Altered arterial muscle ion transport mechanism in the spontaneously hypertensive rat.
The cellular mechanisms that appear to contribute to increased contraction in hypertension involve altered ion movements through cell membranes. The K+ and Na+ gradients and the active transport of Na+ and K+, sometimes electrogenic, are important for the peripheral arteries. There may be other kinds of transport involved, especially the active transport of Ca2+. However, a passive Ca2+-Na+ countertransport mechanism has not been demonstrated in vascular muscle and therefore presently appears unlikely as an explanation of hypertension. The altered transport of Na+ and K+ apparently plays a causative role in the development of hypertension, because there is a cross-over of membrane properties on cross-innervation. Since the prevention of sympathetic innervation prevents that cross-over, it is likely that a long-term influence of the sympathetic nervous system is important in the development of hypertension. The trophic influence of the sympathetic innervation on vascular muscle is now one of the important frontiers in the study of cellular mechanisms that lead to increased blood pressure.
D000818:Animals; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism; D005110:Extracellular Space / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D007473:Ion Channels; D011188:Potassium; D002118:Calcium