Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity

C. M. Boustany-Kari; M. Gong; W. S. Akers; Z. Guo; L. A. Cassis

doi:10.1038/sj.ijo.0803426

Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity

C. M. Boustany-Kari, M. Gong, W. S. Akers, Z. Guo, L. A. Cassis

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

Objective: To determine whether obesity-induced hypertension was associated with alterations in vascular contractility and/or cardiac function. Design: Male Sprague-Dawley rats were fed either a low fat (LF; 11% kcal as fat) or a moderately high fat (MHF; 32% kcal as fat) diet for 11 weeks. Measurements: Body weight; mean arterial pressure; angiotensin peptides; mesenteric contractile response to phenylephrine (PE), potassium chloride (KCl), serotonin, angiotensin II (AngII), calcium chloride; baseline and isoproterenol-induced cardiac contractility; baseline and isoproterenol-induced coronary artery blood flow. Results: Rats fed the MHF diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups. OP rats exhibited elevations in mean arterial pressure (MAP) and elevations in systemic concentrations of angiotensin peptides. Mesenteric arteries from OP rats exhibited a greater contractile response to PE, KCl and serotonin (5-HT). Heightened responses to PE persisted in arteries from OP rats even after normalization of the response to KCl. In contrast, the response of permeabilized mesenteric arteries to a maximal concentration of calcium was similar in rats from each group. Isolated perfused hearts exhibited similar baseline and isoproterenol-induced contractility in rats from each group. However, isoproterenol was unable to increase coronary artery blood flow in hearts from OP rats. Conclusion: Enhanced vascular reactivity may contribute to obesity-induced hypertension, while reductions in coronary artery relaxation would impair the ability of the heart to respond to increased myocardial demand.

Original language	English
Pages (from-to)	1652-1659
Number of pages	8
Journal	International Journal of Obesity
Volume	31
Issue number	11
DOIs	https://doi.org/10.1038/sj.ijo.0803426
State	Published - Nov 2007

Bibliographical note

Funding Information:
This research was supported by National Heart Lung and Blood Institute Grant HL-73085 (L Cassis), and through an American Heart Association Grant-in-Aid 0455159B (W Akers).

Keywords

Angiotensin
Cardiac function
Hypertension
Vascular contractility

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Medicine (miscellaneous)
Nutrition and Dietetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1038/sj.ijo.0803426

Cite this

@article{924c380a198d416b94985d3710c37869,

title = "Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity",

abstract = "Objective: To determine whether obesity-induced hypertension was associated with alterations in vascular contractility and/or cardiac function. Design: Male Sprague-Dawley rats were fed either a low fat (LF; 11% kcal as fat) or a moderately high fat (MHF; 32% kcal as fat) diet for 11 weeks. Measurements: Body weight; mean arterial pressure; angiotensin peptides; mesenteric contractile response to phenylephrine (PE), potassium chloride (KCl), serotonin, angiotensin II (AngII), calcium chloride; baseline and isoproterenol-induced cardiac contractility; baseline and isoproterenol-induced coronary artery blood flow. Results: Rats fed the MHF diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups. OP rats exhibited elevations in mean arterial pressure (MAP) and elevations in systemic concentrations of angiotensin peptides. Mesenteric arteries from OP rats exhibited a greater contractile response to PE, KCl and serotonin (5-HT). Heightened responses to PE persisted in arteries from OP rats even after normalization of the response to KCl. In contrast, the response of permeabilized mesenteric arteries to a maximal concentration of calcium was similar in rats from each group. Isolated perfused hearts exhibited similar baseline and isoproterenol-induced contractility in rats from each group. However, isoproterenol was unable to increase coronary artery blood flow in hearts from OP rats. Conclusion: Enhanced vascular reactivity may contribute to obesity-induced hypertension, while reductions in coronary artery relaxation would impair the ability of the heart to respond to increased myocardial demand.",

keywords = "Angiotensin, Cardiac function, Hypertension, Vascular contractility",

author = "Boustany-Kari, {C. M.} and M. Gong and Akers, {W. S.} and Z. Guo and Cassis, {L. A.}",

note = "Funding Information: This research was supported by National Heart Lung and Blood Institute Grant HL-73085 (L Cassis), and through an American Heart Association Grant-in-Aid 0455159B (W Akers).",

year = "2007",

month = nov,

doi = "10.1038/sj.ijo.0803426",

language = "English",

volume = "31",

pages = "1652--1659",

number = "11",

}

TY - JOUR

T1 - Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity

AU - Boustany-Kari, C. M.

