Membrane ATPase mechanism of K+-return relaxation in arterial muscles of stroke-prone SHR and WKY.
These studies compared the importance of electrogenic Na+-K+ active (ATP driven) transport, changes in K+ conductance, and passive Ca2+-Na+ countertransport in the large relaxation that occurs in the rat caudal and basilar artery on return to K+ from K+-free solutions. Furthermore, we compared the importance of these three membrane electrical mechanisms in stroke-prone spontaneously hypertensive rats (SP-SHR) versus their normotensive Wistar-Kyoto control rats (WKY) in basilar (cerebral) and caudal arteries. We found that in both basilar and caudal arteries the hyperpolarization and relaxation that occurred on return to K+ after exposure to a 0 K+ (extracellular) solution was consistently greater in SP-SHR than in WKY. The change in membrane potential occurring on transition to 0 K+ in arteries maintained at low temperature (16 degrees C), used as an estimate of the change in K+ conductance during the K+ transition, was not different in either basilar or caudal arteries between SP-SHR and WKY. Thus the hyperpolarization on return to K+ at body temperature would depend primarily on the level of activity of the membrane ATPase, referred to as the Na+ pump. We also sought to compare the passive (but electrogenic) Ca2+-Na+ countertransport mechanism between strains for both arteries, but we were unable to detect any evidence of the predicted hyperpolarization-contraction on transition from 145 to 10 mM extracellular Na+. Furthermore, the return to extracellular Na+ solution failed to show the depolarization-relaxation predicted by the Ca2+-Na+ countertransport mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D001693:Biological Transport, Active; D003971:Diastole; D004553:Electric Conductivity; D006973:Hypertension / Q000201:enzymology; D008564:Membrane Potentials; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009131:Muscle, Smooth, Vascular / Q000201:enzymology*; D009206:Myocardium / Q000201:enzymology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012964:Sodium / Q000378:metabolism; D014667:Vasopressins / Q000494:pharmacology
D014667:Vasopressins; D012964:Sodium; D000251:Adenosine Triphosphatases; D011188:Potassium