ABSTRACT
Platonia insignis Mart. (Clusiaceae) is a medicinal plant from the Brazilian Amazon region. The present study evaluated the biological potential of the ethanol extract (Pi-EtOH) and ethyl acetate fraction (Pi-EtOAc) of the P. insignis fruit shells on the cardiovascular system of rats. Pi-EtOH or Pi-EtOAc (12.5, 25, and 50 mg/kg) was administered intravenously in normotensive rats (260-300 g), and the mean arterial pressure and the heart rate were monitored. The Pi-EtOH induced hypotension (-11.56±0.89, -7.43±0.85, and -17.56±1.97 mmHg) followed by bradycardia in two highest doses (-8.89±3.62 and -15.79±1.83 beats/min) and Pi-EtOAc, at the same doses, induced hypotension (-11.2±1.03, -14.48±1.13, -29.89±2.67 mmHg) more intensively, followed by tachycardia at the dose 12.5 and 25 mg/kg (15.64±2.06, 19.31±1.92 beats/min) and bradycardia at a dose of 50 mg/kg (-9.98±7.33 beats/min). The hypotensive response from Pi-EtOAc was not attenuated when used in the pretreatment with L-NAME, verapamil, propranolol, and hexamethonium. However, when using yohimbine, the hypotensive effect was inhibited (-4.42±1.28 (P<.05), -3.29±0.99 (P<.05), 2.06±1.18 mmHg (P<.05); Student's t-test). Hence, the Pi-EtOAc seems to act similarly to the α2-adrenergic agonist in this hypotensive effect.
Subject(s)
Adrenergic alpha-2 Receptor Agonists/administration & dosage , Antihypertensive Agents/administration & dosage , Clusiaceae/chemistry , Hypertension/drug therapy , Plant Extracts/administration & dosage , Receptors, Adrenergic, alpha-2/metabolism , Animals , Blood Pressure/drug effects , Heart Rate/drug effects , Humans , Hypertension/genetics , Hypertension/metabolism , Hypertension/physiopathology , Male , Rats , Rats, Wistar , Receptors, Adrenergic, alpha-2/geneticsABSTRACT
Administration of ethanol extract of stem bark from Z. rhoifolium (EEtOH-ZR) induced hypotension associated with a dual effect in heart rate in normotensive rats. This response was highlighted in spontaneously hypertensive rats (SHR). In rat superior mesenteric artery rings, the cumulative addition of EEtOH-ZR (0.1-750 microg/mL) on a phenylephrine-induced pre-contraction (10(-5) M) promoted a vasorelaxant effect by a concentration-dependent manner and independent of vascular endothelium. A similar effect was obtained on KCl-induced pre-contractions (80 mM). EEtOH-ZR attenuated contractions induced by cumulative addition of CaCl2 (10(-6)-3 x 10(-2) M) in depolarizing medium without Ca2+ only at 500 or 750 microg/mL. Likewise, on S-(-)-Bay K 8644-induced pre-contractions (10(-7) M), the EEtOH-ZR-induced vasorelaxant effect was attenuated. EEtOH-ZR (27, 81, 243 or 500 microg/mL) inhibited contractions induced by cumulative addition of phenylephrine (10(-9) - 10(-5) M) in endothelium-denuded preparations or by a single concentration (10(-5) M) in a Ca(2+)-free medium. The involvement of K+ channels was evaluated by tetraethylammonium (3 mM); the EEtOH-ZR-induced vasorelaxation was not attenuated. Thus, calcium influx blockade through voltage-operated calcium channels (CavL) and inhibition of calcium release from intracellular stores are probably underlying EEtOH-ZR-induced cardiovascular effects.