AU - Gong, M.

AU - Akers, W. S.

AU - Guo, Z.

AU - Cassis, L. A.

N1 - Funding Information: This research was supported by National Heart Lung and Blood Institute Grant HL-73085 (L Cassis), and through an American Heart Association Grant-in-Aid 0455159B (W Akers).

PY - 2007/11

Y1 - 2007/11

N2 - Objective: To determine whether obesity-induced hypertension was associated with alterations in vascular contractility and/or cardiac function. Design: Male Sprague-Dawley rats were fed either a low fat (LF; 11% kcal as fat) or a moderately high fat (MHF; 32% kcal as fat) diet for 11 weeks. Measurements: Body weight; mean arterial pressure; angiotensin peptides; mesenteric contractile response to phenylephrine (PE), potassium chloride (KCl), serotonin, angiotensin II (AngII), calcium chloride; baseline and isoproterenol-induced cardiac contractility; baseline and isoproterenol-induced coronary artery blood flow. Results: Rats fed the MHF diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups. OP rats exhibited elevations in mean arterial pressure (MAP) and elevations in systemic concentrations of angiotensin peptides. Mesenteric arteries from OP rats exhibited a greater contractile response to PE, KCl and serotonin (5-HT). Heightened responses to PE persisted in arteries from OP rats even after normalization of the response to KCl. In contrast, the response of permeabilized mesenteric arteries to a maximal concentration of calcium was similar in rats from each group. Isolated perfused hearts exhibited similar baseline and isoproterenol-induced contractility in rats from each group. However, isoproterenol was unable to increase coronary artery blood flow in hearts from OP rats. Conclusion: Enhanced vascular reactivity may contribute to obesity-induced hypertension, while reductions in coronary artery relaxation would impair the ability of the heart to respond to increased myocardial demand.

AB - Objective: To determine whether obesity-induced hypertension was associated with alterations in vascular contractility and/or cardiac function. Design: Male Sprague-Dawley rats were fed either a low fat (LF; 11% kcal as fat) or a moderately high fat (MHF; 32% kcal as fat) diet for 11 weeks. Measurements: Body weight; mean arterial pressure; angiotensin peptides; mesenteric contractile response to phenylephrine (PE), potassium chloride (KCl), serotonin, angiotensin II (AngII), calcium chloride; baseline and isoproterenol-induced cardiac contractility; baseline and isoproterenol-induced coronary artery blood flow. Results: Rats fed the MHF diet segregated into obesity-prone (OP) and obesity-resistant (OR) groups. OP rats exhibited elevations in mean arterial pressure (MAP) and elevations in systemic concentrations of angiotensin peptides. Mesenteric arteries from OP rats exhibited a greater contractile response to PE, KCl and serotonin (5-HT). Heightened responses to PE persisted in arteries from OP rats even after normalization of the response to KCl. In contrast, the response of permeabilized mesenteric arteries to a maximal concentration of calcium was similar in rats from each group. Isolated perfused hearts exhibited similar baseline and isoproterenol-induced contractility in rats from each group. However, isoproterenol was unable to increase coronary artery blood flow in hearts from OP rats. Conclusion: Enhanced vascular reactivity may contribute to obesity-induced hypertension, while reductions in coronary artery relaxation would impair the ability of the heart to respond to increased myocardial demand.

KW - Angiotensin

KW - Cardiac function

KW - Hypertension

KW - Vascular contractility

UR - http://www.scopus.com/inward/record.url?scp=35648981980&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35648981980&partnerID=8YFLogxK

U2 - 10.1038/sj.ijo.0803426

DO - 10.1038/sj.ijo.0803426

M3 - Article

C2 - 16819529

AN - SCOPUS:35648981980

SN - 0307-0565

VL - 31

SP - 1652

EP - 1659

JO - International Journal of Obesity

JF - International Journal of Obesity

IS - 11

ER -

Enhanced vascular contractility and diminished coronary artery flow in rats made hypertensive from diet-induced obesity

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this