Related Experiment Videos
Piperine, active substance of black pepper, alleviates hypertension induced by NO synthase inhibition
L Hlavackova1, A Urbanova, O Ulicna
1Department 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).
Related Concept Videos
Antihypertensive Drugs: Vasodilators
Treatment for Pulmonary Arterial Hypertension: Phosphodiesterase Inhibitors
Among the PDE5 inhibitors, sildenafil (Revatio) stands out as a competitive and selective inhibitor. It operates by elevating cellular levels of cGMP and augmenting signaling through the cGMP-PKG pathway, promoting vasodilation. Upon oral...
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally, α1-blockers effectively address urinary obstruction...