Hirsch A T, Majzoub J A, Ren C J, Scales K M, Creager M A
Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
J Appl Physiol (1985). 1993 Nov;75(5):1984-8. doi: 10.1152/jappl.1993.75.5.1984.
In animals subjected to hemorrhage, plasma arginine vasopressin concentrations increase to levels sufficient to cause vasoconstriction, thus attenuating the hypotensive response. The purpose of this study was to examine the contribution of vasopressin to blood pressure regulation during hypotension in humans. Hypotension was induced in twelve normal subjects by lower body negative pressure (LBNP) before and after intravenous administration of vasopressin V1 receptor antagonist. Before drug administration, LBNP reduced systolic blood pressure from 125 +/- 4 to 78 +/- 12 mmHg (P < 0.01) as vasopressin concentration increased from 2.9 +/- 0.6 to 17 +/- 6 pg/ml (P < 0.05). After administration of the vasopressin antagonist, LBNP reduced systolic blood pressure from 128 +/- 3 to 89 +/- 11 mmHg (P < 0.01). The hypotensive response to LBNP was not potentiated by inhibiting vasopressin's vasoconstrictive effects (P = NS). Thus hypotension causes marked increases in plasma vasopressin concentration. In contrast to findings in animal studies, however, vasopressin does not contribute to the maintenance of blood pressure during hypotension in humans.
在遭受出血的动物中，血浆精氨酸加压素浓度会升高至足以引起血管收缩的水平，从而减弱低血压反应。本研究的目的是探讨加压素在人类低血压期间对血压调节的作用。在静脉注射加压素V1受体拮抗剂前后，通过下体负压（LBNP）对12名正常受试者诱发低血压。给药前，随着加压素浓度从2.9±0.6升高至17±6 pg/ml（P<0.05），LBNP使收缩压从125±4降至78±12 mmHg（P<0.01）。给予加压素拮抗剂后，LBNP使收缩压从128±3降至89±11 mmHg（P<0.01）。抑制加压素的血管收缩作用并未增强对LBNP的低血压反应（P=无显著性差异）。因此，低血压会导致血浆加压素浓度显著升高。然而，与动物研究结果相反，加压素在人类低血压期间对血压维持并无作用。
