kallikrein and male subfertility. Usefulness of high-unit kallikrein tablets. Andrologia. 1981 Apr;13(2):108–20. 7. Saitoh S, Kumamoto Y, Shimamoto K, Iimura O. Kallikrein in the male reproductive system. Arch Androl. 1987;19(2):133–47. 8. Izzo PL, Canale D, Bianchi B, Meschini P, Esposito G, Menchini Fabris GF, et al. The treatment of male subfertility with kallikrein. Andrologia. 1984 Apr;16(2):156–61. 9. Wang Chang-lin, Zhu You-ling. Clinical effect of urinary kallidinogenese compined with citicoline on treating acute carotisal cerebral infarction. Anhui Medical and Pharmaceutical Journal 2009-01. 10. Iezzi S, Di Padova M, Serra C, Caretti G, Simone C, Maklan E, et al. Deacetylase inhibitors increase muscle cell size by promoting myoblast recruitment and fusion through induction of follistatin. Dev Cell. 2004 May;6(5):673–84. 11. Bonetto A, Penna F, Minero VG, Reffo P, Bonelli G, Baccino FM, et al. Deacetylase inhibitors modulate the myostatin/follistatin axis without improving cachexia in tumor-bearing mice. Curr Cancer Drug Targets. 2009 Aug;9(5):608–16. 12. Vianello S, Yu H, Voisin V, Haddad H, He X, Foutz AS, et al. Arginine butyrate: a therapeutic candidate for Duchenne muscular dystrophy. FASEB J. 2013 Jun;27(6):2256–69. 13. Verdin E. Histone Deacetylases: Transcriptional Regulation and Other Cellular Functions. Springer; 2007. 14. Tapiero H, Mathé G, Couvreur P, Tew KD. I. Arginine. Biomed Pharmacother. 2002 Nov;56(9):439–45. 15. Radomski MW, Palmer RM, Moncada S. The anti-aggregating properties of vascular endothelium: interactions between prostacyclin and nitric oxide. Br J Pharmacol. 1987 Nov;92(3):639–46. 16. Witte MB, Barbul A. Arginine physiology and its implication for wound healing. Wound Repair Regen. 2003 Dec;11(6):419–23. 17. Schuschke DA, Saari JT, Miller FN. A role for dietary copper in nitric oxide-mediated vasodilation. Microcirculation. 1995 Dec;2(4):371–6. 18. Schuschke DA, Percival SS, Saari JT, Miller FN. Relationship between dietary copper concentration and acetylcholine-induced vasodilation in the microcirculation of rats. Biofactors. 1999;10(4):321–7. 19. Burg A, Cohen H, Meyerstein D. The reaction mechanism of nitrosothiols with copper(I). J Biol Inorg Chem. 2000 Apr;5(2):213–7. 20. Perez, A. et al. The flavonoid quercetin induces acute vasodilator effects in healthy volunteers: correlation with beta-glucuronidase activity. Pharmacol. Res. 89, 11–18 (2014). 21. Li, P.G. et al. Quercetin induces rapid eNOS phosphorylation and vasodilation by an Akt-independent and PKA-dependent mechanism. Pharmacology 89, 220–228 (2012). 22. Fayez, M. Al-, Cai, H., Tunstall, R., Steward, W. P. & Gescher, A. J. Differential modulation of cyclooxygenase-mediated prostaglandin production by the putative cancer chemopreventive flavonoids tricin, apigenin and quercetin. Cancer Chemother. Pharmacol. 58, 816–825 (2006). 23. Monori-Kiss, A., Monos, E. & Nádasy, G. L. Quantitative analysis of vasodilatory action of quercetin on intramural coronary resistance arteries of the rat in vitro. PLoS ONE 9, e105587 (2014). 24. Smith, A. J., Kavuru, P., Wojtas, L., Zaworotko, M. J. & Shytle, R. D. Cocrystals of quercetin with improved solubility and oral bioavailability. Mol. Pharm. 8, 1867–1876 (2011). 25. Kelly, G. S. Quercetin. Monograph. Altern Med Rev 16, 172–194 (2011). 26. Allard, J. S., Perez, E., Zou, S. & de Cabo, R. Dietary activators of Sirt1. Mol. Cell. Endocrinol. 299, 58–63 (2009). 27. Hubbard, B. P. & Sinclair, D. A. Small molecule SIRT1 activators for the treatment of aging and age-related diseases. Trends Pharmacol. Sci. 35, 146–154 (2014). 28. Li, X. SIRT1 and energy metabolism. Acta Biochim. Biophys. Sin. (Shanghai) 45, 51–60 (2013). 29. Rauwald, H. W., Brehm, O. & Odenthal, K. P. The involvement of a Ca2+ channel blocking mode of action in the pharmacology of Ammi visnaga fruits. Planta Med. 60, 101–105 (1994). 30. Durate, J. et al. Effects of visnadine on rat isolated vascular smooth muscles. Planta Med. 63, 233–236 (1997).
