Fioretti Alexandre C, Ogihara Cristiana A, Cafarchio Eduardo M, Venancio Daniel P, de Almeida Roberto Lopes, Antonio Bruno B, Sato Monica A
Department of Morphology and Physiology, Faculdade de Medicina do ABC, Santo Andre, SP, Brazil.
Department of Morphology and Physiology, Faculdade de Medicina do ABC, Santo Andre, SP, Brazil.
Vascul Pharmacol. 2017 Dec;99:53-64. doi: 10.1016/j.vph.2017.09.007. Epub 2017 Oct 3.
Venous and arterial walls are responsive to sympathetic system and circulating substances, nevertheless, very few is known about the venous blood flow regulation simultaneously to arterial vascular beds. In this study, we compared the venous and arterial blood flow regulation in visceral and muscular beds upon injection of different doses of vasoactive drugs which act in arterial vascular beds. Anesthetized adult male Wistar rats underwent to right femoral artery and vein cannulation for hemodynamic recordings and infusion of drugs. Doppler flow probes were placed around the left renal artery and vein, and left femoral artery and vein to evaluate the changes in flood flow. Phenylephrine (PHE) injection (α-adrenergic receptor agonist) elicited vasoconstriction in all arteries and veins. Intravenous prazosin (PZS) (1mg/kg, α-adrenergic receptor blocker) caused renal artery vasodilation, but not in the other beds. Vasoconstrictor effect of PHE was abolished by PZS in all vascular beds, except in femoral vein. Phentolamine (PTL) injection (1mg/kg, α/α-adrenergic receptor blocker) produced renal artery vasodilation with no change in other beds. After PTL, the vasoconstriction evoked by PHE was abolished in all vascular beds. Sodium Nitroprusside (SNP), a nitric oxide donor, elicited vasodilation in all beds, and after PTL but not post PZS injection, SNP enhanced the vasodilatory effect in femoral vein. Our findings suggest that the vasoconstriction in renal and femoral veins is mediated by different subtypes of α-adrenoceptors. The nitric oxide-dependent vasodilation in femoral vein enhances when α-adrenoceptors are not under stimulation, but not in the other vascular beds investigated.
静脉壁和动脉壁对交感神经系统和循环物质有反应,然而,关于静脉血流与动脉血管床同时调节的情况却知之甚少。在本研究中,我们比较了在注射作用于动脉血管床的不同剂量血管活性药物后,内脏和肌肉床中静脉和动脉血流的调节情况。对成年雄性Wistar大鼠进行麻醉,然后对其右股动脉和静脉进行插管,以记录血流动力学并输注药物。将多普勒血流探头置于左肾动脉和静脉以及左股动脉和静脉周围,以评估血流变化。注射去氧肾上腺素(PHE)(α-肾上腺素能受体激动剂)可引起所有动脉和静脉的血管收缩。静脉注射哌唑嗪(PZS)(1mg/kg,α-肾上腺素能受体阻滞剂)可使肾动脉血管舒张,但对其他血管床无此作用。除股静脉外,PZS可消除PHE在所有血管床中的血管收缩作用。注射酚妥拉明(PTL)(1mg/kg,α/α-肾上腺素能受体阻滞剂)可使肾动脉血管舒张,而其他血管床无变化。注射PTL后,PHE引起的血管收缩在所有血管床中均被消除。一氧化氮供体硝普钠(SNP)可使所有血管床血管舒张,在注射PTL后而非PZS后,SNP可增强股静脉的血管舒张作用。我们的研究结果表明,肾静脉和股静脉中的血管收缩由不同亚型的α-肾上腺素能受体介导。当α-肾上腺素能受体未受刺激时,股静脉中依赖一氧化氮的血管舒张作用增强,而在其他研究的血管床中则不然。