Effect of myricetin on blood pressure and metabolic alterations in fructose hypertensive rats

Fructose feeding induces a rise in blood pressure in normal rats and is associated with insulin resistance, hyperinsulinemia, and hypertriglyceridemia. We have examined the effect of myricetin (100 and 300?mg/kg, p.o. for 6 weeks) isolated from Vitis vinifera Linn. (Vitaceae) on systolic blood pressure (SBP), vascular reactivity, serum glucose, triglycerides, cholesterol, and insulin in fructose-induced hypertension. Myricetin reduced systolic blood pressure and vascular reactivity changes to catecholamines and reversed the metabolic alterations induced by fructose. The cumulative concentration–response curve (CCRC) of Ang II was shifted toward the right in rats treated with myricetin, using isolated strips of ascending colon. The results suggest that myricetin could prevent the development of high blood pressure induced by a diet rich in fructose, probably by reversing the metabolic alterations induced by fructose. In conclusion, myricetin has antihypertensive action in the fructose model.     

Effects of verapamil on blood pressure and heart rate in neurogenic hypertensive rats

The mechanism(s) underlying the prolactin (PRL)-releasing effect of benserazide (Bz), a peripheral inhibitor of L-aromatic amino-acid decarboxylase, was investigated in the rat. In intact male and female rats, Bz was ineffective to increase significantly plasma PRL at 0.8 mg/kg i.p. but elicited an already maximal effect at 1.6 mg/kg. Bz added to in vitro incubated anterior pituitaries (APs) did not alter PRL secretion at the dose of 3.8 X 10(-6)M but increased PRL release at 10(-4)M. Bz, even at very high doses (up to 10(-3) M), did not displace [3H]spiroperidol binding from AP membrane preparations. In rats having had mechanical ablation of the medio basal hypothalamus (MBH), Bz (15 mg/kg i.p.) induced no rise in plasma PRL and did not counteract the striking inhibitory effect of a dopamine (DA) infusion (5 micrograms/kg per min per 120 min). Administration of Bz (15 mg/kg i.p.) into intact male rats decreased significantly the DA concentrations in the median eminence (ME) but not in the residual hypothalamus and the AP. In the same rats 1-dopa (50 mg/kg i.p.) increased significantly the DA concentrations not only in the ME but also in the hypothalamus and the AP. Bz given concurrently with 1-dopa markedly reduced the rise in DA concentrations induced by 1-dopa in the ME, and greatly potentiated the increase in DA concentrations in the hypothalamus. These data indicate that the mechanism whereby a single administration of Bz increases PRL secretion in the rat is not consistent with the postulated DA receptor antagonist action of the drug, but instead implies inhibition of the decarboxylation of 1-dopa at dopaminergic nerve terminals of the ME.     

Qi盐对肾性和自发性高血压大鼠血压的影响

目的观察Qi盐对肾性和自发性高血压大鼠(SHR)的降压作用.方法通过缩窄左肾动脉而制备2K1C夹的肾性高血压模型,同时选用16周龄的SHR,2种实验鼠均连续给予Qi盐0.4、0.2、0.1 g·kg-1,14 d(ig,qd),观察其对肾性和SHR BP的影响.结果Qi盐各剂量组及普通盐组对肾性高血压模型鼠BP在用药d 7、14均无明显的影响,而对SHR,Qi盐0.4、0.2 g·kg-1给药7d后可显著降低BP,与对照组相比,P<0.05,但14 d后BP有所回升.结论Qi盐对肾性高血压模型无明显的治疗作用,但在给药7 d后能显著地降低SHR的BP.     

原花青素对肾血管性高血压大鼠血压及血清抗氧化能力的影响

目的:探讨原花青素对肾血管性高血压大鼠血压及血清抗氧化能力的影响。方法:采用"两肾一夹"(2K1C)法建立大鼠肾血管性高血压病模型,术后2周,选择40只尾动脉血压升高超过130 mmHg的大鼠按照随机数字表法分为4组,每组10只,分别为:空白对照组高血压模型组、原花青素低剂量治疗组、原花青素高剂量治疗组及氯沙坦组。在对大鼠应用药物治疗后的第4、5、6周,测定2组大鼠的尾动脉血压、血清中超氧化物歧化酶(SOD)活性、一氧化氮(NO)以及丙二醛(MDA)的含量,同时测定总抗氧化能力(T-AOC);应用Western-blot方法检测大鼠腹主动脉中的内皮素-1(ET-1)蛋白表达。结果:治疗4周后,原花青素高、低剂量能显著降低肾血管性高血压大鼠的尾动脉血压(P<0.01,P<0.05),且降压作用维持至第6周;与模型组相比较,原花青素高、低剂量治疗组使肾血管性高血压大鼠血清中MDA含量、ET-1表达值、T-AOC显著降低(P<0.01,P<0.05),使肾血管性高血压大鼠血清中NO含量与SOD活性显著增高(P<0.01,P<0.05)。结论:原青花素能够显著降低肾血管性高血压大鼠尾动脉收缩压,同时对大鼠的血清具有很强的抗氧化能力,主要的作用机制可能与其增加一氧化氮的释放及产生以及降低ET-1的蛋白在血管中的表达相关。     