THUNDERBOLT
$48.00
ULTIMATE PUMP
Advanced Anabolic Vasodilator
90 Capsules
Thunderbolt
Advance Anabolic Vasodilator
The workout pump isn’t just for show – it provides a valuable effect to your training. The increased bloodflow helps supply the muscles with oxygen and nutrients and remove waste products like lactic acid. The temporary swelling of the muscles results in stretching of the muscle fascia which allows for continued muscle growth. The pump is also a powerful motivating factor, by acting as positive feedback on your workout, rewarding your efforts by making you look your best.
Antaeus Labs Thunderbolt isn’t your run-of-the-mill “pump supp”. We’ve only included those things we think will make the biggest difference to your workouts and your progress in the gym. The new and improved Thunderbolt formula also introduces two new bioavailability-enhanced ingredients for maximum pump.
Each dose of Thunderbolt contains:
-Kallidinogenase
-Arginine Butyrate
-Quercetin-Niacinamide Cocrystals
-Visnadine-Cyclodextrin Complex
-Copper (1mg)
Kallidinogenase
Kallidinogenase is a naturally-occurring vasodilatory human enzyme. The kallidinogenase, also known as kallikrein, found in Thunderbolt is a natural human enzyme in recombinant form. We use enteric coated acid-resistant capsules for maximum bioavailability and absorption from the GI tract.
Kallikrein is a serine protease which cleaves kininogen to release the potent vasoactive kinin peptides bradykinin (BK) or kallidin. Within skeletal muscle, bradykinin promotes glucose uptake and improves blood flow. [1]
Kinins have a very short half-life, as they are destroyed in less than 20secs by through the action of kininases (aminopeptidases) present in the tissues and blood. Hence, kinins are unsuitable for use as exogenously administered agents. In plasma, kininogen is in excess, leaving kallikrein as the limiting factor in kinin formation. Therefore, kallikrein is a far better choice for activating the kinin–kallikrein system.
Kallidinogenase is stable for 28 months at room temperature, and about five years if kept refrigerated. [2]
Primary effects:
Kallidinogenase increases peripheral and cerebral bloodflow via Bradykinin B1 and B2 receptors. It is a peripheral vasodilator. [3]
Other beneficial effects:
Kallidinogenase strongly increases prostaglandin levels, which may increase the anabolic response to exercise. [4,5]
It also has significant pro-fertility effects, [6,7,8] is nephroprotective, has diuretic effects via activation of the Bradykinin B2 receptor, and increases bloodflow to the brain. [9]
B2 receptor activation also increases vascular permeability and allows the blood brain barrier to be crossed more easily.
Arginine Butyrate
Arginine Butyrate activates the nitric oxide pathway and inhibits histone deacetylase to increase follistatin and reduce myostatin.
Primary effects:
HDAC inhibitors have potential as anabolic agents as they increase follistatin and reduce myostatin levels. [10,11]
In mouse models of muscular dystrophy arginine butyrate demonstrated beneficial effects including increased muscle strength and increased utrophin expression. [12]
Exposure of myoblasts to HDAC inhibitors results in upregulation of follistatin expression. In turn, follistatin binds to and suppresses the activity of myostatin, a TGF-β family member that negatively regulates muscle mass. [13]
Other beneficial effects:
Arginine’s NO-mediated functions are fairly well known. L-arginine is converted into NO by the enzyme NO synthase (eNOS). Nitric oxide causes relaxation vascular smooth muscle by binding to and activating guanylate cyclase and increasing intracellular levels of cyclic-guanosine 3’,5’-monophosphate, causing vasodilation which lowers arterial pressure. [14] This improves blood flow which increases the “pump”. Nitric oxide also inhibits platelet aggregation and adhesion. [15] Arginine is also a precursor of creatine, and plays a role in accelerating tissue repair following injuries. [16]
Copper
Copper is a trace element required for human health. It is included here to prevent diet-related deficiency, which may impair vasodilation.
