Acute Hypertensive Rats Research Articles

Hypotensive effect of Centella asiatica L. extract in acute Angiotensin II-induced hypertension

Centella asiatica L. (C.asiatica) is a plant with a hypotensive effect. Since this effect has several mechanism(s), therefore in the current study we investigated the effects of hydroalcoholic extract of C.asiatica on cardiovascular parameters in acute hypertensive rats. Animals were divided into four groups; 1) control, 2) Angiotensin II (AngII) that received (50 ng/kg) intravenously (i.v.), 3 and 4) two groups of C.asiatica extract (CA100, and CA200 mg/kg). In treated groups, 30 min after injection of the extract, AngII was injected. Cardiovascular parameters were recorded by the power lab system after the cannulation of the femoral artery. The maximum changes (∆) of systolic blood pressure (SBP), mean arterial pressure (MAP) and heart rate (HR) were calculated and used for statistical analysis. In the AngII group, ΔSBP and ΔMAP significantly increased compared to the control group. The HR also decreased compared to the control group but it was not significant. In CA100+AngII group ΔSBP and ΔMAP significantly decreased compared to the AngII. The use of these doses of CA with AngІІ compared to AngІІ alone had a significant effect on the HR. In CA200+AngII group ΔSBP and ΔMAP significantly decreased compared to the AngII. The change of HR in this dose was not significant to the AngII. In a recent study, we concluded that C.asiatica decreased the cardiovascular responses in hypertensive rats received AngII. Also between two doses of C.asiatica did not observe any significant difference. Therefore, one of the most important hypotensive mechanism(s) of the considered plant can be the effect on Renin-angiotensin system.

Cardiovascular effects of standardized hydroalcoholic extract of Ribes khorasanicum fruit in acute hypertensive rats.

Ribes khorasanicum (R. khorasanicum) traditionally has been used for the treatment of higher blood pressure. In this study, the effect of hydroalcoholic extract of R. khorasanicum fruit in normotensive and hypertensive rats was evaluated. Animals were assigned into the following groups: 1) Control, 2) AngII (50 ng/kg), 3) AngII + losartan (Los, 10 mg/kg) and 4-6) Doses 4, 12 and 24 mg/kg of extract +AngII groups. AngII and Los were injected intravenously and the extract was injected intraperitoneal. In R. khorasanicum groups, AngII injected 30 after injection of the extract. The femoral artery was cannulated and mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) were recorded by Power Lab software. Maximal changes (∆) of cardiovascular responses were determined and compared with those of control and AngII groups. Finally, oxidative stress parameters in the heart and aorta were also determined. In normotensive rats, 12 mg/kg of the extract showed significant hypotensive effects while 24 mg/kg produced significant tachycardia. Increased ∆SBP and ∆MAP in AngII group were significantly blunted by Los. Doses 4 and 12 mg/kg of the plant also significantly attenuate the effect of AngII on ∆SBP and ∆MAP. Tachycardia induced by 24 mg/kg of the extract didn't affect by AngII. Extract also significantly improved the effect of AngII on MDA, total thiol content, CAT and SOD in both heart and aorta tissues. R. khorasanicum at lower doses showed hypotensive effects and attenuated cardiovascular parameters in hypertensive rats via its antioxidant effects.

Preventive Effect of Hydroalcoholic Extract of Rosa damascena on Cardiovascular Parameters in Acute Hypertensive Rats Induced by Angiotensin II.

Background:Rosa damascena (R.D) is an aromatic plant with numerous therapeutic effects including cardiovascular effect. The mechanism cardiovascular effect of R.D is unclear and suggested mediated through renin–angiotensin system (RAS). Therefore, in this study, the role of hydroalcoholic extract of R.D on acute hypertension induced by AngII was evaluated.Methods:After anesthesia, femoral artery and vein of rats were cannulated for recording cardiovascular responses and drug injection, respectively. Systolic blood pressure (SBP), mean arterial blood pressure (MAP), and heart rate (HR) were recorded continuously by power lab software. Rats were divided into saline, AngII (50 ng/kg), AngII + Losartan (10 mg/kg), and three groups of R.D extract (250, 500, and 1000 mg/kg). Losartan and AngII were administered intravenously and the other ones intraperitoneal. In the R.D groups, 30 min after injection of the extract, AngII was injected and the maximum changes in SBP, MAP, and HR were calculated and compared to that in control and AngII groups.Results:Results show that AngII significantly increased SBP, MAP, and decreased HR than the control group which was blocked by losartan. SBP and MAP in R.D + AngII groups were significantly lower than AngII alone (P < 0.05 –P < 0.001). Only MAP in higher dose (1000 mg/kg) was significantly lower than low dose (250 mg/kg; P < 0.05). Two higher doses also significantly decreased bradycardia induced by AngII (P < 0. 01).Conclusions:The preventive effect of hydroalcoholic extract of R.D on cardiovascular parameters maybe is mediated by suppression of AngII activity.