Effects of nifedipine on blood pressure and heart rate in conscious neurogenic hypertensive rats

The effects of nifedipine (15 micrograms/kg, i.v.) on mean blood pressure (MBP) and heart rate were studied in neurogenic hypertensive rats (NHR), compared with renovascular hypertensive (RHR), and control (CR) rats. The maximal MBP reduction reached 32, 37 and 9%, respectively. The baseline MBP was recovered after 120, 150, and 5 min, respectively. The hypotension was not accompanied by changes in the baseline high heart rate of NHR and by tachycardia in CR and RHR groups. The data show the antihypertensive efficacy of nifedipine in both models of hypertension and indicate that under conditions of increased sympathetic tone the cardiac pacemaker cannot be easily inhibited by nifedipine.     

睾酮对去势的肾血管性高血压大鼠肾素-血管紧张素系统及血压的影响

目的探讨去势对肾血管性高血压大鼠肾素-血管紧张素系统及血压的影响,及给予去势的肾血管性高血压大鼠不同剂量的十一酸睾酮后肾素-血管紧张素系统及血压的变化。方法成年雄性Wistar大鼠（180-220g）32只．行左侧肾动脉结扎手术,4周后肾血管性高血压大鼠造模成功。随机分为对照组,单纯去势（双侧睾丸切除）组,小剂量睾酮（TU）组（去势后皮下注射TU13．7μg/g）和大剂量．TU组（去势后皮下注射TU625μg／g）。30d后,测量血压（BP）。测血压后,取血检测血清总睾酮（TT）、血浆肾素活性（RA）、血管紧张素Ⅱ（AngⅡ）。取左侧肾脏,检测组织肾素活性（RA）,血管紧张素Ⅱ（AngⅡ）。结果单纯去势组血清TT水平明显低于对照组（P〈0．01）,小剂量TU组血清TT水平低于对照组（P〈0．05）,大剂量TU组血清TT水平明显高于对照组（P〈0．01）。单纯去势组的血浆RA、AngⅡ水平明显低于对照组（P〈0．01）,小剂量TU组的血浆RA、AngⅡ水平低于对照组（P〈0．05）,大剂量TU组的血浆RA、AngⅡ水平明显高于对照组（P〈0．01）。单纯去势组肾组织的RA、AngⅡ水平明显低于对照组（P〈0．01）,小剂量TU组肾组织的RA、AngⅡ水平低于对照组（P〈0．05）,大剂量TU组肾组织的RA、AngⅡ水平高于对照组（P〈0．05）。单纯去势组BP明显低于对照组（P〈0．01）,小剂量TU组BP低于对照组（P〈0．05）,大剂量TU组BP明显高于对照组（P〈0．01）。结论雄性肾血管性高血压大鼠去势及去势后给予不同剂量的十一酸睾酮可产生不同水平的TT,同时也使血浆及组织局部的肾素-血管紧张素系统、血压发生变化。去势及去势后给予十一酸睾酮可能通过血浆及组织局部的肾素-血管紧张素系统影响肾血管性高血压大鼠的血压。     

Effects of prolyl hydroxylase inhibition on arterial collagen synthesis and blood pressure in hypertensive rats

Changes in arterial collagen synthesis and the effects of P-1894B, a potent inhibitor of prolyl hydroxylase, were investigated on rat hypertension, induced by deoxycorticosterone acetate (DOCA) and salt. In DOCA-salt hypertensive rats, prolyl hydroxylase activity increased significantly in the abdominal aorta and in the mesenteric artery. Incorporation of 14C-proline into the thoracic aorta, abdominal aorta and mesenteric artery was higher and the hydroxyproline content of the abdominal aorta and mesenteric artery was higher than in the control rats. Treatment with P-1894B significantly inhibited prolyl hydroxylase activity, reduced arterial collagen synthesis, but did not prevent or reverse hypertension.     

