Genetic AT1A receptor deficiency attenuates cold-induced hypertension

Zhongjie Sun, Xiuqing Wang, Charles E. Wood, J. Robert Cade

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

The aim of this study was to test our hypotheses that AT1A receptors play a role in the pathogenesis of cold-induced hypertension (CIH) and in the cold-induced increase in drinking responses to ANG II. Two groups of wild-type (WT) and two groups of AT1A receptor gene knockout (AT 1A-KO) mice were used (6/ group). Blood pressures (BP) of the four groups were similar during the control period at room temperature (25°C). After the control period, one group of WT and one group of AT1A-KO mice were exposed to cold (5°C), while the remaining groups were kept at 25°C. BP of the cold-exposed WT group elevated significantly within 1 wk of exposure to cold and increased gradually to a maximum level by week 5. However, there was only a slight increase in BP of the cold-exposed AT1A-KO group. The maximal cold-induced increase in BP (ΔBP) is significantly less in AT1A-KO group (11 ± 3 mmHg) than in WT group (49 ± 6 mmHg), indicating that AT1A receptor deficiency attenuates cold-induced elevation of BP. Interestingly, both WT and AT1A-KO mice developed cardiac and renal hypertrophy to the same extent. AT1A-KO caused a significant increase in urine and plasma levels of nitric oxide (NO), indicating that the renin-angiotensin system inhibits NO formation probably via AT1A receptors. Cold exposure inhibited endothelial NO synthase protein expressions and decreased urine and plasma levels of NO, which may be mediated partially by AT1A receptors. AT1A-KO completely abolished the cold-induced increase in drinking responses to ANG II. We conclude that 1) AT1A receptors play an essential role in the pathogenesis of CIH but not cardiac hypertrophy; 2) the role of AT1A receptors in CIH may be mediated partially by its inhibitory effect on the NO system; and 3) cold-induced increase in drinking response to ANG II is mediated by AT 1A receptors.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume288
Issue number2 57-2
DOIs
StatePublished - Feb 1 2005
Externally publishedYes

Fingerprint

Hypertension
Blood Pressure
Nitric Oxide
Drinking
Cardiomegaly
Urine
Gene Knockout Techniques
Nitric Oxide Synthase Type III
Renin-Angiotensin System
Kidney
Temperature

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Genetic AT1A receptor deficiency attenuates cold-induced hypertension. / Sun, Zhongjie; Wang, Xiuqing; Wood, Charles E.; Cade, J. Robert.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 288, No. 2 57-2, 01.02.2005.

Research output: Contribution to journalArticle

@article{8b54a4d62c5d4e67aef92a6abcd14a0d,
title = "Genetic AT1A receptor deficiency attenuates cold-induced hypertension",
abstract = "The aim of this study was to test our hypotheses that AT1A receptors play a role in the pathogenesis of cold-induced hypertension (CIH) and in the cold-induced increase in drinking responses to ANG II. Two groups of wild-type (WT) and two groups of AT1A receptor gene knockout (AT 1A-KO) mice were used (6/ group). Blood pressures (BP) of the four groups were similar during the control period at room temperature (25°C). After the control period, one group of WT and one group of AT1A-KO mice were exposed to cold (5°C), while the remaining groups were kept at 25°C. BP of the cold-exposed WT group elevated significantly within 1 wk of exposure to cold and increased gradually to a maximum level by week 5. However, there was only a slight increase in BP of the cold-exposed AT1A-KO group. The maximal cold-induced increase in BP (ΔBP) is significantly less in AT1A-KO group (11 ± 3 mmHg) than in WT group (49 ± 6 mmHg), indicating that AT1A receptor deficiency attenuates cold-induced elevation of BP. Interestingly, both WT and AT1A-KO mice developed cardiac and renal hypertrophy to the same extent. AT1A-KO caused a significant increase in urine and plasma levels of nitric oxide (NO), indicating that the renin-angiotensin system inhibits NO formation probably via AT1A receptors. Cold exposure inhibited endothelial NO synthase protein expressions and decreased urine and plasma levels of NO, which may be mediated partially by AT1A receptors. AT1A-KO completely abolished the cold-induced increase in drinking responses to ANG II. We conclude that 1) AT1A receptors play an essential role in the pathogenesis of CIH but not cardiac hypertrophy; 2) the role of AT1A receptors in CIH may be mediated partially by its inhibitory effect on the NO system; and 3) cold-induced increase in drinking response to ANG II is mediated by AT 1A receptors.",
author = "Zhongjie Sun and Xiuqing Wang and Wood, {Charles E.} and Cade, {J. Robert}",
year = "2005",
month = "2",
day = "1",
doi = "10.1152/ajpregu.00466.2004",
language = "English (US)",
volume = "288",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "2 57-2",

}

TY - JOUR

T1 - Genetic AT1A receptor deficiency attenuates cold-induced hypertension

AU - Sun, Zhongjie

AU - Wang, Xiuqing

AU - Wood, Charles E.

