Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure via vasopressin production and secretion in postpartum rats

Taku Matsuura, Keisuke Shinohara, Takeshi Iyonaga, Yoshitaka Hirooka, Hiroyuki Tsutsui

Research output: Contribution to journalArticle

Abstract

Objectives:Women with a history of preeclampsia exhibit increased salt sensitivity of blood pressure at postpartum, which might be responsible for their increased risk of future cardiovascular diseases. However, it is unclear whether preeclampsia can cause increased salt sensitivity at postpartum. Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. Therefore, the aim of this study was to determine whether the exposure to preeclampsia, as elicited by placental ischemia, causes increased salt sensitivity at postpartum, and if so, whether vasopressin is involved in its process.Methods and results:We used a reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. Pregnant Sprague-Dawley rats were categorized into the following two groups: RUPP-operated and sham-operated (SHAM) control groups. A 1-week-long high-salt diet was initiated at 3 weeks postpartum. The high-salt diet-induced increase in mean arterial pressure was significantly greater in the RUPP group than in the SHAM group. In addition, the plasma levels of copeptin, a substitute for plasma vasopressin, increased and serum osmolality decreased in the RUPP group. Double immunostaining revealed that the expression of c-Fos, a marker of neural activity, in vasopressin-producing neurons and presympathetic neurons in the hypothalamic paraventricular nucleus was significantly elevated in the RUPP group. The oral administration of conivaptan, the dual V1a/V2 vasopressin receptor antagonist, during high-salt diet abolished the enhanced increase in mean arterial pressure in RUPP rats.Conclusion:Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure at postpartum probably due to enhanced vasopressin production and secretion.

Original languageEnglish
Pages (from-to)1657-1667
Number of pages11
JournalJournal of hypertension
Volume37
Issue number8
DOIs
Publication statusPublished - Aug 1 2019

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Vasopressins
Postpartum Period
Ischemia
Salts
Blood Pressure
Pre-Eclampsia
Perfusion
Pressure
Diet
Arterial Pressure
Plasma Substitutes
Neurons
Paraventricular Hypothalamic Nucleus
Osmolar Concentration
Oral Administration
Sprague Dawley Rats
Cardiovascular Diseases
Hypertension
Control Groups
Serum

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure via vasopressin production and secretion in postpartum rats. / Matsuura, Taku; Shinohara, Keisuke; Iyonaga, Takeshi; Hirooka, Yoshitaka; Tsutsui, Hiroyuki.

In: Journal of hypertension, Vol. 37, No. 8, 01.08.2019, p. 1657-1667.

Research output: Contribution to journalArticle

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abstract = "Objectives:Women with a history of preeclampsia exhibit increased salt sensitivity of blood pressure at postpartum, which might be responsible for their increased risk of future cardiovascular diseases. However, it is unclear whether preeclampsia can cause increased salt sensitivity at postpartum. Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. Therefore, the aim of this study was to determine whether the exposure to preeclampsia, as elicited by placental ischemia, causes increased salt sensitivity at postpartum, and if so, whether vasopressin is involved in its process.Methods and results:We used a reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. Pregnant Sprague-Dawley rats were categorized into the following two groups: RUPP-operated and sham-operated (SHAM) control groups. A 1-week-long high-salt diet was initiated at 3 weeks postpartum. The high-salt diet-induced increase in mean arterial pressure was significantly greater in the RUPP group than in the SHAM group. In addition, the plasma levels of copeptin, a substitute for plasma vasopressin, increased and serum osmolality decreased in the RUPP group. Double immunostaining revealed that the expression of c-Fos, a marker of neural activity, in vasopressin-producing neurons and presympathetic neurons in the hypothalamic paraventricular nucleus was significantly elevated in the RUPP group. The oral administration of conivaptan, the dual V1a/V2 vasopressin receptor antagonist, during high-salt diet abolished the enhanced increase in mean arterial pressure in RUPP rats.Conclusion:Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure at postpartum probably due to enhanced vasopressin production and secretion.",
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T1 - Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure via vasopressin production and secretion in postpartum rats

AU - Matsuura, Taku

AU - Shinohara, Keisuke

AU - Iyonaga, Takeshi

AU - Hirooka, Yoshitaka

AU - Tsutsui, Hiroyuki

PY - 2019/8/1

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N2 - Objectives:Women with a history of preeclampsia exhibit increased salt sensitivity of blood pressure at postpartum, which might be responsible for their increased risk of future cardiovascular diseases. However, it is unclear whether preeclampsia can cause increased salt sensitivity at postpartum. Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. Therefore, the aim of this study was to determine whether the exposure to preeclampsia, as elicited by placental ischemia, causes increased salt sensitivity at postpartum, and if so, whether vasopressin is involved in its process.Methods and results:We used a reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. Pregnant Sprague-Dawley rats were categorized into the following two groups: RUPP-operated and sham-operated (SHAM) control groups. A 1-week-long high-salt diet was initiated at 3 weeks postpartum. The high-salt diet-induced increase in mean arterial pressure was significantly greater in the RUPP group than in the SHAM group. In addition, the plasma levels of copeptin, a substitute for plasma vasopressin, increased and serum osmolality decreased in the RUPP group. Double immunostaining revealed that the expression of c-Fos, a marker of neural activity, in vasopressin-producing neurons and presympathetic neurons in the hypothalamic paraventricular nucleus was significantly elevated in the RUPP group. The oral administration of conivaptan, the dual V1a/V2 vasopressin receptor antagonist, during high-salt diet abolished the enhanced increase in mean arterial pressure in RUPP rats.Conclusion:Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure at postpartum probably due to enhanced vasopressin production and secretion.

AB - Objectives:Women with a history of preeclampsia exhibit increased salt sensitivity of blood pressure at postpartum, which might be responsible for their increased risk of future cardiovascular diseases. However, it is unclear whether preeclampsia can cause increased salt sensitivity at postpartum. Vasopressin may play a role in the pathogenesis of preeclampsia and salt-sensitive hypertension. Therefore, the aim of this study was to determine whether the exposure to preeclampsia, as elicited by placental ischemia, causes increased salt sensitivity at postpartum, and if so, whether vasopressin is involved in its process.Methods and results:We used a reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. Pregnant Sprague-Dawley rats were categorized into the following two groups: RUPP-operated and sham-operated (SHAM) control groups. A 1-week-long high-salt diet was initiated at 3 weeks postpartum. The high-salt diet-induced increase in mean arterial pressure was significantly greater in the RUPP group than in the SHAM group. In addition, the plasma levels of copeptin, a substitute for plasma vasopressin, increased and serum osmolality decreased in the RUPP group. Double immunostaining revealed that the expression of c-Fos, a marker of neural activity, in vasopressin-producing neurons and presympathetic neurons in the hypothalamic paraventricular nucleus was significantly elevated in the RUPP group. The oral administration of conivaptan, the dual V1a/V2 vasopressin receptor antagonist, during high-salt diet abolished the enhanced increase in mean arterial pressure in RUPP rats.Conclusion:Prior exposure to placental ischemia causes increased salt sensitivity of blood pressure at postpartum probably due to enhanced vasopressin production and secretion.

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