Olson K R, Conklin D J, Farrell A P, Keen J E, Takei Y, Weaver L, Smith M P, Zhang Y
Indiana University School of Medicine, South Bend Center for Medical Education, University of Notre Dame 46556, USA.
Am J Physiol. 1997 Aug;273(2 Pt 2):R527-39. doi: 10.1152/ajpregu.1997.273.2.R527.
Active venous regulation of cardiovascular function is well known in mammals but has not been demonstrated in fish. In the present studies, the natriuretic peptides (NP) rat atrial natriuretic peptide (ANP) and trout ventricular natriuretic peptide (VNP), clearance receptor inhibitor SC-46542, and sodium nitroprusside (SNP) were infused into unanesthetized trout fitted with pressure cannulas in the ventral aorta, dorsal aorta, and ductus Cuvier, and a ventral aorta (VA) flow probe was used to measure cardiac output (CO). In another group, in vivo vascular (venous) capacitance curves were obtained during ANP or SNP infusion. The in vitro effects of NP on vessels and the heart were also examined. ANP, VNP, and SC-46542 decreased central venous pressure (PVen), CO, stroke volume (SV), and gill resistance (RG), whereas systemic resistance (RS) and heart rate (HR) increased. Dorsal aortic pressure (PDA) transiently increased and then fell even though RS remained elevated. ANP decreased mean circulatory filling pressure (MCFP), increased vascular compliance at all blood volumes, and increased unstressed volume in hypovolemic fish. ANP had no direct effect on the heart. ANP responses in vivo were not altered in trout made hypotensive by prior treatment with the angiotensin-converting enzyme inhibitor lisinopril. SNP reduced ventral aortic pressure (PVA), PDA, and RS, increased CO and HR, but did not affect PVen, SV, or RG. SNP slightly decreased MCFP but did not affect compliance or unstressed volume. In vitro, large systemic arteries were more responsive than veins to NP, whereas SNP relaxed both. These results show that, in vivo, NP decrease venous compliance, thereby decreasing venous return, CO, and arterial pressure. Conversely, SNP hypotension is due to decreased RS. This is the first evidence for active regulation of venous capacitance in fish, which probably occurs in small veins or venules. The presence of venous baroreceptors is also suggested.
在哺乳动物中，心血管功能的主动静脉调节是众所周知的，但在鱼类中尚未得到证实。在本研究中，将利钠肽（NP）大鼠心房利钠肽（ANP）和鳟鱼心室利钠肽（VNP）、清除受体抑制剂SC - 46542以及硝普钠（SNP）注入未麻醉的鳟鱼体内，这些鳟鱼在腹主动脉、背主动脉和居维叶氏管中装有压力插管，并使用腹主动脉（VA）流量探头测量心输出量（CO）。在另一组实验中，在注入ANP或SNP期间获得体内血管（静脉）容量曲线。还研究了NP对血管和心脏的体外作用。ANP、VNP和SC - 46542降低中心静脉压（PVen）、CO、每搏输出量（SV）和鳃阻力（RG），而全身阻力（RS）和心率（HR）增加。背主动脉压（PDA）短暂升高，然后下降，尽管RS仍然升高。ANP降低平均循环充盈压（MCFP），在所有血容量下增加血管顺应性，并增加低血容量鱼类的无应激容量。ANP对心脏没有直接作用。在用血管紧张素转换酶抑制剂赖诺普利预先处理使血压降低的鳟鱼中，ANP在体内的反应没有改变。SNP降低腹主动脉压（PVA）、PDA和RS，增加CO和HR，但不影响PVen、SV或RG。SNP略微降低MCFP，但不影响顺应性或无应激容量。在体外，大的全身动脉对NP的反应比静脉更敏感，而SNP使两者都舒张。这些结果表明，在体内，NP降低静脉顺应性，从而减少静脉回心血量、CO和动脉压。相反，SNP引起的低血压是由于RS降低。这是鱼类中静脉容量主动调节的首个证据，这种调节可能发生在小静脉或微静脉中。这也提示了静脉压力感受器的存在。