AU - Cade, J. Robert

PY - 2005/2/1

Y1 - 2005/2/1

N2 - The aim of this study was to test our hypotheses that AT1A receptors play a role in the pathogenesis of cold-induced hypertension (CIH) and in the cold-induced increase in drinking responses to ANG II. Two groups of wild-type (WT) and two groups of AT1A receptor gene knockout (AT 1A-KO) mice were used (6/ group). Blood pressures (BP) of the four groups were similar during the control period at room temperature (25°C). After the control period, one group of WT and one group of AT1A-KO mice were exposed to cold (5°C), while the remaining groups were kept at 25°C. BP of the cold-exposed WT group elevated significantly within 1 wk of exposure to cold and increased gradually to a maximum level by week 5. However, there was only a slight increase in BP of the cold-exposed AT1A-KO group. The maximal cold-induced increase in BP (ΔBP) is significantly less in AT1A-KO group (11 ± 3 mmHg) than in WT group (49 ± 6 mmHg), indicating that AT1A receptor deficiency attenuates cold-induced elevation of BP. Interestingly, both WT and AT1A-KO mice developed cardiac and renal hypertrophy to the same extent. AT1A-KO caused a significant increase in urine and plasma levels of nitric oxide (NO), indicating that the renin-angiotensin system inhibits NO formation probably via AT1A receptors. Cold exposure inhibited endothelial NO synthase protein expressions and decreased urine and plasma levels of NO, which may be mediated partially by AT1A receptors. AT1A-KO completely abolished the cold-induced increase in drinking responses to ANG II. We conclude that 1) AT1A receptors play an essential role in the pathogenesis of CIH but not cardiac hypertrophy; 2) the role of AT1A receptors in CIH may be mediated partially by its inhibitory effect on the NO system; and 3) cold-induced increase in drinking response to ANG II is mediated by AT 1A receptors.

AB - The aim of this study was to test our hypotheses that AT1A receptors play a role in the pathogenesis of cold-induced hypertension (CIH) and in the cold-induced increase in drinking responses to ANG II. Two groups of wild-type (WT) and two groups of AT1A receptor gene knockout (AT 1A-KO) mice were used (6/ group). Blood pressures (BP) of the four groups were similar during the control period at room temperature (25°C). After the control period, one group of WT and one group of AT1A-KO mice were exposed to cold (5°C), while the remaining groups were kept at 25°C. BP of the cold-exposed WT group elevated significantly within 1 wk of exposure to cold and increased gradually to a maximum level by week 5. However, there was only a slight increase in BP of the cold-exposed AT1A-KO group. The maximal cold-induced increase in BP (ΔBP) is significantly less in AT1A-KO group (11 ± 3 mmHg) than in WT group (49 ± 6 mmHg), indicating that AT1A receptor deficiency attenuates cold-induced elevation of BP. Interestingly, both WT and AT1A-KO mice developed cardiac and renal hypertrophy to the same extent. AT1A-KO caused a significant increase in urine and plasma levels of nitric oxide (NO), indicating that the renin-angiotensin system inhibits NO formation probably via AT1A receptors. Cold exposure inhibited endothelial NO synthase protein expressions and decreased urine and plasma levels of NO, which may be mediated partially by AT1A receptors. AT1A-KO completely abolished the cold-induced increase in drinking responses to ANG II. We conclude that 1) AT1A receptors play an essential role in the pathogenesis of CIH but not cardiac hypertrophy; 2) the role of AT1A receptors in CIH may be mediated partially by its inhibitory effect on the NO system; and 3) cold-induced increase in drinking response to ANG II is mediated by AT 1A receptors.

UR - http://www.scopus.com/inward/record.url?scp=12344269888&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=12344269888&partnerID=8YFLogxK

U2 - 10.1152/ajpregu.00466.2004

DO - 10.1152/ajpregu.00466.2004

M3 - Article

VL - 288

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 2 57-2

ER -