Effects of indomethacin on hormonal and blood pressure responses to captopril in spontaneously hypertensive rats

The possible role of vasodilatory prostanoids in the antihypertensive action of captopril was investigated in spontaneously hypertensive rats (SHR). Captopril (100 mg/kg/day for 5 days) decreased systolic blood pressure and increased water consumption, urine excretion and plasma renin activity (PRA). It also enhanced the urinary excretion of the prostacyclin metabolite 6-keto-PGF1 alpha, but did not change the excretion of PGE2. Indomethacin (3 mg/kg/day), given both alone and in combination with captopril, reduced markedly the urinary excretions of 6-keto-PGF1 alpha and PGE2 but did not alter PRA, compared with corresponding groups without indomethacin. The suppression of prostanoid synthesis caused by indomethacin did not affect the antihypertensive effect of captopril or the basal blood pressure in SHR. Neither did indomethacin influence drinking or urine excretion in SHR not receiving captopril, but it reduced the dipsogenic and diuretic effects of captopril. The results suggest that captopril augments the production of vasodilatory prostacyclin. Yet prostanoids have no significant role in the antihypertensive mechanism of captopril in SHR.     

香荚兰乙酮对DOCA盐高血压大鼠血压及大动脉结构的影响

目的观察香荚兰乙酮对醋酸脱氧皮质酮(DOCA)盐高血压大鼠血压及大动脉结构的影响。方法 34只SD大鼠分为假手术组(n=10),DOCA盐高血压模型组(模型组,n=13)和香荚兰乙酮治疗组(治疗组,n=11),模型组和治疗组大鼠于左肾切除术1 wk后开始给药(DOCA 12.5 mg.wk-1皮下注射,1%NaCl饮水;治疗组饮水中加入1.5 mmol.L-1香荚兰乙酮),共5 wk。所有动物在术后wk 2,4,6测定尾动脉血压;6 wk后通过超声活体观察颈总动脉内膜-中膜厚度(IMT),并取胸主动脉测定血管中层厚度。结果模型组大鼠血压呈逐步升高趋势,wk 6治疗组大鼠血压明显下降[(140.6±10.5)mmHg vs.(166.6±13.5)mmHg,P<0.01],胸主动脉中层厚度[(165.52±33.65)μm vs.(194.25±17.91)μm,P<0.05]及颈动脉IMT[(53.33±10.22)μm vs.(78.00±12.96)μm,P<0.05]均显著降低。结论香荚兰乙酮干预可明显降低DOCA盐高血压大鼠尾动脉血压,抑制颈动脉内IMT的增厚,降低胸主动脉中层厚度。     

Effects of beta-adrenergic receptor blocking agents on blood pressure in conscious hypertensive rats.

The effects of beta-adrenergic receptor blocking agents administered i.v. on the blood pressure in conscious spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR) and normotensive Wistar strain rats (NR) were studied. dl-Propranolol and dl-YB-2, 1 mg/kg i.v., caused a sustained rise in blood pressure in SHR and RHR. The maximum response of each beta-blocking agent after phentolamine, 10 mg/kg i.v., in SHR and RHR was significantly larger than that in NR. The potency ratio for the hypertensive activities of the 1- and d-isomers of propranolol and YB-2 was similar to the ratio of their beta-blocking activities. The pressor effects of the beta-blocking agents after phentolamine were significantly inhibited by adrenalectomy, reserpinization and pretreatment with hexamethonium. The results suggest that the pressor effect of the beta-blocking agents may be due to their beta-blocking activities and the unmasking of alpha-receptor activities of the blood vessels. Furthermore, the greater pressor effect of the agents observed in hypertensive rats is attributed to a greater activity of the sympathetic nervous system in these rats as compared to normotensive rats.     

Hypotensive and hypertensive effects of acetaldehyde on blood pressure in rats

Intravenous injection of acetaldehyde produced hypotensive actions in pentobarbital-anaesthetised whole rats, but hypertensive actions in pithed rats. The hypotensive effects of acetaldehyde in whole rats were abolished by pre-treatment with yohimbine. In pithed rats, the hypertensive effects of acetaldehyde were significantly attenuated by prazosin and phentolamine, and in rats that had been pre-treated with reserpine. Our results suggest that the hypertensive actions of acetaldehyde in pithed rats are due to the release of catecholamines, which subsequently leads to vasoconstriction. In whole rats the hypotensive actions of acetaldehyde may be due to alpha2-adrenoceptor stimulation in the central nervous or peripheral system.     

