Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade.

Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Research Abstract Details 

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Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Abstract Text:

Jean LeFebvre,Ayumi Shintani,Tebeb Gebretsadik,Jeffery R Petro,Laine J Murphey,Nancy J Brown,

This study tested the hypothesis that endogenous bradykinin contributes to the effects of angiotensin AT(1) receptor blockade in humans. The effect of the bradykinin B(2) receptor antagonist d-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-d-Tic-Oic-Arg (HOE-140) (18 microg/kg/h i.v. for 6 h) on hemodynamic and endocrine responses to acute and chronic (1-month) treatment with valsartan (160 mg/day) was determined in 13 normotensive and 12 hypertensive salt-deplete subjects. Acute valsartan increased plasma renin activity (PRA) from 5.3 +/- 9.9 to 15.6 +/- 19.8 ng of angiotensin (Ang) I/ml/h (P < 0.001) and decreased aldosterone from 18.3 +/- 10.5 to 12.0 +/- 9.6 ng/dl (P < 0.001). Chronic valsartan significantly increased baseline PRA (10.5 +/- 15.5 ng of Ang I/ml/h; P = 0.004) but did not affect baseline angiotensin-converting enzyme activity or aldosterone. HOE-140 tended to increase the PRA response to valsartan, and it attenuated the decrease in aldosterone following chronic valsartan (P = 0.03). Acute valsartan decreased mean arterial pressure 12.7 +/- 6.9% (from 100.2 +/- 8.4 to 87.5 +/- 9.8 mm Hg in hypertensives and from 82.4 +/- 8.6 to 70.3 +/- 8.4 mm Hg in normotensives). HOE-140 did not affect the blood pressure response to either acute (effect of valsartan, P < 0.001; effect of HOE-140, P = 0.98) or chronic (valsartan, P = 0.01; HOE-140, P = 0.84) valsartan. Plasma cGMP was increased significantly during chronic valsartan (P = 0.048) through a bradykinin receptor-independent mechanism (effect of HOE-140, P = 0.13). Both acute (P < 0.001) and chronic (P < 0.001) valsartan increased heart rate. HOE-140 augmented the heart rate response to chronic valsartan (P = 0.04). These data suggest that endogenous bradykinin does not contribute significantly to the blood pressure-lowering effect of valsartan through its B(2) receptor.

Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Publishing Authors By Initials

J LeFebvre,A Shintani,T Gebretsadik,JR Petro,LJ Murphey,NJ Brown,

For similar amino acids, peptides, and proteins: amino acids: amino acids, branched-chain: valine research abstracts see: amino acids, peptides, and proteins: amino acids: amino acids, branched-chain: valine research

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MEDLINE DATE:

Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of pharmacology and experimental thera

VOLUME: 320

Page Numbers: 1261-7

Journal Abbreviation: J. Pharmacol. Exp. Ther.

ISSN: 0022-3565

DAY: 20

MONTH: 12

YEAR: 2006

Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 376362

Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Keywords Mesh Terms:

KEYWORDS: Valine

MESH TERMS: therapeutic use

Chemical & Substance for Abstract: Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade. Information

Substance Name: Renin

Registry Number: EC 3.4.23.15

Grant and Affiliation Information for Bradykinin B(2) receptor does not contribute to blood pressure lowering during AT(1) receptor blockade.

AFFILIATION: Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-6602, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01HL067308

ACRONYM: HL

MEDLINETA: J Pharmacol Exp Ther

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