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Oleanolic Acid Prevents Increase in Blood Pressure and Nephrotoxicity in Nitric Oxide Dependent Type of Hypertension in Rats.

Bachhav SS, Bhutada MS, Patil SP, Sharma KS, Patil SD - Pharmacognosy Res (2014 Oct-Dec)

Bottom Line: OA produced a small, though nonsignificant, increase in the NOx level.L-NAME administration did not affect cardiac mass index.However, OA has nonsignificantly affected the NO levels.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Dhule, Maharashtra, India.

ABSTRACT

Background: Recently, we have reported antihypertensive activity of oleanolic acid (OA) in glucocorticoid-induced hypertension with restoration of nitric oxide (NO) level. However, the involvement of NO-releasing action of OA was unclear.

Objective: To explore antihypertensive activity of OA in N(ω)-nitro-L-arginine methyl ester (L-NAME) hypertensive rats wherein NO is completely blocked, which would allow exploring the possibility of involvement of NO-releasing action of OA.

Materials and methods: Five groups of rats were investigated as normal control, L-NAME (40 mg/kg/day), L-NAME + enalapril (15 mg/kg/day), L-NAME + l-arginine (100 mg/kg/day), and L-NAME + OA (60 mg/kg/day) for 4 weeks. The systolic blood pressure, body weight, and heart rate were measured weekly for 4 weeks. Serum nitrate/nitrite (NOx) level, urine electrolytes concentration, cardiac mass index, and serum creatinine level were determined followed by organ histopathology.

Results: OA and enalapril delayed the rise in blood pleasure following L-NAME administration. Decreased serum NOx level was not significantly increased with any of the treatment. OA produced a small, though nonsignificant, increase in the NOx level. L-NAME administration did not affect cardiac mass index. There was an increase in serum creatinine upon L-NAME administration which was prevented by OA. Decreased urine volume, urine sodium and potassium were reversed by OA.

Conclusion: These results suggest that the antihypertensive effect of OA in L-NAME hypertension is due to diuresis and nephroprotection. However, OA has nonsignificantly affected the NO levels.

No MeSH data available.


Related in: MedlinePlus

Effect of different treatments on blood pressure: (A) Time course of systolic blood pressure (SBP in mmHg) measured using the tail cuff method; (B) Mean arterial blood pressure (MABP in mmHg) on Day 28 measured by invasive carotid artery cannulation. Data expressed as mean ± SEM. N= number of rats **p < 0.01, ***p < 0.001 compared with basal SBP (at week 0) (within the group comparison) using one-way ANOVA followed by Bonferroni as a post-ANOVA test. ap < 0.05, bp < 0.01, cp < 0.001 compared with NORM-CON; αp < 0.05, βp < 0.01, γp < 0.001 compared with L-NAME control (inter-group comparison) using two-way (for SBP) and one way ANOVA (for MABP on Day 28) followed by Bonferroni as a post-ANOVA test
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Figure 1: Effect of different treatments on blood pressure: (A) Time course of systolic blood pressure (SBP in mmHg) measured using the tail cuff method; (B) Mean arterial blood pressure (MABP in mmHg) on Day 28 measured by invasive carotid artery cannulation. Data expressed as mean ± SEM. N= number of rats **p < 0.01, ***p < 0.001 compared with basal SBP (at week 0) (within the group comparison) using one-way ANOVA followed by Bonferroni as a post-ANOVA test. ap < 0.05, bp < 0.01, cp < 0.001 compared with NORM-CON; αp < 0.05, βp < 0.01, γp < 0.001 compared with L-NAME control (inter-group comparison) using two-way (for SBP) and one way ANOVA (for MABP on Day 28) followed by Bonferroni as a post-ANOVA test

Mentions: Figure 1a and b shows the time course effects of different treatments on the SBP of rats and day 28 MABP from different groups, respectively. At the beginning of the experiment, the baseline SBP values did not differ among the different experimental groups. SBP of the L-NAME group was raised by 47.3% after L-NAME administration for 28 days (p < 0.001 vs. day 0) which was significantly different from NORM-CON rats (p < 0.001). Similarly, MABP of rats of L-NAME group after invasive BP measurement was significantly increased from that of NORM-CON (p < 0.001). On day 28, the SBP and MABP of the rats in the ENALAPRIL (p < 0.001) and OA60 (p < 0.001 and p < 0.05, respectively) groups were lower than that of those in the L-NAME group. An increase in the SBP and MABP due to NO inhibition was not prevented significantly in the L-ARG group.


