Vasopressin lowers pulmonary artery pressure in hypoxic rats by releasing atrial natriuretic peptide

H. Jin, Y. F. Chen, R. H. Yang, T. M. McKenna, Robert Jackson, S. Oparil

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

The authors previously demonstrated that arginine vasopressin (AVP) lowers pulmonary artery pressure in rats with hypoxic pulmonary hypertension by activation of the V1 receptor. The pulmonary depressor effect of AVP in hypoxia-adapted rats is not due to its effect on cardiac output. The current study tested two alternative hypotheses: that AVP lowers pulmonary artery pressure in the hypoxia-adapted lung by (1) dilating pulmonary vasculature directly, or (2) releasing atrial natriuretic peptide (ANP) from the heart. The first hypothesis was tested by injecting AVP into the pulmonary arteries of isolated, buffer perfused lungs and monitoring pulmonary artery pressure, and by exposing preconstricted pulmonary artery rings to graded doses of AVP and monitoring the tension generated. AVP caused minimal vasodilation in perfused lungs and only a small vasodilator effect in pulmonary artery rings. The second hypothesis was tested by injecting AVP (160 ng/kg) or vehicle intravenously in conscious hypoxia-adapted (4 weeks) or air control rats and measuring ANP in arterial blood and atria, and by testing pretreatment with the V1 receptor antagonist d(CH2)5 Tyr(Me)AVP (130 μg/kg) on the AVP-induced increase in plasma ANP. AVP produced a 7-fold increase in plasma ANP (209 ± 33 to 1346 ± 233 pg/ml; p < 0.05) in hypoxia-adapted rats and a 5-fold increase in ANP (122 ± 22 to 573 ± 174 pg/ml; p < 0.05) in air controls. ANP release was abolished by pretreatment of both groups with d(CH2)5 Tyr(Me)AVP. The AVP-induced ANP release came mainly from left atrium. These data strongly suggest that the pulmonary depressor effects of AVP in hypoxia-adapted rats is due to augmented V1 receptor-induced release of ANP from left atrium.

Original languageEnglish
Pages (from-to)227-236
Number of pages10
JournalAmerican Journal of the Medical Sciences
Volume298
Issue number4
StatePublished - Jan 1 1989
Externally publishedYes

Fingerprint

Arginine Vasopressin
Vasopressins
Pulmonary Artery
Pressure
Atrial Natriuretic Factor
Vasopressin Receptors
Lung
Heart Atria
rat atrial natriuretic peptide
Air
Vasodilator Agents
Pulmonary Hypertension
Vasodilation
Cardiac Output
Buffers

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Vasopressin lowers pulmonary artery pressure in hypoxic rats by releasing atrial natriuretic peptide. / Jin, H.; Chen, Y. F.; Yang, R. H.; McKenna, T. M.; Jackson, Robert; Oparil, S.

In: American Journal of the Medical Sciences, Vol. 298, No. 4, 01.01.1989, p. 227-236.

Research output: Contribution to journalArticle

Jin, H. ; Chen, Y. F. ; Yang, R. H. ; McKenna, T. M. ; Jackson, Robert ; Oparil, S. / Vasopressin lowers pulmonary artery pressure in hypoxic rats by releasing atrial natriuretic peptide. In: American Journal of the Medical Sciences. 1989 ; Vol. 298, No. 4. pp. 227-236.
@article{38165f0f783440eba55f6265181bf10f,
title = "Vasopressin lowers pulmonary artery pressure in hypoxic rats by releasing atrial natriuretic peptide",
abstract = "The authors previously demonstrated that arginine vasopressin (AVP) lowers pulmonary artery pressure in rats with hypoxic pulmonary hypertension by activation of the V1 receptor. The pulmonary depressor effect of AVP in hypoxia-adapted rats is not due to its effect on cardiac output. The current study tested two alternative hypotheses: that AVP lowers pulmonary artery pressure in the hypoxia-adapted lung by (1) dilating pulmonary vasculature directly, or (2) releasing atrial natriuretic peptide (ANP) from the heart. The first hypothesis was tested by injecting AVP into the pulmonary arteries of isolated, buffer perfused lungs and monitoring pulmonary artery pressure, and by exposing preconstricted pulmonary artery rings to graded doses of AVP and monitoring the tension generated. AVP caused minimal vasodilation in perfused lungs and only a small vasodilator effect in pulmonary artery rings. The second hypothesis was tested by injecting AVP (160 ng/kg) or vehicle intravenously in conscious hypoxia-adapted (4 weeks) or air control rats and measuring ANP in arterial blood and atria, and by testing pretreatment with the V1 receptor antagonist d(CH2)5 Tyr(Me)AVP (130 μg/kg) on the AVP-induced increase in plasma ANP. AVP produced a 7-fold increase in plasma ANP (209 ± 33 to 1346 ± 233 pg/ml; p < 0.05) in hypoxia-adapted rats and a 5-fold increase in ANP (122 ± 22 to 573 ± 174 pg/ml; p < 0.05) in air controls. ANP release was abolished by pretreatment of both groups with d(CH2)5 Tyr(Me)AVP. The AVP-induced ANP release came mainly from left atrium. These data strongly suggest that the pulmonary depressor effects of AVP in hypoxia-adapted rats is due to augmented V1 receptor-induced release of ANP from left atrium.",
author = "H. Jin and Chen, {Y. F.} and Yang, {R. H.} and McKenna, {T. M.} and Robert Jackson and S. Oparil",
year = "1989",
month = "1",
day = "1",
language = "English",
volume = "298",
pages = "227--236",
journal = "American Journal of the Medical Sciences",
issn = "0002-9629",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - Vasopressin lowers pulmonary artery pressure in hypoxic rats by releasing atrial natriuretic peptide

