Chronic effects of ACE-inhibition (quinapril) and angiotensin-II type-1 receptor blockade (losartan) on atrial natriuretic peptide in brain nuclei of rats with experimental myocardial infarction

Autor: Kai Hu, Udo Bahner, Markus Ring, Andrea Fehle, Peter Gaudron, Georg Ertl, Bernhard Kruse, Miklós Palkovits
Rok vydání: 2001
Předmět:
Male
medicine.medical_specialty
Physiology
Myocardial Infarction
Angiotensin-Converting Enzyme Inhibitors
Receptor
Angiotensin
Type 2
Losartan
Receptor
Angiotensin
Type 1
Ventricular Function
Left
Angiotensin Receptor Antagonists
Atrial natriuretic peptide
Tetrahydroisoquinolines
Physiology (medical)
Internal medicine
Renin–angiotensin system
medicine
Animals
Rats
Wistar
Receptors
Angiotensin
Angiotensin II receptor type 1
Dose-Response Relationship
Drug
biology
business.industry
Hemodynamics
Models
Cardiovascular
Quinapril
Brain
Angiotensin-converting enzyme
Isoquinolines
Angiotensin II
Subfornical organ
Rats
Treatment Outcome
medicine.anatomical_structure
Endocrinology
Cerebellar Nuclei
cardiovascular system
biology.protein
Vascular Resistance
Cardiology and Cardiovascular Medicine
business
Atrial Natriuretic Factor
hormones
hormone substitutes
and hormone antagonists
circulatory and respiratory physiology
medicine.drug
Zdroj: Basic Research in Cardiology. 96:258-266
ISSN: 1435-1803
0300-8428
DOI: 10.1007/s003950170056
Popis: Alterations of the central nervous system may be important for imbalance of cardiovascular and fluid regulation in heart failure. The central renin-angiotensin and atrial natriuretic peptide (ANP) systems act as mutual antagonists. The effects of angiotensin converting enzyme (ACE) inhibition (quinapril, 6 mg/kg/day) and angiotensin II type 1 (AT1) receptor blockade (losartan, 10 mg/kg/day) on ANP levels in 18 selected, microdissected brain nuclei were determined in sham-operated rats and rats with left ventricular dysfunction 8 weeks after myocardial infarction (MI). Plasma ANP tended to increase in MI rats and was further increased by quinapril. ANP was decreased in 12 brain areas of MI rats. ANP concentration was also significantly decreased by quinapril in six brain nuclei including subfornical organ and organum vasculosum laminae terminalis (areas lacking blood-brain barrier), and by losartan in 16 brain nuclei outside and within the blood-brain barrier in sham operated rats. However, both quinapril and losartan prevented a further reduction of central ANP as a result of myocardial infarction. These data suggest that there are effects on central ANP that result from chronic left ventricular dysfunction as well as an ACE-inhibitor and AT1-antagonist. Mechanisms and consequences of central ANP depression remain unclear. They could, however, support systemic vasoconstriction and sodium and fluid retention.
Databáze: OpenAIRE
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