NDLI: Dual influence of spontaneous hypertension on membrane properties and ATP production in heart and kidney mitochondria in rat: effect of captopril and nifedipine, adaptation and dysadaptation.

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Dual influence of spontaneous hypertension on membrane properties and ATP production in heart and kidney mitochondria in rat: effect of captopril and nifedipine, adaptation and dysadaptation.

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Dual influence of spontaneous hypertension on membrane properties and ATP production in heart and kidney mitochondria in rat: effect of captopril and nifedipine, adaptation and dysadaptation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ziegelhöffer, A. Mujkosová, J. Ferko, M. Vrbjar, N. Ravingerová, T. Ulicná, O. Waczulíková, I. Ziegelhöffer, B.
Description	Author Affiliation: Ziegelhöffer A ( Institute for Heart Research, Slovak Academy of Sciences, Centre of Excellence NOREG, Bratislava, Slovak Republic. usrdzigy@savba.sk)
Abstract	This study deals with changes, induced by hypertension and its treatment, in the function and properties of mitochondria in the heart and kidneys. Male, 16-week-old hypertensive rats were allocated to 3 groups: (i) animals treated daily for 4 weeks with captopril (CAP, 80 mg·(kg body mass)(-1), n = 45), (ii) animals treated with CAP + nifedipine (NIF, 10 mg·kg(-1), n = 45), or (iii) untreated hypertensive controls (n = 96). Wistar rats (n = 96) were used as normotensive controls. Systolic blood pressure (SBP), heart rate (HR), and heart mass / body mass (HW/BW) ratio were measured at the beginning and end of the experiments; measurements for mitochondrial Mg(2+)-ATPase activity, O(2)-consumption (QO(2)), respiratory control index (RCI), ADP/O, oxidative phosphorylation rate (OPR), conjugated diene content (CD), and membrane fluidity (MF) were also taken at different time intervals. In the heart, elevated SBP, HR, and HW/BW accompanied increased QO(2), OPR, and Mg(2+)-ATPase activity, indicating an adaptive response to hypertension-induced increase in the energy demands of the myocardium. Treatments with CAP or with CAP + NIF were very similar in their prevention of increase in SBP, HR, HW/BW, and the rise in OPR (all p < 0.05-0.01). In the kidneys, hypertension induced a drop in OPR; however, antihypertensive therapy aggravated the resulting energy deficiency, whereby treatment with CAP + NIF was more detrimental than treatment with CAP alone. Heart and kidney mitochondria exhibited negligible changes in CD and moderately increased MF, which was more potentiated by treatment with CAP alone than with CAP + NIF.
File Format	HTM / HTML
ISSN	00084212
e-ISSN	12057541
Journal	Canadian Journal of Physiology and Pharmacology
Issue Number	9
Volume Number	90
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2012-09-01
Publisher Place	Canada
Access Restriction	Open
Subject Keyword	Discipline Physiology Discipline Pharmacology Adaptation, Physiological Drug Effects Adenosine Triphosphate Metabolism Antihypertensive Agents Therapeutic Use Hypertension Drug Therapy Kidney Mitochondria Mitochondrial Membranes Myocardium Animals Administration & Dosage Pharmacology Blood Pressure Captopril Drug Therapy, Combination Heart Rate Physiopathology Membrane Fluidity Mitochondria, Heart Nifedipine Rats, Inbred Shr Rats, Wistar Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Pharmacology

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