Literature DB >> 2530000

Decreased cardiac concentration of cGMP kinase in hypertensive animals. An index for cardiac vascularization?

T Ecker1, C Göbel, R Hullin, R Rettig, G Seitz, F Hofmann.   

Abstract

Cyclic GMP (cGMP) kinase is intimately involved in the regulation of vascular smooth muscle tone. Its tissue concentration was determined in normotensive and hypertensive rats by use of monospecific anti-cGMP kinase antibodies. Hearts of spontaneously hypertensive rats and renovascular (Goldblatt II) hypertensive rats contained half the concentration of cGMP kinase than those of the respective normotensive animals. The increase in blood pressure and the resulting left ventricular hypertrophy were correlated inversely with the left ventricular cGMP kinase concentration. This decrease was specific for the left ventricle and was not observed in other tissues. In addition, the cardiac concentration of cGMP kinase was unchanged in hyperthyroid animals that had comparable left ventricular hypertrophy and mild hypertension. This suggested that in severe renovascular hypertension the decrease in cardiac cGMP kinase concentration is caused by a relative lack of cardiac vessel growth during the development of hypertrophy. In agreement with this conclusion, immunohistochemistry of cardiac cross sections showed that cGMP kinase was exclusively located in cardiac vessels. In support of this localization, the maximal arterial blood flow of heart, liver, skeletal muscle, and kidney correlated excellently with the cGMP kinase content of the respective organ. These results suggest that the cGMP kinase concentration of nonsmooth muscle tissues depends on the amount of organ-specific vascular smooth muscle and may be used as an index for the vascularization of these organs.

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Year:  1989        PMID: 2530000     DOI: 10.1161/01.res.65.5.1361

Source DB:  PubMed          Journal:  Circ Res        ISSN: 0009-7330            Impact factor:   17.367


  8 in total

1.  Ca2+ current is regulated by cyclic GMP-dependent protein kinase in mammalian cardiac myocytes.

Authors:  P F Méry; S M Lohmann; U Walter; R Fischmeister
Journal:  Proc Natl Acad Sci U S A       Date:  1991-02-15       Impact factor: 11.205

2.  Long-term potentiation in the hippocampal CA1 region of mice lacking cGMP-dependent kinases is normal and susceptible to inhibition of nitric oxide synthase.

Authors:  T Kleppisch; A Pfeifer; P Klatt; P Ruth; A Montkowski; R Fässler; F Hofmann
Journal:  J Neurosci       Date:  1999-01-01       Impact factor: 6.167

3.  Cardiac hypertrophy is not amplified by deletion of cGMP-dependent protein kinase I in cardiomyocytes.

Authors:  Robert Lukowski; Sergei D Rybalkin; Florian Loga; Veronika Leiss; Joseph A Beavo; Franz Hofmann
Journal:  Proc Natl Acad Sci U S A       Date:  2010-03-08       Impact factor: 11.205

4.  Guanosine 3': 5'-cyclic monophosphate-dependent pathway alterations in ventricular cardiomyocytes of spontaneously hypertensive rats.

Authors:  L Mazzetti; C Ruocco; L Giovannelli; M Ciuffi; S Franchi-Micheli; F Marra; L Zilletti; P Failli
Journal:  Br J Pharmacol       Date:  2001-10       Impact factor: 8.739

5.  Pressure-overload-induced subcellular relocalization/oxidation of soluble guanylyl cyclase in the heart modulates enzyme stimulation.

Authors:  Emily J Tsai; Yuchuan Liu; Norimichi Koitabashi; Djahida Bedja; Thomas Danner; Jean-Francois Jasmin; Michael P Lisanti; Andreas Friebe; Eiki Takimoto; David A Kass
Journal:  Circ Res       Date:  2011-11-17       Impact factor: 17.367

6.  Determinants of aortic cyclic guanosine monophosphate in hypertension induced by chronic inhibition of nitric oxide synthase.

Authors:  J F Arnal; L Warin; J B Michel
Journal:  J Clin Invest       Date:  1992-08       Impact factor: 14.808

7.  Expression of vascular endothelial growth factor during the development of cardiac hypertrophy in spontaneously hypertensive rats.

Authors:  A M McAinsh; M Geyer; J Fandrey; J C Rüegg; R J Wiesner
Journal:  Mol Cell Biochem       Date:  1998-10       Impact factor: 3.396

8.  The Effect of Sorafenib, Tadalafil and Macitentan Treatments on Thyroxin-Induced Hemodynamic Changes and Cardiac Abnormalities.

Authors:  Nancy S Saad; Kyle Floyd; Amany A E Ahmed; Peter J Mohler; Paul M L Janssen; Mohammad T Elnakish
Journal:  PLoS One       Date:  2016-04-15       Impact factor: 3.240

  8 in total

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