Bilirubin, renal hemodynamics, and blood pressure

David E. Stec, Peter A. Hosick, Joey P. Granger

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Bilirubin is generated from the breakdown of heme by heme oxygenase and the reduction of biliverdin by the enzyme biliverdin reductase. Several large population studies have reported a significant inverse correlation between plasma bilirubin levels and the incidence of cardiovascular disease. Protection from cardiovascular disease is also observed in patients with Gilbert's syndrome which is a disease characterized by mutations in hepatic UGT1A1, the enzyme responsible for the conjugation of bilirubin into the bile. Despite the strong correlation between plasma bilirubin levels and the protection from cardiovascular disease, the mechanism by which increases in plasma bilirubin acts to protect against cardiovascular disease is unknown. Since the chronic antihypertensive actions of bilirubin are likely due to its renal actions, the effects of moderate increases in plasma bilirubin on renal hemodynamics as well as bilirubin's potential effects on renal tubule function will be discussed in this review. Mechanisms of action as well as the potential for antihypertensive therapies targeting moderate increases in plasma bilirubin levels will also be highlighted.

Original languageEnglish
Article numberArticle 18
JournalFrontiers in Pharmacology
Volume3 FEB
DOIs
StatePublished - 13 Sep 2012

Fingerprint

Bilirubin
Hemodynamics
Blood Pressure
Kidney
Cardiovascular Diseases
biliverdin reductase
Antihypertensive Agents
Gilbert Disease
Biliverdine
Heme Oxygenase (Decyclizing)
Heme
Bile
Mutation
Liver
Incidence
Enzymes
Population

Keywords

  • Biliverdin
  • Biliverdin reductase
  • Carbon monoxide
  • Glomerular filtration rate
  • Heme oxygenase
  • Liver
  • Renal blood flow
  • UGT1A1

Cite this

Stec, David E. ; Hosick, Peter A. ; Granger, Joey P. / Bilirubin, renal hemodynamics, and blood pressure. In: Frontiers in Pharmacology. 2012 ; Vol. 3 FEB.
@article{d9b6499e5b554ebbb508eab47893a4f5,
title = "Bilirubin, renal hemodynamics, and blood pressure",
abstract = "Bilirubin is generated from the breakdown of heme by heme oxygenase and the reduction of biliverdin by the enzyme biliverdin reductase. Several large population studies have reported a significant inverse correlation between plasma bilirubin levels and the incidence of cardiovascular disease. Protection from cardiovascular disease is also observed in patients with Gilbert's syndrome which is a disease characterized by mutations in hepatic UGT1A1, the enzyme responsible for the conjugation of bilirubin into the bile. Despite the strong correlation between plasma bilirubin levels and the protection from cardiovascular disease, the mechanism by which increases in plasma bilirubin acts to protect against cardiovascular disease is unknown. Since the chronic antihypertensive actions of bilirubin are likely due to its renal actions, the effects of moderate increases in plasma bilirubin on renal hemodynamics as well as bilirubin's potential effects on renal tubule function will be discussed in this review. Mechanisms of action as well as the potential for antihypertensive therapies targeting moderate increases in plasma bilirubin levels will also be highlighted.",
keywords = "Biliverdin, Biliverdin reductase, Carbon monoxide, Glomerular filtration rate, Heme oxygenase, Liver, Renal blood flow, UGT1A1",
author = "Stec, {David E.} and Hosick, {Peter A.} and Granger, {Joey P.}",
year = "2012",
month = "9",
day = "13",
doi = "10.3389/fphar.2012.00018",
language = "English",
volume = "3 FEB",
journal = "Frontiers in Pharmacology",
issn = "1663-9812",
publisher = "Frontiers Media S.A.",

}

Bilirubin, renal hemodynamics, and blood pressure. / Stec, David E.; Hosick, Peter A.; Granger, Joey P.

In: Frontiers in Pharmacology, Vol. 3 FEB, Article 18, 13.09.2012.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Bilirubin, renal hemodynamics, and blood pressure

AU - Stec, David E.

AU - Hosick, Peter A.

AU - Granger, Joey P.

PY - 2012/9/13

Y1 - 2012/9/13

N2 - Bilirubin is generated from the breakdown of heme by heme oxygenase and the reduction of biliverdin by the enzyme biliverdin reductase. Several large population studies have reported a significant inverse correlation between plasma bilirubin levels and the incidence of cardiovascular disease. Protection from cardiovascular disease is also observed in patients with Gilbert's syndrome which is a disease characterized by mutations in hepatic UGT1A1, the enzyme responsible for the conjugation of bilirubin into the bile. Despite the strong correlation between plasma bilirubin levels and the protection from cardiovascular disease, the mechanism by which increases in plasma bilirubin acts to protect against cardiovascular disease is unknown. Since the chronic antihypertensive actions of bilirubin are likely due to its renal actions, the effects of moderate increases in plasma bilirubin on renal hemodynamics as well as bilirubin's potential effects on renal tubule function will be discussed in this review. Mechanisms of action as well as the potential for antihypertensive therapies targeting moderate increases in plasma bilirubin levels will also be highlighted.

AB - Bilirubin is generated from the breakdown of heme by heme oxygenase and the reduction of biliverdin by the enzyme biliverdin reductase. Several large population studies have reported a significant inverse correlation between plasma bilirubin levels and the incidence of cardiovascular disease. Protection from cardiovascular disease is also observed in patients with Gilbert's syndrome which is a disease characterized by mutations in hepatic UGT1A1, the enzyme responsible for the conjugation of bilirubin into the bile. Despite the strong correlation between plasma bilirubin levels and the protection from cardiovascular disease, the mechanism by which increases in plasma bilirubin acts to protect against cardiovascular disease is unknown. Since the chronic antihypertensive actions of bilirubin are likely due to its renal actions, the effects of moderate increases in plasma bilirubin on renal hemodynamics as well as bilirubin's potential effects on renal tubule function will be discussed in this review. Mechanisms of action as well as the potential for antihypertensive therapies targeting moderate increases in plasma bilirubin levels will also be highlighted.

KW - Biliverdin

KW - Biliverdin reductase

KW - Carbon monoxide

KW - Glomerular filtration rate

KW - Heme oxygenase

KW - Liver

KW - Renal blood flow

KW - UGT1A1

UR - http://www.scopus.com/inward/record.url?scp=84865997488&partnerID=8YFLogxK

U2 - 10.3389/fphar.2012.00018

DO - 10.3389/fphar.2012.00018

M3 - Article

C2 - 22347861

AN - SCOPUS:84865997488

VL - 3 FEB

JO - Frontiers in Pharmacology

JF - Frontiers in Pharmacology

SN - 1663-9812

M1 - Article 18

ER -