AU - Jin, H.

AU - Chen, Y. F.

AU - Yang, R. H.

AU - McKenna, T. M.

AU - Jackson, Robert

AU - Oparil, S.

PY - 1989/1/1

Y1 - 1989/1/1

N2 - The authors previously demonstrated that arginine vasopressin (AVP) lowers pulmonary artery pressure in rats with hypoxic pulmonary hypertension by activation of the V1 receptor. The pulmonary depressor effect of AVP in hypoxia-adapted rats is not due to its effect on cardiac output. The current study tested two alternative hypotheses: that AVP lowers pulmonary artery pressure in the hypoxia-adapted lung by (1) dilating pulmonary vasculature directly, or (2) releasing atrial natriuretic peptide (ANP) from the heart. The first hypothesis was tested by injecting AVP into the pulmonary arteries of isolated, buffer perfused lungs and monitoring pulmonary artery pressure, and by exposing preconstricted pulmonary artery rings to graded doses of AVP and monitoring the tension generated. AVP caused minimal vasodilation in perfused lungs and only a small vasodilator effect in pulmonary artery rings. The second hypothesis was tested by injecting AVP (160 ng/kg) or vehicle intravenously in conscious hypoxia-adapted (4 weeks) or air control rats and measuring ANP in arterial blood and atria, and by testing pretreatment with the V1 receptor antagonist d(CH2)5 Tyr(Me)AVP (130 μg/kg) on the AVP-induced increase in plasma ANP. AVP produced a 7-fold increase in plasma ANP (209 ± 33 to 1346 ± 233 pg/ml; p < 0.05) in hypoxia-adapted rats and a 5-fold increase in ANP (122 ± 22 to 573 ± 174 pg/ml; p < 0.05) in air controls. ANP release was abolished by pretreatment of both groups with d(CH2)5 Tyr(Me)AVP. The AVP-induced ANP release came mainly from left atrium. These data strongly suggest that the pulmonary depressor effects of AVP in hypoxia-adapted rats is due to augmented V1 receptor-induced release of ANP from left atrium.

AB - The authors previously demonstrated that arginine vasopressin (AVP) lowers pulmonary artery pressure in rats with hypoxic pulmonary hypertension by activation of the V1 receptor. The pulmonary depressor effect of AVP in hypoxia-adapted rats is not due to its effect on cardiac output. The current study tested two alternative hypotheses: that AVP lowers pulmonary artery pressure in the hypoxia-adapted lung by (1) dilating pulmonary vasculature directly, or (2) releasing atrial natriuretic peptide (ANP) from the heart. The first hypothesis was tested by injecting AVP into the pulmonary arteries of isolated, buffer perfused lungs and monitoring pulmonary artery pressure, and by exposing preconstricted pulmonary artery rings to graded doses of AVP and monitoring the tension generated. AVP caused minimal vasodilation in perfused lungs and only a small vasodilator effect in pulmonary artery rings. The second hypothesis was tested by injecting AVP (160 ng/kg) or vehicle intravenously in conscious hypoxia-adapted (4 weeks) or air control rats and measuring ANP in arterial blood and atria, and by testing pretreatment with the V1 receptor antagonist d(CH2)5 Tyr(Me)AVP (130 μg/kg) on the AVP-induced increase in plasma ANP. AVP produced a 7-fold increase in plasma ANP (209 ± 33 to 1346 ± 233 pg/ml; p < 0.05) in hypoxia-adapted rats and a 5-fold increase in ANP (122 ± 22 to 573 ± 174 pg/ml; p < 0.05) in air controls. ANP release was abolished by pretreatment of both groups with d(CH2)5 Tyr(Me)AVP. The AVP-induced ANP release came mainly from left atrium. These data strongly suggest that the pulmonary depressor effects of AVP in hypoxia-adapted rats is due to augmented V1 receptor-induced release of ANP from left atrium.

UR - http://www.scopus.com/inward/record.url?scp=0024466704&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024466704&partnerID=8YFLogxK

M3 - Article

C2 - 2529763

AN - SCOPUS:0024466704

VL - 298

SP - 227

EP - 236

JO - American Journal of the Medical Sciences

JF - American Journal of the Medical Sciences

SN - 0002-9629

IS - 4

ER -