Chiranthodendron pentadactylon Larreat is a tree native to southeastern Mexico and Guatemala. Its flower is used in Mexican folk medicine to treat a variety of diseases, including conditions of blood pressure. However, scientific information on its usefulness in this pathology is lacking. The present study evaluates the effect of a methanolic extract (ME) from the flower and its active constituents on heart rate (HR) and mean arterial pressure (MAP) in anesthetized rats (MAPHR). The study also analyzed the effects on rat-isolated aortic rings (RIAR) and the rat mesenteric arterial bed (MABR). Active fractions were chromatographed, which led to the isolation of cyanidin 3-O-glucoside (C3G) identified through HPLC. The Chiranthodendron pentadactylon flowers produced hypotensive and vasorelaxant effects associated with C3G. The vasorelaxant effect is a mechanism underlying the synthesis and release of nitric oxide (NO). Neither cholinergic receptors nor prostaglandins are involved. ME and C3G cause cardiovascular depression in anesthetized rats via cholinergic and prostanoid mechanisms. Our research expands the scientific understanding of the flowers on the rat cardiovascular system. This amplifies the appreciation of the flower’s ethnomedicine employed to control blood pressure. However, researchers need to conduct toxicity studies to determine the safety of this plant.

This study aimed to explore the effects of raloxifene (Rx) and estradiol (E₂) on prothrombin time (PT), partial thromboplastin time (APTT), coagulation factors (VII, X, XI), and fibrinogen concentrations in rats. Female rats were ovariectomized 11 days prior to starting the treatment. Afterward, they received Rx or E₂ (1, 10, 100, and 1000 µg/kg) or propylene glycol (0.3 mL; vehicle, V) subcutaneously for 3 consecutive days. Plasma was collected to measure the hemostatic parameters. Rx significantly increased PT (8%, at 1000 µg/kg; p < 0.05) and APTT at all doses evaluated (32, 70, 67, 30%; p < 0.05, respectively). Rx (1, 10, 100, and 1000 µg/kg) decreased the activity of factor VII by −20, −40, −37, and −17% (p < 0.05), respectively, and E₂ increased it by 9, 34, 52, and 29%. Rx reduced factor X activity at 10 and 100 µg/kg doses (−30, and −30% p < 0.05), and E₂ showed an increment of 24% with 1000 µg/kg dose only. Additionally, Rx (1, 10, 100 µg/kg) diminished FXI activity (−71, −62, −66; p < 0.05), E₂ (1 and 10 µg/kg) in −60 and −38, respectively (p < 0.05), and Rx (1000 µg/kg) produced an increment of 29% (p < 0.05) in fibrinogen concentration, but not E₂. Our findings suggest that raloxifene has a protective effect on hemostasis in rats.

This study aimed to explore the effects of raloxifene (Rx) and estradiol (E2) on prothrombin time (PT), partial thromboplastin time (APTT), coagulation factors (VII, X, XI), and fibrinogen concen-trations in rats. Rats were ovariectomized 11 days prior to starting the treatment. Then they re-ceived Rx or E2 (1 to 1000 µg/Kg) or propylene glycol (0.3 ml; vehicle, V) subcutaneously for three consecutive days. Plasmas were collected to measure the hemostatic parameters. Rx significantly increased PT (8%, at 1000 µg/Kg; p<0.05) and APTT at all doses evaluated (32, 70, 67, 30%; p<0.05, respectively). Rx (1 to 1000 µg/Kg) decreased the activity of factor VII by -20, -40, -37, and -17% (p<0.05), respectively, while E2 increased it by 9, 34, 52, and 29%; Rx reduced factor X activity at 10 and 100 µg/kg doses (-30, and -30% p<0.05), while E2 showed an increment of 24% with 1000 µg/kg dose only; Rx (1-100 µg/Kg) diminished FXI activity (-71, -62, -66; p<0.05), while E2 (1 and 10 µg/Kg) diminished it in -60 and -38, respectively (p<0.05); Rx (1000 µg/Kg) produced an increment of 29% (p<0.05) in fibrinogen concentration, but not E2. Our findings suggest that raloxifene has a pro-tective effect on hemostasis in rats.