These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: An intracellular calcium release inhibitor TMB-8 suppresses renal nerve stimulation-induced antinatriuresis in dogs.
    Author: Ogasawara A, Hisa H, Satoh S.
    Journal: J Pharmacol Exp Ther; 1993 Jan; 264(1):117-21. PubMed ID: 8423524.
    Abstract:
    Effects of nifedipine and TMB-8 on antinatriuresis induced by renal nerve stimulation (RNS) were examined in pentobarbital-anesthetized dogs. RNS (1 Hz) decreased urine flow rate, urinary sodium excretion rate and fractional excretion of sodium and increased renal norepinephrine efflux and renal venous plasma renin activity with little changes in renal hemodynamics. Intrarenal arterial infusion of nifedipine (0.1 microgram/kg/min) or TMB-8 (50 and 100 micrograms/kg/min) increased basal urine flow rate, urinary sodium excretion rate and fractional excretion of sodium without affecting renal venous plasma norepinephrine concentration or plasma renin activity. Neither nifedipine nor TMB-8 affected the RNS-induced increases in norepinephrine efflux and plasmin renin activity. The RNS-induced decreases in urinary sodium excretion rate and fractional excretion of sodium were suppressed during the TMB-8 infusion, whereas nifedipine failed to affect these urinary responses. These results raise the possibility that the release of intracellular calcium from TMB-8-sensitive stores, but not the influx of extracellular calcium through dihydropyridine-sensitive calcium channels, participates in neural control of tubular sodium reabsorption in the dog kidney.
    [Abstract] [Full Text] [Related] [New Search]