Nifedipine inhibits the hypoxia-induced decrease in plasma renin activity in conscious dogs

• Autorzy: Hohne C. , Arntz E. , Krebs M.O. , Boemke W. , Kaczmarczyk G.
• Języki publikacji: EN

Abstrakty

EN

Acute hypoxia induces a decrease in plasma renin activity (PRA), mediated, e.g., by an increase in adenosine concentration, calcium channel activity, or inhibition of ATP-sensitive potassium channels. The decrease in PRA results in a decrease in angiotensin II (AngII) and plasma aldosterone concentration (PAC). This study investigates whether these hypoxia-induced mechanisms can be inhibited by the L-type voltage-dependent calcium channel antagonist nifedipine. Eight conscious, chronically tracheotomized dogs received a low sodium diet (0.5 mmol Na·kg body wt-1·day-1). The dogs were studied twice in randomized order, either with nifedipine infusion (1.5 µg·kg body wt-1·min-1, Nifedipine) or without (Control). The dogs were breathing spontaneously: first hour, normoxia [inspiratory oxygen fraction (FiO2)=0.21]; second and third hour hypoxia (FiO2=0.1). In Controls, PRA (6.8±0.8 vs. 3.0±0.5 ngAngI·ml-1·min-1), AngII (13.3±1.9 vs. 7.3±1.9 pg/ml), and PAC (316±50 vs. 69±12 pg/ml) decreased during hypoxia (P<0.05). In Nifedipine experiments, PRA (6.5±0.9 vs. 10.5±2.4 ngAngI·ml-1·min-1) and AngII (14±1.1 vs. 18±3.9 pg/ml) increased during hypoxia, whereas the decrease in PAC (292±81 vs. 153±41 pg/ml) was blunted (P<0.05). These results foster the idea that the hypoxia-induced decrease in PRA involves L-type calcium channel activity.

Słowa kluczowe

EN

calcium channel; activity; antagonist; adenosine; renin-angiotensin-aldosterone system; nifedipine; dog; hypoxia; potassium channel; plasma renin; angiotensin II

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2003
• Tom: 54
• Numer: 2
• Opis fizyczny: p.137-149,fig.

Twórcy

autor

Hohne C.

• Humboldt-Universitat zu Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany

autor

Arntz E.

autor

Krebs M.O.

autor

Boemke W.

autor

Kaczmarczyk G.