Haemodynamic effects of the flavonoid quercetin in rats revisited

Figures

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  Figure 1. Comparison of phenylephrine‐induced pressor responses as recorded in unanaesthetized normotensive Wistar Kyoto rats (n = 8) and spontaneously hypertensive rats (n = 8) in vehicle‐ and quercetin‐treated animals. (a) The changes in mean arterial pressure (MAP) to intravenous bolus injections of phenylephrine before and after the intravenous administration of the α1‐antagonist tamsulosin. Tamsulosin attenuated, significantly and equipotently, the pressor responses to phenylephrine in both treatment arms. (b) Wistar Kyoto rats (n = 8) and (c) spontaneously hypertensive rats (n = 8) compare the averaged phenylephrine‐induced increments in MAP (averaged over the four injections) as shown in (a) and expressed as the cumulative AUC, before and after the intravenous injection of the vehicle or quercetin as well as at 10, 40 and 120 min after intravenous tamsulosin treatment. In both rat strains, blood pressure responses to α‐adrenoceptor stimulation or α‐adrenoceptor blockade were very comparable and not influenced by treatment of quercetin

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  Figure 2. Comparison of the cumulative tamsulosin‐induced depressor responses as recorded in conscious normotensive Wistar Kyoto rats (WKY, n = 8) and spontaneously hypertensive rats (SHR, n = 8) in vehicle‐ and quercetin‐treated animals. (a, b) The changes in mean arterial pressure (MAP) in both strains. (c, d) The associated changes in heart rate (HR). While absolute depressor responses to tamsulosin were significantly greater in SHR than in WKY, blood pressure responses to α‐adrenoceptor blockade were not very different between vehicle‐ and quercetin‐treated rats

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  Figure 3. Comparison of the regional haemodynamic changes (mean arterial pressure (MAP; Figure 3a) and heart rate (HR; Figure 3b)) induced by acute intravenous injection of quercetin (n = 8) or its vehicle solution (n = 8) as recorded in isoflurane anaesthetized Wistar Kyoto rats instrumented with Doppler flow probes to record simultaneously blood velocity changes as observed in the four indicated vascular beds (carotid conductance (Figure 3c), hindquarter conductance (Figure 3d), mesenteric conductance (Figure 3e) and renal conductance (Figure 3f)). Data on tamsulosin‐induced haemodynamic changes were taken at 3, 10, 20 and 30 min after injection of the α1‐antagonist. Compared with vehicle treatment, quercetin treatment did not amplify tamsulosin‐induced changes in any of the vascular beds. Absolute baseline values (±SD) of MAP and HR under anaesthesia were not significantly different, being 70 ± 11 mmHg and 311 ± 34 bpm in the vehicle‐treated (n = 13) and 78 ± 11 mmHg and 325 ± 28 bpm in the quercetin‐treated (n = 10) rats, respectively

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  Figure 4. Comparison of the regional haemodynamic changes induced by a 2 min, 45° head‐up tilt in isoflurane anaesthetized Wistar Kyoto rats instrumented with Doppler flow probes. Data are presented for changes in mean arterial pressure (MAP; Figures 4a,c and e) and mesenteric conductance (Figures 4b, d and f) recorded after injection of vehicle or quercetin and hence 10 and 30 min after additional tamsulosin administration. Data are compared for vehicle‐ and quercetin‐treated rats. There was no difference in tilt responses between vehicle‐ and quercetin‐treated rats

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  Figure 5. Comparison of telemetry‐based 24‐hr patterns of mean arterial pressure (MAP; Figure 5a) and heart rate (HR; Figure 5b) and locomotor activity (Figure 5c) in adult spontaneously hypertensive rats as recorded over 3 days at the age of 16–17 weeks (defined as week 0) and 5 weeks later (defined as week 5) after chronic oral feeding of quercetin (10 mg·kg−1, n = 6) or normal food (n = 6). In both treatment arms, MAP rose significantly with ageing of the spontaneously hypertensive rats and HR fell. These age‐related changes in haemodynamics were not different between animals on control food and those on quercetin