Effect of dietary taurine on blood pressure in spontaneously hypertensive rats

Previous studies have shown the dietary supplementation with sulfur amino acids modified the development of hypertension in rats. In the current study, it was found that the addition of taurine (3%) to the drinking water of rats during the period of 4–14 weeks of age had little effect on blood pressure in normotensive Wistar-Kyoto rats (WKR), and slightly retarded the development of hypertension in spontaneously hypertensive rats (SHR). In the stroke-prone substrain (SHR-SP), however, there is a highly significant reduction in the development of hypertension. The endogenous content of taurine in the liver of SHR-SP is less than 50 per cent of that measured in WKR. The livers of the SHR contain an intermediate amount of taurine. The cysteic acid decarboxylase activity of liver is similar in all three strains. The tissues of animals treated chronically with taurine contain only slightly greater amounts of taurine, with small but significant increases in brain taurine being noted. It appears that genetically hypertensive rats, particularly the SHR-SP substrain, have a defect in taurine metabolism, and that this may be related to the severity of hypertension. There is no evidence to suggest that taurine plays a normal regulatory role in blood pressure maintenance.     

Synergism of hydrochlorothiazide and nitrendipine on reduction of blood pressure and blood pressure variability in spontaneously hypertensive rats

AIM: To investigate the possible synergism of hydrochlorothiazide and nitrendipine on reducing both blood pressure (BP) and blood pressure variability (BPV) in spontaneously hypertensive rats (SHR). METHODS: Seventy animals were randomly divided into seven groups. The doses were 5 and 10 mg/kg for nitrendipine, 10 and 20 mg/kg for hydrochlorothiazide and 10 + 5, 20 + 10 mg/kg, respectively, for the combination of these two drugs and 0.8% carboxymethylcellulose as control. The drugs were given via a catheter of gastric fistula. BP was then continuously recorded for 5 h from 1 h before drug administration to the end of 4th hour after drug administration, in conscious and freely moving rats. RESULTS: The effects on both BP and BPV reduction of the combination of hydrochlorothiazide and nitrendipine were greater than the single drug in SHR. The two drugs possessed an obvious synergism on both systolic blood pressure (q = 1.79 with small dose and q = 1.23 with large dose) and systolic blood pressure variability reduction (q = 1.79 with small dose and q = 1.39 with large dose) in SHR. CONCLUSION: The present work clearly demonstrated that there was a synergistic effect between hydrochlorothiazide and nitrendipine in lowering and stabilizing BP in SHR.     

Effects of potassium adaptation on blood pressure and pressor responses in normotensive and renal hypertensive Wistar rats

Potassium adaptation reduces blood pressure (BP) in hypertensive humans and animals but its effects on normotensive BP and the nature of pressor responses to vasoactive drugs are not known. We measured directly, the mean arterial pressure (MAP) of normotensive control, normotensive potassium-adapted (given 0.75% potassium chloride solution for 5 weeks), renal hypertensive (RHP), and renal hypertensive Wistar rats later adapted to potassium. The maximum percentage change, the ED25, and recovery times after bolus injections of noradrenaline (NA), angiotensin II (Ang. II), sodium nitroprusside (SNP), and acetylcholine (ACh) were compared. The MAP of normotensive potassium-adapted rats was significantly lower than that of the normotensive controls (95.6+/-5.0 vs. 110.8+/-2.8 mmHg, p<0.05). The potassium-adapted hypertensive rats (RHP-A) also had significantly lower MAP values than the non-adapted hypertensive ones (116.0+/-4.4 vs. 138.2+/-4.1 mmHg, p<0.01). Potassium adaptation significantly blunted responses to NA and augmented responses to SNP but while the duration of action of Ang. II was significantly shortened, that of SNP was significantly increased. We conclude that potassium adaptation reduces BP in the normotensive and hypertensive rats and may influence both the degree and duration of action of vasoactive drugs given as bolus injections.     

Effects of potassium supplementation on blood pressure, electrolytes and 3H-norepinephrine release in spontaneously hypertensive rats

Potassium supplementation has been shown to decrease blood pressure in human and animal models of hypertension. The purpose of this study was to determine if potassium supplementation altered sympathetic nerve activity by altering 3H-norepinephrine release in caudal artery preparations of spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Supplementation in the drinking water with 0.5 or 1.0% KCl for 5 weeks lowered blood pressure (19 and 25 mm Hg, respectively) in SHR but had no effect on WKY. The decrease in blood pressure with 0.5% KCl was not accompanied by significant changes in either plasma or cerebrospinal fluid (CSF) sodium or potassium levels in either SHR or WKY. 3H-Norepinephrine release induced by 56 mmol/l KCl was not altered in either SHR or WKY. However, the ability of yohimbine to enhance 3H-norepinephrine release in caudal artery preparations was significantly decreased by potassium supplementation in SHR, but was not affected in WKY. These data suggest that potassium supplementation may alter alpha 2-adrenoceptor activity. Further studies are required to determine if this altered alpha 2-adrenoceptor activity plays a direct role in the blood-pressure-lowering effects of potassium supplementation.