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Objective: To compare the action mechanisms of human and porcine derived erythrocyte-derived depressing factor (h-EDDF and p-EDDF) as well as the effects on blood pressure., Methods: The experiments were carried out in spontaneously hypertensive rats (SHR, n = 5) and two kidney-one click renal hypertensive rats (2K-1C, n = 7). The acute and chronic effects of h-EDDF and p-EDDF on blood pressure were observed, blood pressure test using tail plethysmography under unanaesthetic state. Both EDDF were administrated via jugular vein and/or oral respectively. The isolated thoracic aorta ring perfusion assay was used to examine the effect of EDDF on the asodilation. Primary cultured VSMCs were prepared from the thoracic aorta media of 2K-1C and normal Wistar rats. The effect of EDDF on proliferation of VSMCs were determined by MTT assay. The cell cycle of VSMCs was evaluated by flow cytometric., Results: Both h-EDDF and p-EDDF could significantly decrease blood pressure of Wistar rats through intravenous administration and/or orally (P < 0.01 and P < 0.05 respectively). The contractile response of aorta in 2K-1C rats to PE was significantly enhanced compared with that of the control (P < 0.01) and both EDDF (10(-3) g/ml) remarkably induced a vasodilation with endothelium-dependent manner in SHR and 2K-1C rats (P < 0.05). h-EDDF and p-EDDF could significantly inhibit the proliferation of VSMCs from 2K-1C and control rats. After 24 hours of exposure to EDDFs the cell number of G0/G1 phase obviously increased and cell number in S phase was decreased (P < 0.01, respectively)., Conclusions: It seems that the effects of h-EDDF and p-EDDF on blood pressure and vasodilation as well as inhibition of VSMCs proliferation and regulation of cell cycle have no significant difference.

This study observed the depressor effects of erythrocyte antihypertensive factor (AHF) from spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats on SHR, renal hypertensive rats (RHR) and their control animals. Blood pressure (BP) tests were carried out in two parts. Chronic experiment: Six-month-old male rats weighing 200-300 g were divided into six groups: (1) Stroke prone SHR (SHRsp, n = 5); (2) WKY (n = 4); (3) RHR (n = 4); (4) Wistar (n = 4). The rats in each group were given intraperitoneal injections of AHF (10 mg/100 g BW) once. The rats in groups (5) and (6) were injected with normal saline as control. BP was measured just prior to injection and at 0.5, 1, 3, 6, 24 h and 24 h intervals thereafter. BP in SHRsp dropped (from 180.0 +/- 11.5 to 145.0 +/- 12.6, P less than 0.05). Within 24 h there was a further reduction, and the average value of the fall was 65 mmHg (P less than 0.01). BP remained significantly depressed for 4 days and did not recover until the seventh day. In contrast to the effect of this extract on SHR, the BP in WKY rats did not appear to be affected. Normal saline injected intraperitoneally did not lower BP in either SHRsp or WKY rats. BP in RHR rats showed a profound decrease within 3 h, with the average value for the drop being 56 mmHg (P less than 0.001). BP recovered to normal at 6 h. Acute group: Three SHRsp rats with BP 180.0 +/- 5.8 mmHg and weighing 231.0 +/- 11.2 g were anesthetized with sodium pentobarbital. AHF was injected into the femoral vein (0.35 mg/100 g BW). The results showed that the BP markedly decreased after administration of the extract, and the average value for the drop was 35 mmHg (P less than 0.05). The BP did not show any obvious change after injection of WKY rat extract.

Aorta segments (A) and mesenteric arteries (MA) from stroke prone spontaneously hypertensive rats (SHRsp) and control Wistar Kyoto rats (WKY) were used in the present study to assess the effect of AHF on Ca2+ influx in vascular smooth muscle (VSM). The results indicated that Ca2+ influx in VSM of SHRsp was much higher than that of WKY rats (P less than 0.05). AHF at 10(-7), 10(-6) and 10(-5) g/ml can significantly inhibit Ca2+ influx in a dose-dependent manner in VSM of both A and MA (P less than 0.05 and less than 0.01). The suppression effect of AHF on Ca2+ influx and the concentration-dependent relationship were more obvious in MA than in A. The Ca2+ influx in VSM of WKY rats was unaffected by administration of AHF.