Renal arteriolar angiotensin responses during varied adenosine receptor activation

Pamela K. Carmines, Edward W. Inscho

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

We performed experiments to test the hypothesis that endogenous adenosine acts as an essential cofactor required for eliciting angiotensin II (Ang II)-induced afferent and/or efferent arteriolar vasoconstriction. Enalaprilat (2 mg IV) was administered to anesthetized rats to reduce endogenous Ang II levels. Kidneys and blood were harvested from these animals and used for study of renal microvascular function using the in vitro blood-perfused juxtamedullary nephron technique. Arteriolar inside diameter was monitored videomicroscopically in (1) normal kidneys, (2) kidneys subjected to adenosine receptor blockade (100 μmol/L 1,3-dipropyl- 8-p-sulfophenylxanthine), and (3) kidneys continuously exposed to 1 /wnol/L adenosine. Under resting conditions, arteriolar diameters were similar in all three groups of kidneys, averaging 24.8 ±1.0 μn (n=23) in afferent arterioles and 24.0±0.9 fim (n=16) in efferent arterioles. In normal kidneys, adenosine (10 μmol/L) decreased both afferent (10.2±2.0%) and efferent (6.5 ±0.8%) diameters, an effect that was absent in kidneys subjected to adenosine receptor blockade. Ang II (10 pmol/L to 100 nmol/L) elicited dose-dependent vasoconstriction of both vascular segments in normal kidneys. At a concentration of 100 nmol/L, Ang II decreased afferent diameter by 36.8±8.5% and efferent diameter by 3O.8±9.6%. Neither afferent nor efferent arteriolar Ang II dose-response relations were significantly different in kidneys treated with low-dose adenosine or the adenosine receptor blocker. These observations refute the hypothesis that a receptor-mediated action of adenosine is required for Ang II-induced constriction of juxtamedullary afferent or efferent arterioles. Furthermore, subconstrictor adenosine levels do not potently modulate renal arteriolar vasoconstrictor responses to Ang II.

Original languageEnglish (US)
Pages (from-to)I-114-I-119
JournalHypertension
Volume23
Issue number1
StatePublished - Jan 1994

Fingerprint

Purinergic P1 Receptors
Angiotensins
Kidney
Angiotensin II
Adenosine
Arterioles
Vasoconstriction
Enalaprilat
Nephrons
Vasoconstrictor Agents
Constriction
Blood Vessels

Keywords

  • Adenosine
  • Angiotensin II
  • Arterioles
  • Purinergic
  • Receptors
  • Renal circulation

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Renal arteriolar angiotensin responses during varied adenosine receptor activation. / Carmines, Pamela K.; Inscho, Edward W.

In: Hypertension, Vol. 23, No. 1, 01.1994, p. I-114-I-119.

Research output: Contribution to journalArticle

@article{e73bc46d29b74cafb337f1b398a90723,
title = "Renal arteriolar angiotensin responses during varied adenosine receptor activation",
abstract = "We performed experiments to test the hypothesis that endogenous adenosine acts as an essential cofactor required for eliciting angiotensin II (Ang II)-induced afferent and/or efferent arteriolar vasoconstriction. Enalaprilat (2 mg IV) was administered to anesthetized rats to reduce endogenous Ang II levels. Kidneys and blood were harvested from these animals and used for study of renal microvascular function using the in vitro blood-perfused juxtamedullary nephron technique. Arteriolar inside diameter was monitored videomicroscopically in (1) normal kidneys, (2) kidneys subjected to adenosine receptor blockade (100 μmol/L 1,3-dipropyl- 8-p-sulfophenylxanthine), and (3) kidneys continuously exposed to 1 /wnol/L adenosine. Under resting conditions, arteriolar diameters were similar in all three groups of kidneys, averaging 24.8 ±1.0 μn (n=23) in afferent arterioles and 24.0±0.9 fim (n=16) in efferent arterioles. In normal kidneys, adenosine (10 μmol/L) decreased both afferent (10.2±2.0%) and efferent (6.5 ±0.8%) diameters, an effect that was absent in kidneys subjected to adenosine receptor blockade. Ang II (10 pmol/L to 100 nmol/L) elicited dose-dependent vasoconstriction of both vascular segments in normal kidneys. At a concentration of 100 nmol/L, Ang II decreased afferent diameter by 36.8±8.5% and efferent diameter by 3O.8±9.6%. Neither afferent nor efferent arteriolar Ang II dose-response relations were significantly different in kidneys treated with low-dose adenosine or the adenosine receptor blocker. These observations refute the hypothesis that a receptor-mediated action of adenosine is required for Ang II-induced constriction of juxtamedullary afferent or efferent arterioles. Furthermore, subconstrictor adenosine levels do not potently modulate renal arteriolar vasoconstrictor responses to Ang II.",
keywords = "Adenosine, Angiotensin II, Arterioles, Purinergic, Receptors, Renal circulation",
author = "Carmines, {Pamela K.} and Inscho, {Edward W.}",
year = "1994",
month = "1",
language = "English (US)",
volume = "23",
pages = "I--114--I--119",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Renal arteriolar angiotensin responses during varied adenosine receptor activation

AU - Carmines, Pamela K.

