Pullan P T, Johnston C I, Anderson W P, Korner P I
Am J Physiol. 1980 Jul;239(1):H81-7. doi: 10.1152/ajpheart.1980.239.1.H81.
The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension was investigated in the conscious dog. Intravenous infusion of synthetic arginine vasopressin to elevate plasma levels approximately fivefold to 31 pg/ml caused bradycardia in normal dogs, together with suppression of plasma renin activity and angiotensin II. This plasma level of vasopressin also caused elevation of mean arterial blood pressure in dogs with pharmacological total autonomic blockade. A similar degree of elevation of plasma vasopressin concentration was observed following mild nonhypotensive hemorrhage; more severe hemorrhage resulted in an approximate 100-fold increase in plasma vasopressin levels. Severe renal artery constriction in unilaterally nephrectomized dogs caused a marked rise in mean arterial blood pressure, but only a doubling of plasma vasopressin concentration. A suppressor infusion of vasopressin did not potentiate the pressor response to infused angiotensin II. It is concluded that vasopressin may play a role in normal cardiovascular homeostatic responses, but it is unlikely to have a significant direct vasoconstrictor role in the pathogenesis of this form of experimental renal hypertension.
在清醒犬中研究了血管升压素在血压控制及一侧肾性 Goldblatt 高血压发病机制中的作用。向正常犬静脉输注合成精氨酸血管升压素使血浆水平升高约五倍至 31 pg/ml,导致心动过缓,同时抑制血浆肾素活性和血管紧张素 II。这种血管升压素血浆水平也使药理学上完全自主神经阻滞的犬平均动脉血压升高。轻度非低血压性出血后观察到血浆血管升压素浓度有类似程度的升高;更严重的出血导致血浆血管升压素水平约增加 100 倍。单侧肾切除犬的严重肾动脉狭窄导致平均动脉血压显著升高,但血浆血管升压素浓度仅加倍。血管升压素的抑制性输注并未增强对输注血管紧张素 II 的升压反应。得出结论,血管升压素可能在正常心血管稳态反应中起作用,但在这种实验性肾性高血压的发病机制中不太可能具有显著的直接血管收缩作用。