Oleanolic Acid Prevents Increase in Blood Pressure and Nephrotoxicity in Nitric Oxide Dependent Type of Hypertension in Rats.

Bachhav SS, Bhutada MS, Patil SP, Sharma KS, Patil SD - Pharmacognosy Res (2014 Oct-Dec)

Effect of different treatments on blood pressure: (A) Time course of systolic blood pressure (SBP in mmHg) measured using the tail cuff method; (B) Mean arterial blood pressure (MABP in mmHg) on Day 28 measured by invasive carotid artery cannulation. Data expressed as mean ± SEM. N= number of rats **p < 0.01, ***p < 0.001 compared with basal SBP (at week 0) (within the group comparison) using one-way ANOVA followed by Bonferroni as a post-ANOVA test. ap < 0.05, bp < 0.01, cp < 0.001 compared with NORM-CON; αp < 0.05, βp < 0.01, γp < 0.001 compared with L-NAME control (inter-group comparison) using two-way (for SBP) and one way ANOVA (for MABP on Day 28) followed by Bonferroni as a post-ANOVA test
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4660519&req=5

Figure 1: Effect of different treatments on blood pressure: (A) Time course of systolic blood pressure (SBP in mmHg) measured using the tail cuff method; (B) Mean arterial blood pressure (MABP in mmHg) on Day 28 measured by invasive carotid artery cannulation. Data expressed as mean ± SEM. N= number of rats **p < 0.01, ***p < 0.001 compared with basal SBP (at week 0) (within the group comparison) using one-way ANOVA followed by Bonferroni as a post-ANOVA test. ap < 0.05, bp < 0.01, cp < 0.001 compared with NORM-CON; αp < 0.05, βp < 0.01, γp < 0.001 compared with L-NAME control (inter-group comparison) using two-way (for SBP) and one way ANOVA (for MABP on Day 28) followed by Bonferroni as a post-ANOVA test
Mentions: Figure 1a and b shows the time course effects of different treatments on the SBP of rats and day 28 MABP from different groups, respectively. At the beginning of the experiment, the baseline SBP values did not differ among the different experimental groups. SBP of the L-NAME group was raised by 47.3% after L-NAME administration for 28 days (p < 0.001 vs. day 0) which was significantly different from NORM-CON rats (p < 0.001). Similarly, MABP of rats of L-NAME group after invasive BP measurement was significantly increased from that of NORM-CON (p < 0.001). On day 28, the SBP and MABP of the rats in the ENALAPRIL (p < 0.001) and OA60 (p < 0.001 and p < 0.05, respectively) groups were lower than that of those in the L-NAME group. An increase in the SBP and MABP due to NO inhibition was not prevented significantly in the L-ARG group.

Bottom Line: OA produced a small, though nonsignificant, increase in the NOx level.L-NAME administration did not affect cardiac mass index.However, OA has nonsignificantly affected the NO levels.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, R. C. Patel Institute of Pharmaceutical Education and Research, Shirpur, Dhule, Maharashtra, India.

ABSTRACT

Background: Recently, we have reported antihypertensive activity of oleanolic acid (OA) in glucocorticoid-induced hypertension with restoration of nitric oxide (NO) level. However, the involvement of NO-releasing action of OA was unclear.

Objective: To explore antihypertensive activity of OA in N(ω)-nitro-L-arginine methyl ester (L-NAME) hypertensive rats wherein NO is completely blocked, which would allow exploring the possibility of involvement of NO-releasing action of OA.

Materials and methods: Five groups of rats were investigated as normal control, L-NAME (40 mg/kg/day), L-NAME + enalapril (15 mg/kg/day), L-NAME + l-arginine (100 mg/kg/day), and L-NAME + OA (60 mg/kg/day) for 4 weeks. The systolic blood pressure, body weight, and heart rate were measured weekly for 4 weeks. Serum nitrate/nitrite (NOx) level, urine electrolytes concentration, cardiac mass index, and serum creatinine level were determined followed by organ histopathology.

Results: OA and enalapril delayed the rise in blood pleasure following L-NAME administration. Decreased serum NOx level was not significantly increased with any of the treatment. OA produced a small, though nonsignificant, increase in the NOx level. L-NAME administration did not affect cardiac mass index. There was an increase in serum creatinine upon L-NAME administration which was prevented by OA. Decreased urine volume, urine sodium and potassium were reversed by OA.

Conclusion: These results suggest that the antihypertensive effect of OA in L-NAME hypertension is due to diuresis and nephroprotection. However, OA has nonsignificantly affected the NO levels.

No MeSH data available.


Related in: MedlinePlus