Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension

Authors:
  • JMJ. Mohring
    J. Mohring
  • BMB. Mohring
    B. Mohring
  • MPM. Petri
    M. Petri
  • DHD. Haack
    D. Haack
  • JAJoanna M. Abrams
    Joanna M. Abrams
  • WEWilliam C. Engeland
    William C. Engeland
  • JOJohn W. Osborn
    John W. Osborn
  • MNMasato Nishimura
    Masato Nishimura
  • KOKen Ohtsuka
    Ken Ohtsuka
  • ANAkira Nanbu
    Akira Nanbu
  • HTHakuo Takahashi
    Hakuo Takahashi
  • MYManabu Yoshimura
    Manabu Yoshimura
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Abstract
During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.