Document Detail


Altered relationship between cyclic GMP and myocardial O2 consumption in renal hypertension-induced cardiac hypertrophy.
MedLine Citation:
PMID:  9706666     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We tested the hypothesis that preventing cyclic GMP degradation with zaprinast, (a selective cyclic GMP-phosphodiesterase inhibitor) would produce a blunted reduction in myocardial O2 consumption in renal hypertension (One Kidney-One Clip, 1K1C)-induced cardiac hypertrophy. Four groups of anesthetized open-chest New Zealand white rabbits (n = 26) were utilized. Either vehicle or zaprinast (3 x 10(-3) M) was applied topically to the left ventricular surface of control or 1K1C rabbits. Coronary blood flow (radioactive microspheres) and O2 extraction (microspectrophotometry) were used to determine O2 consumption. Myocardial cyclic GMP levels were determined by radioimmunoassay. The 1K1C rabbits had a greater heart weight-to-body weight ratio (2.94 +/- 0.08 g/kg) than controls (2.58 +/- 0.17). Systolic blood pressure was higher in 1K1C (102 +/- 9 mm Hg) than in controls (86 +/- 3). Zaprinast significantly and similarly increased cyclic GMP in both control (3.90 +/- 0.47 to 4.66 +/- 0.89 pmol/g) subepicardium (EPI) and (5.08 +/- 0.69 to 7.06 +/- 1.36) subendocardium (ENDO) and 1K1C hearts (5.53 +/- 0.61 to 7.48 +/- 1.51 EPI and 6.48 +/- 0.42 to 8.88 +/- 1.08 ENDO). Myocardial O2 consumption (ml O2/min/ 100 g) was significantly lower in controls treated with zaprinast (EPI: 8.8 +/- 0.1; ENDO: 9.5 +/- 1.9) than in controls treated with vehicle (EPI: 13.6 +/- 1.3; ENDO: 16.2 +/- 2.9). This effect was diminished in 1K1C rabbits treated with zaprinast (EPI: 10.3 +/- 2.4; ENDO: 11.2 +/- 2.6) compared with the vehicle-treated 1K1C group (EPI: 13.3 +/- 1.2; ENDO: 14.5 +/- 2.4). There was a similar increase in myocardial cyclic GMP after treatment with zaprinast, but a greater depression of myocardial O2 consumption in control animals than in 1K1C after treatment with zaprinast. This suggested that the reduction in myocardial O2 consumption, related to increases in cyclic GMP caused by cyclic GMP-phosphodiesterase blockade, was less in 1K1C cardiac hypertrophy.
Authors:
P Rabindranauth; P M Scholz; J Tse; K L Naim; H R Weiss
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Research in experimental medicine. Zeitschrift für die gesamte experimentelle Medizin einschliesslich experimenteller Chirurgie     Volume:  198     ISSN:  0300-9130     ISO Abbreviation:  Res Exp Med (Berl)     Publication Date:  1998 Jul 
Date Detail:
Created Date:  1998-10-27     Completed Date:  1998-10-27     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0324736     Medline TA:  Res Exp Med (Berl)     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  11-21     Citation Subset:  IM    
Affiliation:
Department of Physiology & Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854-5635, USA.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Cardiomegaly / etiology,  metabolism*
Coronary Circulation / drug effects
Cyclic GMP / analysis,  metabolism*
Hemodynamics
Hypertension, Renovascular / complications
Microspheres
Myocardium / metabolism*
Oxygen Consumption*
Phosphodiesterase Inhibitors / pharmacology*
Purinones / pharmacology*
Rabbits
Grant Support
ID/Acronym/Agency:
HL40320/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Phosphodiesterase Inhibitors; 0/Purinones; 37762-06-4/zaprinast; 7665-99-8/Cyclic GMP

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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