| Quercetin (3, 3', 4', 5, 7-pentahydroxyflavone), a member of the flavonoids family, is widely consumed in the human diet and is particularly abundant in onions, kale, tea and red wine, which commonly presents in the form of quercetin glycosides. In recent years, domestic and foreign medical workers have focused on the study of quercetin and revealed that quercetin has a wide range of biological effects such as scavenging oxygen free radicals and anti-oxidation, lowering the blood pressure, reducing ischemic-reperfusion injury. Quercetin has been shown to be an excellent antioxidant in vitro. Within the flavonoid family, it is the most potent scavenger of reactive oxygen species (ROS) including singlet oxygen (1O2), superoxide (O2?) and hydroxyl radical (·OH). Moreover, its antioxidant capacity is much higher than the classic antioxidants such as vitamin C and vitamin E. Quercetin has a positive role in vasodilation and lowering the blood pressure, but the mechanism is not yet clear. It may be related to endothelium and regulation of ion channels. Using the whole-cell configuration of the patch-clamp technique, quercetin increases the frequency of spontaneous transient outward currents (STOCs) carried by large conductance Ca2+-activated K+ channels (BKCa) to make the coronary arteries relax. Epidemiological studies have reported that quercetin can restore endothelial dysfunction and inhibit vascular smooth muscle cell proliferation. Meanwhile, endothelial dysfunction and vascular smooth muscle cell proliferation are the major risk factors for developing atherosclerosis and hypertension. Therefore, quercetin plays an important role in the prevention and treatment of cardiovascular diseases. It is well known that baroreflex is a major way to modulate blood pressure. The effects of quercetin on carotid sinus baroreceptor activity and baroreflex have not been reported yet. The goals of the present research were to observe these effects of quercetin. 1 Quercetin inhibits carotid sinus baroreflex in anesthetized male rats Objective: To study the effects of quercetin on carotid sinus baroreflex (CSB).Methods: The functional curve of carotid sinus baroreflex was measured by recording the changes of arterial pressure in 36 anesthetized male rats with perfusing isolated carotid sinus.Results: Quercetin (1, 10, 100μmol/L) inhibited CSB, which shifted the functional curve of the baroreflex to the right and upward, with a marked decrease in peak slope (PS) and reflex decrease (RD) in blood pressure in a concentration-dependent manner. PS decreased from 0.45±0.01 to 0.38±0.01 (P<0.01), 0.33±0.02 (P<0.01), 0.25±0.02 (P<0.01) respectively. RD decreased from (47.83±0.98) mmHg to (41.00±1.26 mmHg, P<0.01), (35.67±1.21 mmHg, P<0.01), (30.00±1.55 mmHg, P<0.01); threshold pressure (TP) increased from (64.96±1.84) mmHg to (71.49±0.52 mmHg, P<0.01), (75.51±1.22 mmHg, P<0.01), (85.39±1.95 mmHg, P<0.01); equilibrium pressure (EP) increased from (94.60±1.04) mmHg to (97.12±0.99 mmHg, P<0.01), (99.13±0.76 mmHg, P<0.01), (101.81±1.05 mmHg, P<0.01); saturation pressure (SP) increased from (187.24±1.88) mmHg to (192.93±1.48 mmHg, P<0.01), (197.12±1.64 mmHg, P<0.01), (206.67±1.48 mmHg, P<0.01) respectively. (2) Pretreatment with charybdotoxin (ChTX, 100 nmol/L), an inhibitor of calcium-activated potassium channel, completely abolished the effect of quercetin (10μmol/L) on the CSB. (3) Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 100μmol/L), an inhibitor of nitric oxide synthase, did not influence the inhibitory effect of quercetin (10μmol/L). (4) Pretreatment with indomethacin (10μmol/L), an inhibitor of cyclooxygenase, did not affect the inhibitory effect of quercetin (10μmol/L).Conclusion: Quercetin inhibits carotid sinus baroreflex in anesthetized rats, which is mediated by opening the calcium-activated potassium channel to increase potassium efflux in baroreceptor nerve endings. However, NO and prostacyclin (PGI2) released from the endothelium seem not to be involved in the mechanism of this effect.2 Quercetin inhibits carotid sinus baroreceptor activity in anesthetized male ratsObjective: To study the effect of quercetin on carotid baroreceptor activity (CBA).Methods: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in 36 anesthetized male rats with perfusing isolated carotid sinus.Results: (1) Quercetin (1, 10, 100μmol/L) inhibits CBA, which shifted FCCB to the right and downward. There was a marked decrease in peak slope (PS) and peak integral value (PIV) of carotid sinus nerve discharge in a concentration-dependent manner. PS decreased from (3.06±0.06) %/mmHg to (2.53±0.04 %/mmHg, P<0.001), (2.23±0.05 %/mmHg, P<0.001), (2.02±0.09 %/mmHg, P<0.001), respectively. PIV decreased from (330.33±3.20) % to (274.17±4.17 %, P<0.001), (244.17±3.66 %, P<0.001), (213.33±3.27 %, P<0.001), respectively; threshold pressure (TP) increased from (44.77±1.33) mmHg to (51.63±1.73 mmHg, P<0.001), (57.96±2.56 mmHg, P<0.001), (64.65±2.15 mmHg, P<0.001); saturation pressure (SP) increased from (158.92±2.05) mmHg to (168.59±1.72 mmHg, P<0.001), (177.21±2.08 mmHg, P<0.001), (186.36±1.94 mmHg, P<0.001). (2) Pretreatment with charybdotoxin (ChTX, 100 nmol/L), an inhibitor of calcium-activated potassium channel, completely abolished the effect of quercetin (10μmol/L) on the CBA. (3) Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 100μmol/L), an inhibitor of nitric oxide synthase, did not influence the inhibitory effect of quercetin (10μmol/L). (4) Pretreatment with indomethacin (10μmol/L), an inhibitor of cyclooxygenase, did not affect the inhibitory effect of quercetin (10μmol/L) on the CBA.Conclusion: Quercetin inhibits carotid sinus baroreceptor activity in anesthetized rats, which is mediated by opening the calcium-activated potassium channel to increase potassium efflux in baroreceptor nerve endings. However, NO and prostacyclin (PGI2) released from the endothelium seem not to be involved in the mechanism of this effect.
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