Relationship between cGMP and myocardial O2 consumption is altered in T4-induced cardiac hypertrophy

Harvey Weiss, E. Rodriguez, J. Tse

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Abstract

We tested the hypothesis that increases in guanosine 3',5'-cyclic monophosphate (cGMP) would reduce myocardial O2 consumption and that thyroxine (T4)-induced (0.5 mg/kg for 16 days) cardiac hypertrophy would change this relationship. Anesthetised open-chest New Zealand White rabbits were divided into four groups: control vehicle (CV, n = 7), control nitroprusside (CN, n = 6), T4 vehicle (T4V, n = 8), and T4 nitroprusside (T4N, n = 8). Vehicle or sodium nitroprusside (10-4 M) was topically applied to the left ventricular subepicardium for 15 min. Coronary blood flow (radioactive microspheres) and O2 extraction (microspectrophotometry) were used to determine O2 consumption. Gunnylate cyclase activity and cGMP were determined by radioimmunoassay. T4 increased the heart weight-to-body weight ratio from 2.7 ± 0.1 to 3.4 ± 0.2. Topical application of nitroprusside had no significant hemodynamic effects. Nitroprusside significantly increased myocardial cGMP in control hearts (CV = 4.1 ± 0.3 to CN = 12.4 ± 5.0 pmol/g) and T4 hearts (T4V = 3.9 ± 0.3 to T4N = 5.2 ± 0.4). The increase in the level of myocardial cGMP was significantly greater in CN (+202%) than in T4N (+33%). There were no significant differences in basal or total gunnylate cyclase activity between control and T4 rabbits. Myocardial O2 consumption significantly declined in both groups during nitroprusside (10.8 ± 1.4 for CV to 7.3 ± 1.0 for CN (-32%) and 13.6 ± 1.2 for T4V to 9.9 ± 1.4 ml O2 · min-1 · 100 g-1 for T4N (-27%)). Thus, although basal levels of cGMP were not altered, T4-treated hearts responded to nitroprusside with a lesser increase in cGMP, and O2 consumption was diminished similarly. This indicates a change in the inverse relationship between the myocardial level of cGMF and O2 consumption with T4.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume268
Issue number2 37-2
StatePublished - Jan 1 1995

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Cardiomegaly
Nitroprusside
Microspectrophotometry
Rabbits
Cyclic GMP
Thyroxine
Microspheres
Radioimmunoassay
Thorax
Hemodynamics
Body Weight
Weights and Measures
Control Groups

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)
  • Physiology

Cite this

@article{26ec6161e8764d4f911e4e600c8fcb8b,
title = "Relationship between cGMP and myocardial O2 consumption is altered in T4-induced cardiac hypertrophy",
abstract = "We tested the hypothesis that increases in guanosine 3',5'-cyclic monophosphate (cGMP) would reduce myocardial O2 consumption and that thyroxine (T4)-induced (0.5 mg/kg for 16 days) cardiac hypertrophy would change this relationship. Anesthetised open-chest New Zealand White rabbits were divided into four groups: control vehicle (CV, n = 7), control nitroprusside (CN, n = 6), T4 vehicle (T4V, n = 8), and T4 nitroprusside (T4N, n = 8). Vehicle or sodium nitroprusside (10-4 M) was topically applied to the left ventricular subepicardium for 15 min. Coronary blood flow (radioactive microspheres) and O2 extraction (microspectrophotometry) were used to determine O2 consumption. Gunnylate cyclase activity and cGMP were determined by radioimmunoassay. T4 increased the heart weight-to-body weight ratio from 2.7 ± 0.1 to 3.4 ± 0.2. Topical application of nitroprusside had no significant hemodynamic effects. Nitroprusside significantly increased myocardial cGMP in control hearts (CV = 4.1 ± 0.3 to CN = 12.4 ± 5.0 pmol/g) and T4 hearts (T4V = 3.9 ± 0.3 to T4N = 5.2 ± 0.4). The increase in the level of myocardial cGMP was significantly greater in CN (+202{\%}) than in T4N (+33{\%}). There were no significant differences in basal or total gunnylate cyclase activity between control and T4 rabbits. Myocardial O2 consumption significantly declined in both groups during nitroprusside (10.8 ± 1.4 for CV to 7.3 ± 1.0 for CN (-32{\%}) and 13.6 ± 1.2 for T4V to 9.9 ± 1.4 ml O2 · min-1 · 100 g-1 for T4N (-27{\%})). Thus, although basal levels of cGMP were not altered, T4-treated hearts responded to nitroprusside with a lesser increase in cGMP, and O2 consumption was diminished similarly. This indicates a change in the inverse relationship between the myocardial level of cGMF and O2 consumption with T4.",
author = "Harvey Weiss and E. Rodriguez and J. Tse",
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T1 - Relationship between cGMP and myocardial O2 consumption is altered in T4-induced cardiac hypertrophy

AU - Weiss, Harvey

AU - Rodriguez, E.

