Short-term saralasin blockade of renal hypertension in fetal lambs

Debra Anderson, N. D. Binder

    Research output: Contribution to journalArticle

    1 Citation (Scopus)

    Abstract

    In the fetal lamb, suprarenal aortic blood flow reduction is known to lead to an upper body hypertension. The dependency of this hypertension on the renin-angiotensin system was investigated. Intravenous infusions of saralasin or saline vehicle were begun before suprarenal aortic blood flow reduction and continued for 24 h. In those fetuses receiving saline, upper body arterial blood pressure was significantly elevated both 60 min (P <0.05) and 24 h (P <0.05) after blood flow reduction. In those fetuses receiving an infusion of saralasin, upper body arterial blood pressure failed to rise after 60 min of blood flow reduction. However, 24 h later, blood pressure was elevated (P <0.05), though the increase was not as great as that seen in the saline infused fetuses (P <0.05). From these results, we conclude that the initial increase in upper body arterial blood pressure seen after suprarenal aortic blood flow reduction is dependent upon the renin-angiotensin system. However, as early as 1 day later, some other mechanism is responsible for sustaining the hypertension.

    Original languageEnglish (US)
    Pages (from-to)383-392
    Number of pages10
    JournalJournal of Physiology
    Volume433
    StatePublished - 1991

    Fingerprint

    Saralasin
    Renal Hypertension
    Arterial Pressure
    Fetus
    Renin-Angiotensin System
    Hypertension
    Intravenous Infusions
    Blood Pressure

    ASJC Scopus subject areas

    • Physiology

    Cite this

    Short-term saralasin blockade of renal hypertension in fetal lambs. / Anderson, Debra; Binder, N. D.

    In: Journal of Physiology, Vol. 433, 1991, p. 383-392.

    Research output: Contribution to journalArticle

    Anderson, D & Binder, ND 1991, 'Short-term saralasin blockade of renal hypertension in fetal lambs', Journal of Physiology, vol. 433, pp. 383-392.
    Anderson, Debra ; Binder, N. D. / Short-term saralasin blockade of renal hypertension in fetal lambs. In: Journal of Physiology. 1991 ; Vol. 433. pp. 383-392.
    @article{c997888b9a34495bb8211da80f04eaff,
    title = "Short-term saralasin blockade of renal hypertension in fetal lambs",
    abstract = "In the fetal lamb, suprarenal aortic blood flow reduction is known to lead to an upper body hypertension. The dependency of this hypertension on the renin-angiotensin system was investigated. Intravenous infusions of saralasin or saline vehicle were begun before suprarenal aortic blood flow reduction and continued for 24 h. In those fetuses receiving saline, upper body arterial blood pressure was significantly elevated both 60 min (P <0.05) and 24 h (P <0.05) after blood flow reduction. In those fetuses receiving an infusion of saralasin, upper body arterial blood pressure failed to rise after 60 min of blood flow reduction. However, 24 h later, blood pressure was elevated (P <0.05), though the increase was not as great as that seen in the saline infused fetuses (P <0.05). From these results, we conclude that the initial increase in upper body arterial blood pressure seen after suprarenal aortic blood flow reduction is dependent upon the renin-angiotensin system. However, as early as 1 day later, some other mechanism is responsible for sustaining the hypertension.",
    author = "Debra Anderson and Binder, {N. D.}",
    year = "1991",
    language = "English (US)",
    volume = "433",
    pages = "383--392",
    journal = "Journal of Physiology",
    issn = "0022-3751",
    publisher = "Wiley-Blackwell",

    }

    TY - JOUR

    T1 - Short-term saralasin blockade of renal hypertension in fetal lambs

    AU - Anderson, Debra

    AU - Binder, N. D.

    PY - 1991

    Y1 - 1991

    N2 - In the fetal lamb, suprarenal aortic blood flow reduction is known to lead to an upper body hypertension. The dependency of this hypertension on the renin-angiotensin system was investigated. Intravenous infusions of saralasin or saline vehicle were begun before suprarenal aortic blood flow reduction and continued for 24 h. In those fetuses receiving saline, upper body arterial blood pressure was significantly elevated both 60 min (P <0.05) and 24 h (P <0.05) after blood flow reduction. In those fetuses receiving an infusion of saralasin, upper body arterial blood pressure failed to rise after 60 min of blood flow reduction. However, 24 h later, blood pressure was elevated (P <0.05), though the increase was not as great as that seen in the saline infused fetuses (P <0.05). From these results, we conclude that the initial increase in upper body arterial blood pressure seen after suprarenal aortic blood flow reduction is dependent upon the renin-angiotensin system. However, as early as 1 day later, some other mechanism is responsible for sustaining the hypertension.

    AB - In the fetal lamb, suprarenal aortic blood flow reduction is known to lead to an upper body hypertension. The dependency of this hypertension on the renin-angiotensin system was investigated. Intravenous infusions of saralasin or saline vehicle were begun before suprarenal aortic blood flow reduction and continued for 24 h. In those fetuses receiving saline, upper body arterial blood pressure was significantly elevated both 60 min (P <0.05) and 24 h (P <0.05) after blood flow reduction. In those fetuses receiving an infusion of saralasin, upper body arterial blood pressure failed to rise after 60 min of blood flow reduction. However, 24 h later, blood pressure was elevated (P <0.05), though the increase was not as great as that seen in the saline infused fetuses (P <0.05). From these results, we conclude that the initial increase in upper body arterial blood pressure seen after suprarenal aortic blood flow reduction is dependent upon the renin-angiotensin system. However, as early as 1 day later, some other mechanism is responsible for sustaining the hypertension.

    UR - http://www.scopus.com/inward/record.url?scp=0026090333&partnerID=8YFLogxK

    UR - http://www.scopus.com/inward/citedby.url?scp=0026090333&partnerID=8YFLogxK

    M3 - Article

    C2 - 1841947

    AN - SCOPUS:0026090333

    VL - 433

    SP - 383

    EP - 392

    JO - Journal of Physiology

    JF - Journal of Physiology

    SN - 0022-3751

    ER -