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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

Light photomicrographs of rat (i) heart (ii) kidney and (iii) thoracic aorta in different experimental groups
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Figure 5: Light photomicrographs of rat (i) heart (ii) kidney and (iii) thoracic aorta in different experimental groups

Mentions: Chronic oral administration of L-NAME over 4 weeks caused morphological abnormalities such as moderate diffuse myocardial degeneration and necrosis with inflammatory infiltration in heart muscles [Figure 5(i)] while cystic dilation of tubules, atrophy of the tubular epithelium and fewer glomeruli with mild degree increase in glomerular filtration space in the kidney [Figure 5(ii)]. These abnormalities were partially prevented by treatment with OA. There was no abnormality detected in the thoracic aorta in any of the group [Figure 5(iii) c].


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)

Light photomicrographs of rat (i) heart (ii) kidney and (iii) thoracic aorta in different experimental groups
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Light photomicrographs of rat (i) heart (ii) kidney and (iii) thoracic aorta in different experimental groups
Mentions: Chronic oral administration of L-NAME over 4 weeks caused morphological abnormalities such as moderate diffuse myocardial degeneration and necrosis with inflammatory infiltration in heart muscles [Figure 5(i)] while cystic dilation of tubules, atrophy of the tubular epithelium and fewer glomeruli with mild degree increase in glomerular filtration space in the kidney [Figure 5(ii)]. These abnormalities were partially prevented by treatment with OA. There was no abnormality detected in the thoracic aorta in any of the group [Figure 5(iii) c].

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