AU - Tse, J.

PY - 1995/1/1

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N2 - We tested the hypothesis that increases in guanosine 3',5'-cyclic monophosphate (cGMP) would reduce myocardial O2 consumption and that thyroxine (T4)-induced (0.5 mg/kg for 16 days) cardiac hypertrophy would change this relationship. Anesthetised open-chest New Zealand White rabbits were divided into four groups: control vehicle (CV, n = 7), control nitroprusside (CN, n = 6), T4 vehicle (T4V, n = 8), and T4 nitroprusside (T4N, n = 8). Vehicle or sodium nitroprusside (10-4 M) was topically applied to the left ventricular subepicardium for 15 min. Coronary blood flow (radioactive microspheres) and O2 extraction (microspectrophotometry) were used to determine O2 consumption. Gunnylate cyclase activity and cGMP were determined by radioimmunoassay. T4 increased the heart weight-to-body weight ratio from 2.7 ± 0.1 to 3.4 ± 0.2. Topical application of nitroprusside had no significant hemodynamic effects. Nitroprusside significantly increased myocardial cGMP in control hearts (CV = 4.1 ± 0.3 to CN = 12.4 ± 5.0 pmol/g) and T4 hearts (T4V = 3.9 ± 0.3 to T4N = 5.2 ± 0.4). The increase in the level of myocardial cGMP was significantly greater in CN (+202%) than in T4N (+33%). There were no significant differences in basal or total gunnylate cyclase activity between control and T4 rabbits. Myocardial O2 consumption significantly declined in both groups during nitroprusside (10.8 ± 1.4 for CV to 7.3 ± 1.0 for CN (-32%) and 13.6 ± 1.2 for T4V to 9.9 ± 1.4 ml O2 · min-1 · 100 g-1 for T4N (-27%)). Thus, although basal levels of cGMP were not altered, T4-treated hearts responded to nitroprusside with a lesser increase in cGMP, and O2 consumption was diminished similarly. This indicates a change in the inverse relationship between the myocardial level of cGMF and O2 consumption with T4.

AB - We tested the hypothesis that increases in guanosine 3',5'-cyclic monophosphate (cGMP) would reduce myocardial O2 consumption and that thyroxine (T4)-induced (0.5 mg/kg for 16 days) cardiac hypertrophy would change this relationship. Anesthetised open-chest New Zealand White rabbits were divided into four groups: control vehicle (CV, n = 7), control nitroprusside (CN, n = 6), T4 vehicle (T4V, n = 8), and T4 nitroprusside (T4N, n = 8). Vehicle or sodium nitroprusside (10-4 M) was topically applied to the left ventricular subepicardium for 15 min. Coronary blood flow (radioactive microspheres) and O2 extraction (microspectrophotometry) were used to determine O2 consumption. Gunnylate cyclase activity and cGMP were determined by radioimmunoassay. T4 increased the heart weight-to-body weight ratio from 2.7 ± 0.1 to 3.4 ± 0.2. Topical application of nitroprusside had no significant hemodynamic effects. Nitroprusside significantly increased myocardial cGMP in control hearts (CV = 4.1 ± 0.3 to CN = 12.4 ± 5.0 pmol/g) and T4 hearts (T4V = 3.9 ± 0.3 to T4N = 5.2 ± 0.4). The increase in the level of myocardial cGMP was significantly greater in CN (+202%) than in T4N (+33%). There were no significant differences in basal or total gunnylate cyclase activity between control and T4 rabbits. Myocardial O2 consumption significantly declined in both groups during nitroprusside (10.8 ± 1.4 for CV to 7.3 ± 1.0 for CN (-32%) and 13.6 ± 1.2 for T4V to 9.9 ± 1.4 ml O2 · min-1 · 100 g-1 for T4N (-27%)). Thus, although basal levels of cGMP were not altered, T4-treated hearts responded to nitroprusside with a lesser increase in cGMP, and O2 consumption was diminished similarly. This indicates a change in the inverse relationship between the myocardial level of cGMF and O2 consumption with T4.

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