Urapidil has been determined to aid in the recovery of torsion detorsion (T/D) injuries in ovaries and testes, as well as ischemia-reperfusion (I/R) renal injuries. Both of these conditions are directly associated with one another as T/D injuries commonly lead to ischemia, or the lack of blood flow.[7][8][9] Urapidil is able to reduce inflammatory response, apoptosis and act as an antioxidant through a variety of pathways.[8] During the detorsion phase of an injury, reperfusion, or the restoration of blood flow is important, but can also cause injuries to the affected tissue through apoptosis and the generation of ROS.[8][7] Oxidative stress also plays a vital role in D/T and I/R injuries and is marked by malondialdehyde, or MDA, levels.[7][9] MDA can also contribute to tissue damage, particularly by encouraging polymerization and cross-linking of the membranes of the affected cells.[8] Through various studies performed within the past decade, it has been found that urapidil can treat T/D and I/R injuries, particularly stemming from autophagy, apoptosis, and inflammation, by elevating levels of SOD, TAS, and GPx within the cell.[8][9] Both SOD and GPx help to counteract the negative effects of ROS which injures tissue through lipid peroxidation and by damaging DNA.[8] Additionally, urapidil has the ability to counteract autophagy by lowering the quantity of autophagosome marker LC3B and caspase-3 which also plays a critical role in autophagy regulation.[8]
^Eltze M (October 1979). "Investigations on the mode of action of a new antihypertensive drug, urapidil, in the isolated rat vas deferens". European Journal of Pharmacology. 59 (1–2): 1–9.
doi:
10.1016/0014-2999(79)90018-9.
PMID228944.
^Schoetensack W, Bruckschen EG, Zech K (1983). "Urapidil". New Drugs Annual: Cardiovascular Drugs. p. 19.
^Verberne AJ, Rand MJ (January 1985). "Effect of urapidil on beta-adrenoceptors of rat atria". European Journal of Pharmacology. 108 (2): 193–196.
doi:
10.1016/0014-2999(85)90725-3.
PMID2984023.
Urapidil has been determined to aid in the recovery of torsion detorsion (T/D) injuries in ovaries and testes, as well as ischemia-reperfusion (I/R) renal injuries. Both of these conditions are directly associated with one another as T/D injuries commonly lead to ischemia, or the lack of blood flow.[7][8][9] Urapidil is able to reduce inflammatory response, apoptosis and act as an antioxidant through a variety of pathways.[8] During the detorsion phase of an injury, reperfusion, or the restoration of blood flow is important, but can also cause injuries to the affected tissue through apoptosis and the generation of ROS.[8][7] Oxidative stress also plays a vital role in D/T and I/R injuries and is marked by malondialdehyde, or MDA, levels.[7][9] MDA can also contribute to tissue damage, particularly by encouraging polymerization and cross-linking of the membranes of the affected cells.[8] Through various studies performed within the past decade, it has been found that urapidil can treat T/D and I/R injuries, particularly stemming from autophagy, apoptosis, and inflammation, by elevating levels of SOD, TAS, and GPx within the cell.[8][9] Both SOD and GPx help to counteract the negative effects of ROS which injures tissue through lipid peroxidation and by damaging DNA.[8] Additionally, urapidil has the ability to counteract autophagy by lowering the quantity of autophagosome marker LC3B and caspase-3 which also plays a critical role in autophagy regulation.[8]
^Eltze M (October 1979). "Investigations on the mode of action of a new antihypertensive drug, urapidil, in the isolated rat vas deferens". European Journal of Pharmacology. 59 (1–2): 1–9.
doi:
10.1016/0014-2999(79)90018-9.
PMID228944.
^Schoetensack W, Bruckschen EG, Zech K (1983). "Urapidil". New Drugs Annual: Cardiovascular Drugs. p. 19.
^Verberne AJ, Rand MJ (January 1985). "Effect of urapidil on beta-adrenoceptors of rat atria". European Journal of Pharmacology. 108 (2): 193–196.
doi:
10.1016/0014-2999(85)90725-3.
PMID2984023.