Endothelin-induced contraction of human peripheral resistance vessels is partly dependent on stimulation of sodium-hydrogen exchange.
The role of Na-H exchange in endothelin-induced contraction of human peripheral resistance vessels was investigated. Endothelin produced a dose-dependent contraction which was greatly attenuated in the presence of a low extracellular sodium concentration. Inhibition of Na-H exchange by the amiloride analogue 5-(N,N-hexamethylene) amiloride (5-NNHA) resulted in a greater than 65% relaxation of a maximal endothelin-induced contraction in the presence of normal extracellular sodium. However, in the presence of a low extracellular sodium concentration, inhibition of Na-H exchange only resulted in a 25% relaxation. These data suggest that endothelin-induced vasoconstriction of human peripheral resistance vessels is mediated in part by stimulation of Na-H exchange.
Richards
N T
NT
Renal Laboratory, St Thomas' Hospital, London, UK.
Poston
L
L
Goldsmith
D J
DJ
Cragoe
E J
EJ
Hilton
P J
PJ
D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D002352:Carrier Proteins; D004305:Dose-Response Relationship, Drug; D016232:Endothelins; D004730:Endothelium, Vascular / Q000502:physiology*; D006801:Humans; D007962:Leukocytes / Q000187:drug effects; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D010455:Peptides / Q000494:pharmacology*; D017923:Sodium-Hydrogen Exchangers; D014655:Vascular Resistance / Q000187:drug effects
D002352:Carrier Proteins; D016232:Endothelins; D010455:Peptides; D017923:Sodium-Hydrogen Exchangers; C057360:5-(N,N-hexamethylene)amiloride; D000584:Amiloride