Antihypertensive Responses Elicited by Central Moxonidine in Rats: Possible Role of Nitric Oxide

In the present study, we investigated the effects of pretreatment with NG-nitro-L-arginine methyl ester (L-NAME) (nitric oxide synthase inhibitor) injected intravenously (IV) on the hypotension, bradycardia, and vasodilation produced by moxonidine (alpha2-adrenergic/imidazoline receptor agonist) injected into the fourth brain ventricle (4th V) in rats submitted to acute hypertension that results from baroreflex blockade by bilateral injections of kynurenic acid (kyn, glutamatergic receptor antagonist) into the nucleus of the solitary tract (NTS) or in normotensive rats. Male Wistar rats (n=5 to 7/group) anesthetized with IV urethane (1.0 g kg(-1) of body weight) and alpha-chloralose (60 mg kg(-1) of body weight) were used. Bilateral injections of kyn (2.7 nmol 100 nL(-1)) into the NTS increased baseline mean arterial pressure (148 +/- 11 mm Hg, vs. control: 102 +/- 4 mm Hg) and baseline heart rate (417 +/- 11 bpm, vs. control: 379 +/- 6 bpm). Moxonidine (20 nmol microL(-1)) into the 4th V reduced mean arterial pressure and heart rate to similar levels in rats treated with kyn into the NTS (68 +/- 9 mm Hg and 359 +/- 7 bpm) or in control normotensive rats (66 +/- 7 mm Hg and 362 +/- 8 bpm, respectively). The pretreatment with L-NAME (25 micromol kg, IV) attenuated the hypotension produced by moxonidine into the 4th V in rats treated with kyn (104 +/- 6 mm Hg) or in normotensive rats (95 +/- 8 mm Hg), without changing bradycardia. Moxonidine into the 4th V also reduced renal, mesenteric, and hindquarter vascular resistances in rats treated or not with kyn into the NTS and the pretreatment with L-NAME IV reduced these effects of moxonidine. Therefore, these data indicate that nitric oxide mechanisms are involved in hypotension and mesenteric, renal, and hindquarter vasodilation induced by central moxonidine in normotensive and in acute hypertensive rats.

A new inorganic vasodilator, trans-[Ru(NO)(NH 3) 4(POEt) 3](PF 6) 3: hypotensive effect of endothelium-dependent and -independent vasodilators in different hypertensive animals models

The hypotensive effect of RuNO was investigated in acute and chronic hypertensive rats, as well as in normotensive rats. Acute hypertension rats were used with 30% increase on basal BP (phenylephrine, angiotensin II (Ang II), N G-nitro- l-arginine methyl ester ( l-NAME), and adult spontaneously hypertensive rats (SHR) (basal BP 168±3 mm Hg) were used as models for chronic hypertension. Rats were implanted with catheters (iv/ia) for BP measurements and for in bolus administration of RuNO, sodium nitroprusside (SNP), and acetylcholine (Ach) (10, 20, 40 nmol/kg, iv). The principal findings of this study were: (i) The hypotensive response to RuNO was 150% higher in acutely (phenylephrine and Ang II) and chronically (SHR) hypertensive rats than in normotensive rats, except in the case of l-NAME-induced hypertension ( ΔMAP=10±1.4 mm Hg). Chronic SHR showed 60% increase ( ΔMAP=19±0.8 mm Hg) in the effect compared to normotensive rats. (ii) The hypotensive response to SNP was lower (60%) in hypertensive rats than in normotensive rats, when compared to RuNO. However, the responses were similar in l-NAME-induced hypertension ( ΔMAP=30±2 mm Hg). (iii) The vasodilator response to Ach was increased in rats with Ang II-induced hypertension ( ΔMAP=53±1 mm Hg) and in SHR ( ΔMAP=67±3 mm Hg). RuNO response was more potent than SNP in hypertensive models and the increment in relation to normotensive was observed in the phenylephrine- and l-NAME-treated rats. This response could be correlated to the different endothelial dysfunction present in each model.

In vivo effects of the controlled NO donor/scavenger ruthenium cyclam complexes on blood pressure

Ruthenium(II/III) complexes able to bind and release NO • were tested in vivo, in conscious Wistar rats instrumented for continuous blood pressure (BP) measurement and administration of in bolus injections (5 to 100 nmol/Kg i.v.) of trans-[Ru IICl(NO +)(cyclam)](PF 6) 2 (cyclam-NO) or sodium nitroprusside (SNP). For normotensive rats, cyclam-NO produced a sustained 10% BP reduction of basal MAP during 7 ± 0.4 to 11 ± 0.3 min. In acute hypertensive rats, cyclam-NO produced BP reduction 3-fold larger than in normotensive rats and similar to that of SNP (maximal effect: 41 ± 1.3 vs. 45 ± 2.2 mmHg, respectively). However, the duration of the effect of cyclam-NO was 13 to 21-fold longer than that of SNP. The hypotensive effect of cyclam-NO was fully blocked in presence of continuous infusion of a NO • scavenger, carboxy-PTIO (6 mmol/Kg/min), or of the inhibitor of cGMP activation, methylene blue (83 nmol/Kg/min), or of the cyclam-NO precursor, trans-[RuCl(tfms)(cyclam)](tfms) (cyclam-tfms) (500 mmol/Kg/min). The long lasting BP reduction of cyclam-NO can be interpreted in terms of a slower rate of NO • release (k -NO = 2.2 × 10 −3 s −1 at 35 °C) following chemical reduction (E 0′ = 0.10 V vs NHE). In summary, cyclam-NO showed an hypotensive effect around 20 times longer than SNP in either normotensive or hypertensive rats, which was completely inhibited by methylene blue or carboxy-PTIO. Continuous infusion of cyclam-tfms completely blocked the hypotensive effect of cyclam-NO by scavenging the NO • released by the reduced cyclam-NO.

Silicon in the blood vessel wall: A biological entity?

Frequent observations showing the presence of high Si-peaks in X-ray microanalytical spectra from Epon-embedded periphery blood vessels in the rat resulted in a more detailed and specific study of this problem. Experiments on two untreated, four metabolically disordered and four hypertensive rats are described from 411 measurements. Si was confined to the lumina of the vessels, the erythrocytes, the cytoplasm of endothelia and smooth muscle cells. The nuclei of all the cells analysed were found to be free, or nearly free, of Si. Acute hypertensive rats contained two to three times more Si than the control animals. The validity of these findings and values is discussed in relation to the possibility of artificial contamination, resolution problems and dislocation of ions, together with the pathogenic role of Si in hypertension and atherosclerosis.