Gynura procumbens inhibit angiotensin-converting enzyme in spontaneously hypertensive rats. - GreenMedInfo Summary
Inhibition of angiotensin-converting enzyme activity by a partially purified fraction of Gynura procumbens in spontaneously hypertensive rats.
Med Princ Pract. 2007;16(3):203-8. PMID: 17409755
Department of Physiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
OBJECTIVES: To investigate the hypotensive and angiotensin-converting enzyme (ACE) inhibitory activities of a partially purified fraction (FA-I) of the leaves of Gynura procumbens and to qualitatively analyse the putative compounds present in the fraction.
MATERIALS AND METHODS: The hypotensive effect of FA-I was tested in both spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) by an intravenous administration of 0-10 mg/kg of the FA-I. Administration of captopril (20 microg/kg) served as the control. In vitro 0.0-2.0 mg/ml FA-I was added to a mixture of ACE and hippuryl-L-histidyl-L-leucine and assayed by a modification of the colourimetric method of Hurst and Lovell-Smith. All blood pressure measurements were monitored by the Macintosh MacLab set-up. ACE activity was measured by an in vitro assay in which the enzymatic cleavage of hippuryl-L-histidyl-L-leucine to form histidyl-leucine and hippurate was determined colourimetrically by a cyanuric chloride/dioxane reagent.
RESULTS: The FA-I produced a marked dose-dependent reduction in mean arterial pressure (MAP) in SHR and WKY rats, with an ED(50) of 1.09 and 1.05 mg/kg, respectively (p<0.01). Furthermore, FA-I at 10 mg/kg strongly inhibited the angiotensin I-induced rise in MAP (p<0.01). This response was comparable to that of captopril at 20 microg/kg. In the in vitro assay, ACE activity was inhibited with an IC(50) of 0.8 mg/ml. The qualitative phytochemical analysis of FA-I indicated the presence of glycoconjugates and peptides.
CONCLUSION: These results suggest that the hypotensive effect of G. procumbens may be due, in part, to the glycoconjugated or peptidal substances found in FA-I that exhibit an inhibitory effect on ACE.