Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits

Masayo Fukuhara, Kiyoshi Matsumura, Isao Abe, Masatoshi Fujishima

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICV) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICV Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 μg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9±2.2 vs. 16.2±0.7%, P<0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICV Ang II (20±1 vs. 16±2 mmHg, p<0.05, and 30.9±3.7 vs. 16.2±0.7%, p<0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central presser action of Ang II in conscious rabbits.

Original languageEnglish
Pages (from-to)89-95
Number of pages7
JournalHypertension Research
Volume21
Issue number2
Publication statusPublished - Jun 1 1998

Fingerprint

Vasopressins
Angiotensin II
Opioid Analgesics
Rabbits
Arginine Vasopressin
Vasopressin Receptors
Naloxone
Kidney
Arterial Pressure
Narcotic Antagonists
Sympathetic Nervous System
Angiotensins
Renin
Intravenous Injections
Epinephrine
Heart Rate

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Fukuhara, M., Matsumura, K., Abe, I., & Fujishima, M. (1998). Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits. Hypertension Research, 21(2), 89-95.

Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits. / Fukuhara, Masayo; Matsumura, Kiyoshi; Abe, Isao; Fujishima, Masatoshi.

In: Hypertension Research, Vol. 21, No. 2, 01.06.1998, p. 89-95.

Research output: Contribution to journalArticle

Fukuhara, M, Matsumura, K, Abe, I & Fujishima, M 1998, 'Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits', Hypertension Research, vol. 21, no. 2, pp. 89-95.
Fukuhara, Masayo ; Matsumura, Kiyoshi ; Abe, Isao ; Fujishima, Masatoshi. / Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits. In: Hypertension Research. 1998 ; Vol. 21, No. 2. pp. 89-95.
@article{88fe6b2de5fb4171af9fc0cdea417253,
title = "Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits",
abstract = "It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICV) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICV Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 μg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9±2.2 vs. 16.2±0.7{\%}, P<0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICV Ang II (20±1 vs. 16±2 mmHg, p<0.05, and 30.9±3.7 vs. 16.2±0.7{\%}, p<0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central presser action of Ang II in conscious rabbits.",
author = "Masayo Fukuhara and Kiyoshi Matsumura and Isao Abe and Masatoshi Fujishima",
year = "1998",
month = "6",
day = "1",
language = "English",
volume = "21",
pages = "89--95",
journal = "Hypertension Research",
issn = "0916-9636",
publisher = "Nature Publishing Group",
number = "2",

}

TY - JOUR

T1 - Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits

AU - Fukuhara, Masayo

AU - Matsumura, Kiyoshi

AU - Abe, Isao

AU - Fujishima, Masatoshi

PY - 1998/6/1

Y1 - 1998/6/1

N2 - It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICV) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICV Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 μg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9±2.2 vs. 16.2±0.7%, P<0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICV Ang II (20±1 vs. 16±2 mmHg, p<0.05, and 30.9±3.7 vs. 16.2±0.7%, p<0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central presser action of Ang II in conscious rabbits.

AB - It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous systems. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (ICV) Ang II in conscious rabbits. ICV Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to ICV Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 μg/kg) augmented the maximum increase in RSNA caused by ICV Ang II (8.9±2.2 vs. 16.2±0.7%, P<0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICV Ang II (20±1 vs. 16±2 mmHg, p<0.05, and 30.9±3.7 vs. 16.2±0.7%, p<0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central presser action of Ang II in conscious rabbits.

UR - http://www.scopus.com/inward/record.url?scp=0031927889&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031927889&partnerID=8YFLogxK

M3 - Article

C2 - 9661804

AN - SCOPUS:0031927889

VL - 21

SP - 89

EP - 95

JO - Hypertension Research

JF - Hypertension Research

SN - 0916-9636

IS - 2

ER -