Primary effects:
Copper deficiency has been shown to block acetylcholine-mediated vascular smooth muscle relaxation. [17,18]
Other beneficial effects:
Copper potentiates the vasodilatory and antiplatelet actions of endogenous nitrosothiols: Copper ions are important catalysts in the decomposition of low molecular weight nitrosothiols (like GSNO) by superoxide dismutase (Cu/Zn SOD). [19]. Copper also enables many metabolic functions, the absorption of iron and formation of red blood cells, and the function of the immune system.
Quercetin-Niacinamide Cocrystals
Quercetin is a hydrophobic and lipophilic aglycone flavonol present in a wide variety of fruits and vegetables. Niacinamide is a form of Vitamin B3. As cocrystals the two compounds form a solid-state crystalline lattice structure, stabilized by hydrogen bonds.
Primary effects:
Quercetin induces vasodilatory effects in humans in both in vivo and ex vivo experiments. [20] Quercetin achieves this vasodilation by inducing phosphorylation of endothelial nitric oxide synthase (eNOS) in endothelial cells, [21] and also by the production of endogenous vasodilatory prostanoids through cyclooxygenase enzyme inhibition. [22] In vitro experiments suggest quercetin is capable of increasing blow flow in blood vessels by up to 50%. [23]
Quercetin-Niacinamide cocrystals have improved solubility and oral bioavailability profiles compared to free quercetin, with much faster time to maximum concentration (Tmax). [24]
Other beneficial effects:
Quercetin has many potential beneficial effects, which have been studied to varying degrees of scientific rigour. Research has suggested anti-inflammatory properties (through the inhibition of histamine release from mast cells), inhibition of platelet aggregation, blood pressure-lowering effects (which may be dependent on an individual’s genetics), while evidence of improvements in human endurance has been equivocal. [25]
Niacinamide and quercetin are both SIRT1 activators. [26] Though the exact function of the sirtuin family of enzymes in mammals is not fully understood, SIRT1 facilitates longevity in “lower” organisms, and has been implicated in human aging and metabolic- and age-related conditions. [27,28]
Visnadine-Cyclodextrin Complex
Visnadine is a component of the plant Ammi visnaga (Bishop’s Weed), a member of the carrot family which has been used as a folk remedy around the Mediterranean since the time of the ancient Egyptians. Bishop’s Weed contains several compounds with vasodilatory properties including visnadine, visnagin, and khellin, of which visnadine is the most potent. [29] It is used in Thunderbolt complexed with cyclodextrins, for improved bioavailability.
Primary effects:
Visnadine is a peripheral and coronary vasodilator. It is believed to be vasodilatory through inhibition of calcium entry through voltage-gated L-type channels, and not through the release of endothelium-derived relaxing factors. [29][30]
Get maximum pump with new Antaeus Labs Thunderbolt.
Look and perform your best with Antaeus Labs.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
References:
1. Wicklmayr M, Dietze G, Brunnbauer H, Rett K, Mehnert H. Dose-dependent effect of bradykinin on muscular blood flow and glucose uptake in man. Hoppe-Seyler’s Z Physiol Chem. 1983 Jul;364(7):831–3.
2. Tanimoto T, Fukuda H, Kimura T. [Long-term stability of Kallidinogenase Reference Standard]. Eisei Shikenjo Hokoku. 1989;(107):119–20.
3. Ogawa K, Ito T, Ban M, Motizuki M, Satake T. Effects of kallidinogenase on urinary kallikrein excretion and plasma prostanoid concentrations in patients with essential hypertension. Experientia. 1986 Sep 15;42(9):1014–5.
4. Honda M, Nagashima Y, Hatano M, Nishino T, Awaya J, Washino N, et al. Effects of purified hog pancreatic kallikrein on the kinin-prostaglandin system and renin-angiotensin-aldosterone system. Nephron. 1985;41(1):34–8.
5. Ogawa K, Ito T, Ban M, Motizuki M, Satake T. Effects of kallidinogenase on urinary kallikrein excretion and plasma prostanoid concentrations in patients with essential hypertension. Experientia. 1986 Sep 15;42(9):1014–5.
6. Kamidono S, Hazama M, Matsumoto O, Takada KI, Tomioka O, Ishigami J. Kallikrein and male subfertility. Usefulness of high-unit kallikrein tablets. Andrologia. 1981 Apr;13(2):108–20.
7. Saitoh S, Kumamoto Y, Shimamoto K, Iimura O. Kallikrein in the male reproductive system. Arch Androl. 1987;19(2):133–47.
8. Izzo PL, Canale D, Bianchi B, Meschini P, Esposito G, Menchini Fabris GF, et al. The treatment of male subfertility with kallikrein. Andrologia. 1984 Apr;16(2):156–61.
