Abstract Title:

Piperine, active substance of black pepper, alleviates hypertension induced by NO synthase inhibition.

Abstract Source:

Bratisl Lek Listy. 2010;111(8):426-31. PMID: 21033621

Abstract Author(s):

L Hlavackova, A Urbanova, O Ulicna, P Janega, A Cerna, P Babal

Article Affiliation:

Department of Pathology, Faculty of Medicine, Comenus University, Bratislava, Slovakia.


OBJECTIVES: The presented study is aimed on exploring the effects of black pepper on blood pressure in the rat model of experimental hypertension induced by chronic NO synthesis inhibition.

BACKGROUND: Piperine, the compound of black pepper, can cause a significant decrease of blood pressure in normotensive rats possibly via calcium channel blockade, a pathway that is known to be effective in prevention of L-NAME (N(G)-nitro-L-arginine methyl ester) induced hypertension.

METHODS: Wistar rats were administered clear water (C), L-NAME (40 mg/kg/day, L), piperine (20 mg/kg/day) in corn oil by oral gavage with L-NAME (LP) or without it (P) for 6 weeks. The systolic blood pressure was measured weekly. Specimens of thoracic aorta were processed in paraffin and histological slices were stained with hematoxylin and eosin, Mallory's phosphotungstic acid hematoxylin (PTAH), orcein, antibodies against inducible NO synthase (iNOS) and smooth muscle cells actin (SMCA). Microscopic pictures were digitally processed and morphometrically evaluated.

RESULTS: L-NAME increased the blood pressure, cross-sectional area of aorta, media thickness, elastin and SMCA synthesis and PTAH positive myofibrils relative and absolute content in the aortic media, wheras it decreased percentual content of iNOS, elastin and SMCA. Piperine decreased the blood pressure rise from the third week of treatment, synthesis of elastin and the percentual and absolute content of PTAH positive myofibrils, however, it did not affect other parameters.

CONCLUSION: Oral administration of piperine is able to partially prevent the increase of blood pressure caused by chronic L-NAME administration. This effect is probably caused by the blockage of voltage-dependent calcium channels and supported by filamentous actin disassembly (Tab. 1, Fig. 2, Ref. 35).

Study Type : Animal Study
Additional Links
Pharmacological Actions : Hypotensive : CK(467) : AC(63)

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