AU - Inscho, Edward W.

PY - 1994/1

Y1 - 1994/1

N2 - We performed experiments to test the hypothesis that endogenous adenosine acts as an essential cofactor required for eliciting angiotensin II (Ang II)-induced afferent and/or efferent arteriolar vasoconstriction. Enalaprilat (2 mg IV) was administered to anesthetized rats to reduce endogenous Ang II levels. Kidneys and blood were harvested from these animals and used for study of renal microvascular function using the in vitro blood-perfused juxtamedullary nephron technique. Arteriolar inside diameter was monitored videomicroscopically in (1) normal kidneys, (2) kidneys subjected to adenosine receptor blockade (100 μmol/L 1,3-dipropyl- 8-p-sulfophenylxanthine), and (3) kidneys continuously exposed to 1 /wnol/L adenosine. Under resting conditions, arteriolar diameters were similar in all three groups of kidneys, averaging 24.8 ±1.0 μn (n=23) in afferent arterioles and 24.0±0.9 fim (n=16) in efferent arterioles. In normal kidneys, adenosine (10 μmol/L) decreased both afferent (10.2±2.0%) and efferent (6.5 ±0.8%) diameters, an effect that was absent in kidneys subjected to adenosine receptor blockade. Ang II (10 pmol/L to 100 nmol/L) elicited dose-dependent vasoconstriction of both vascular segments in normal kidneys. At a concentration of 100 nmol/L, Ang II decreased afferent diameter by 36.8±8.5% and efferent diameter by 3O.8±9.6%. Neither afferent nor efferent arteriolar Ang II dose-response relations were significantly different in kidneys treated with low-dose adenosine or the adenosine receptor blocker. These observations refute the hypothesis that a receptor-mediated action of adenosine is required for Ang II-induced constriction of juxtamedullary afferent or efferent arterioles. Furthermore, subconstrictor adenosine levels do not potently modulate renal arteriolar vasoconstrictor responses to Ang II.

AB - We performed experiments to test the hypothesis that endogenous adenosine acts as an essential cofactor required for eliciting angiotensin II (Ang II)-induced afferent and/or efferent arteriolar vasoconstriction. Enalaprilat (2 mg IV) was administered to anesthetized rats to reduce endogenous Ang II levels. Kidneys and blood were harvested from these animals and used for study of renal microvascular function using the in vitro blood-perfused juxtamedullary nephron technique. Arteriolar inside diameter was monitored videomicroscopically in (1) normal kidneys, (2) kidneys subjected to adenosine receptor blockade (100 μmol/L 1,3-dipropyl- 8-p-sulfophenylxanthine), and (3) kidneys continuously exposed to 1 /wnol/L adenosine. Under resting conditions, arteriolar diameters were similar in all three groups of kidneys, averaging 24.8 ±1.0 μn (n=23) in afferent arterioles and 24.0±0.9 fim (n=16) in efferent arterioles. In normal kidneys, adenosine (10 μmol/L) decreased both afferent (10.2±2.0%) and efferent (6.5 ±0.8%) diameters, an effect that was absent in kidneys subjected to adenosine receptor blockade. Ang II (10 pmol/L to 100 nmol/L) elicited dose-dependent vasoconstriction of both vascular segments in normal kidneys. At a concentration of 100 nmol/L, Ang II decreased afferent diameter by 36.8±8.5% and efferent diameter by 3O.8±9.6%. Neither afferent nor efferent arteriolar Ang II dose-response relations were significantly different in kidneys treated with low-dose adenosine or the adenosine receptor blocker. These observations refute the hypothesis that a receptor-mediated action of adenosine is required for Ang II-induced constriction of juxtamedullary afferent or efferent arterioles. Furthermore, subconstrictor adenosine levels do not potently modulate renal arteriolar vasoconstrictor responses to Ang II.

KW - Adenosine

KW - Angiotensin II

KW - Arterioles

KW - Purinergic

KW - Receptors

KW - Renal circulation

UR - http://www.scopus.com/inward/record.url?scp=0028105813&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028105813&partnerID=8YFLogxK

M3 - Article

C2 - 8282342

AN - SCOPUS:0028105813

VL - 23

SP - I-114-I-119

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 1

ER -