9. Wang Chang-lin, Zhu You-ling. Clinical effect of urinary kallidinogenese compined with citicoline on treating acute carotisal cerebral infarction. Anhui Medical and Pharmaceutical Journal 2009-01.
10. Iezzi S, Di Padova M, Serra C, Caretti G, Simone C, Maklan E, et al. Deacetylase inhibitors increase muscle cell size by promoting myoblast recruitment and fusion through induction of follistatin. Dev Cell. 2004 May;6(5):673–84.
11. Bonetto A, Penna F, Minero VG, Reffo P, Bonelli G, Baccino FM, et al. Deacetylase inhibitors modulate the myostatin/follistatin axis without improving cachexia in tumor-bearing mice. Curr Cancer Drug Targets. 2009 Aug;9(5):608–16.
12. Vianello S, Yu H, Voisin V, Haddad H, He X, Foutz AS, et al. Arginine butyrate: a therapeutic candidate for Duchenne muscular dystrophy. FASEB J. 2013 Jun;27(6):2256–69.
13. Verdin E. Histone Deacetylases: Transcriptional Regulation and Other Cellular Functions. Springer; 2007.
14. Tapiero H, Mathé G, Couvreur P, Tew KD. I. Arginine. Biomed Pharmacother. 2002 Nov;56(9):439–45.
15. Radomski MW, Palmer RM, Moncada S. The anti-aggregating properties of vascular endothelium: interactions between prostacyclin and nitric oxide. Br J Pharmacol. 1987 Nov;92(3):639–46.
16. Witte MB, Barbul A. Arginine physiology and its implication for wound healing. Wound Repair Regen. 2003 Dec;11(6):419–23.
17. Schuschke DA, Saari JT, Miller FN. A role for dietary copper in nitric oxide-mediated vasodilation. Microcirculation. 1995 Dec;2(4):371–6.
18. Schuschke DA, Percival SS, Saari JT, Miller FN. Relationship between dietary copper concentration and acetylcholine-induced vasodilation in the microcirculation of rats. Biofactors. 1999;10(4):321–7.
19. Burg A, Cohen H, Meyerstein D. The reaction mechanism of nitrosothiols with copper(I). J Biol Inorg Chem. 2000 Apr;5(2):213–7.
20. Perez, A. et al. The flavonoid quercetin induces acute vasodilator effects in healthy volunteers: correlation with beta-glucuronidase activity. Pharmacol. Res. 89, 11–18 (2014).
21. Li, P.G. et al. Quercetin induces rapid eNOS phosphorylation and vasodilation by an Akt-independent and PKA-dependent mechanism. Pharmacology 89, 220–228 (2012).
22. Fayez, M. Al-, Cai, H., Tunstall, R., Steward, W. P. & Gescher, A. J. Differential modulation of cyclooxygenase-mediated prostaglandin production by the putative cancer chemopreventive flavonoids tricin, apigenin and quercetin. Cancer Chemother. Pharmacol. 58, 816–825 (2006).
23. Monori-Kiss, A., Monos, E. & Nádasy, G. L. Quantitative analysis of vasodilatory action of quercetin on intramural coronary resistance arteries of the rat in vitro. PLoS ONE 9, e105587 (2014).
24. Smith, A. J., Kavuru, P., Wojtas, L., Zaworotko, M. J. & Shytle, R. D. Cocrystals of quercetin with improved solubility and oral bioavailability. Mol. Pharm. 8, 1867–1876 (2011).
25. Kelly, G. S. Quercetin. Monograph. Altern Med Rev 16, 172–194 (2011).
26. Allard, J. S., Perez, E., Zou, S. & de Cabo, R. Dietary activators of Sirt1. Mol. Cell. Endocrinol. 299, 58–63 (2009).
27. Hubbard, B. P. & Sinclair, D. A. Small molecule SIRT1 activators for the treatment of aging and age-related diseases. Trends Pharmacol. Sci. 35, 146–154 (2014).
28. Li, X. SIRT1 and energy metabolism. Acta Biochim. Biophys. Sin. (Shanghai) 45, 51–60 (2013).
29. Rauwald, H. W., Brehm, O. & Odenthal, K. P. The involvement of a Ca2+ channel blocking mode of action in the pharmacology of Ammi visnaga fruits. Planta Med. 60, 101–105 (1994).
30. Durate, J. et al. Effects of visnadine on rat isolated vascular smooth muscles. Planta Med. 63, 233–236 (1997).
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