Chronic ANG II infusion and reflex control of norepinephrine and corticosterone in conscious rabbits

Virginia Brooks, Daniel C. Hatton

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The hypothesis that long-term increases in angiotensin II (ANG II) produce pressure-independent resetting of baroreflex control of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis was tested in rabbits by determining the effect of chronic ANG II infusion on reflex relationships between mean arterial pressure (MAP) and plasma concentrations of norepinephrine (NE) and corticosterone (CS). After 2 wk, ANG II increased MAP from 61 ± 1 to 99 ± 2 mmHg (P <0.05) without altering heart rate or plasma NE concentration, but increased CS from 9.8 ± 1.3 to 29.5 ± 13.7 ng/ml (P <0.05). Heart rate, NE, and CS baroreflex curves were all reset to a higher pressure level (P <0.05) after 24 h, 1 wk, and 2 wk of ANG II. Forty minutes after stopping ANG II on the same days, MAP decreased, and curves were shifted back toward control (P <0.05), indicating that ANG II was required for the resetting. Two findings suggest that the resetting action of ANG II is distinct from the presser effect. First, although stopping ANG II reversed the hypertension as it reversed the resetting, reversal of the hypertension instead by prolonged infusion of nitroprusside along with ANG II did not have the same effect. Second, NE and heart rate baroreflex curves returned toward preinfusion positions after stopping ANG II (P <0.05), even when the hypertension was nearly maintained by phenylephrine infusion. In conclusion, chronic increases in ANG II may have a global baroreflex resetting effect by a mechanism that is in part independent of the hypertension.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume272
Issue number2 41-2
StatePublished - 1997

Fingerprint

Corticosterone
Angiotensin II
Reflex
Norepinephrine
Rabbits
Baroreflex
Hypertension
Arterial Pressure
Heart Rate
Pressure
Sympathetic Nervous System
Nitroprusside
Phenylephrine

Keywords

  • baroreceptor reflex
  • blood pressure
  • heart rate
  • hypertension
  • hypothalamic-pituitary-adrenal axis
  • sympathetic nervous system

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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abstract = "The hypothesis that long-term increases in angiotensin II (ANG II) produce pressure-independent resetting of baroreflex control of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis was tested in rabbits by determining the effect of chronic ANG II infusion on reflex relationships between mean arterial pressure (MAP) and plasma concentrations of norepinephrine (NE) and corticosterone (CS). After 2 wk, ANG II increased MAP from 61 ± 1 to 99 ± 2 mmHg (P <0.05) without altering heart rate or plasma NE concentration, but increased CS from 9.8 ± 1.3 to 29.5 ± 13.7 ng/ml (P <0.05). Heart rate, NE, and CS baroreflex curves were all reset to a higher pressure level (P <0.05) after 24 h, 1 wk, and 2 wk of ANG II. Forty minutes after stopping ANG II on the same days, MAP decreased, and curves were shifted back toward control (P <0.05), indicating that ANG II was required for the resetting. Two findings suggest that the resetting action of ANG II is distinct from the presser effect. First, although stopping ANG II reversed the hypertension as it reversed the resetting, reversal of the hypertension instead by prolonged infusion of nitroprusside along with ANG II did not have the same effect. Second, NE and heart rate baroreflex curves returned toward preinfusion positions after stopping ANG II (P <0.05), even when the hypertension was nearly maintained by phenylephrine infusion. In conclusion, chronic increases in ANG II may have a global baroreflex resetting effect by a mechanism that is in part independent of the hypertension.",
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AU - Brooks, Virginia

AU - Hatton, Daniel C.

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AB - The hypothesis that long-term increases in angiotensin II (ANG II) produce pressure-independent resetting of baroreflex control of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis was tested in rabbits by determining the effect of chronic ANG II infusion on reflex relationships between mean arterial pressure (MAP) and plasma concentrations of norepinephrine (NE) and corticosterone (CS). After 2 wk, ANG II increased MAP from 61 ± 1 to 99 ± 2 mmHg (P <0.05) without altering heart rate or plasma NE concentration, but increased CS from 9.8 ± 1.3 to 29.5 ± 13.7 ng/ml (P <0.05). Heart rate, NE, and CS baroreflex curves were all reset to a higher pressure level (P <0.05) after 24 h, 1 wk, and 2 wk of ANG II. Forty minutes after stopping ANG II on the same days, MAP decreased, and curves were shifted back toward control (P <0.05), indicating that ANG II was required for the resetting. Two findings suggest that the resetting action of ANG II is distinct from the presser effect. First, although stopping ANG II reversed the hypertension as it reversed the resetting, reversal of the hypertension instead by prolonged infusion of nitroprusside along with ANG II did not have the same effect. Second, NE and heart rate baroreflex curves returned toward preinfusion positions after stopping ANG II (P <0.05), even when the hypertension was nearly maintained by phenylephrine infusion. In conclusion, chronic increases in ANG II may have a global baroreflex resetting effect by a mechanism that is in part independent of the hypertension.

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