Crocin prevents acute angiotensin II-induced hypertension in anesthetized rats

OBJECTIVE Angiotensin II (Ang II), the main product of renin-angiotensin system (RAS) has a well-known role in cardiovascular regulation. Over-production of Ang II is one of the important underlying mechanisms of hypertension. In this study, the effect of crocin on cardiovascular responses in rats with acute hypertension induced by Ang II was evaluated. MATERIALS AND METHODS Rats were divided into six groups (n = 6): 1) Control: rats that received saline, 2) Ang II: rats that received Ang II (300 ng/kg) infused in two min, 3) Losartan (Los) + Ang II : rats that received Los (10 mg/kg, i.v) before Ang II, and 4-6) Crocin (Cro) + Ang II groups: rats that received three doses of crocin (50, 100 and 200 mg/kg, slow i.v) 10 min before Ang II. Femoral artery and vein were cannulated for recording of cardiovascular parameters and injection of drugs, respectively. Systolic blood pressure (SBP), mean arterial blood pressure (MAP) and heart rate (HR) were continuously recorded by power lab system. After injection of reagents and extracts, maximum changes (∆) of MAP, SBP and HR were recorded and compared with control group. RESULTS Ang II (300 ng/kg) increased maximal changes in MAP, SBP and HR compared to control group (p<0.001) and Los significantly attenuated these effects of Ang II (p<0.001). Maximal changes of MAP, SBP and HR induced by Ang II, were significantly attenuated by pretreatment with all doses of crocin (50,100 and 200) (p<0.05 and p<0.001). Also, changes of MAP, SBP and HR in Crocin + Ang II groups were significantly different from Los + Ang II group (p<0.05 and p<0. 01). CONCLUSION Based on the effects of crocin on acute Ang II-induced hypertension, it is hypothesized that the cardiovascular improving effects of crocin may be mediated via suppressing of RAS.