Vascular muscle membrane cation mechanisms and total peripheral resistance.
Passive and active carrier-mediated transport of sodium across vascular muscle membranes has been suggested to be more important in the increased total peripheral resistance found in genetic hypertension. Using manipulations of ion gradients and recordings of ion currents, membrane potentials, and tension, I have found evidence for calcium regulation as the central pathophysiological mechanism in spontaneously hypertensive rats. Increased sodium pump activity, which may be a partial compensation for the increased sodium influx in hypertension, may thus be secondary to altered calcium channel regulation in hypertension. The calcium channel, and the membrane potentials governing it, seem to be the most immediately important membrane mechanisms for hypertension research.
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism*; D008564:Membrane Potentials; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014655:Vascular Resistance
D002352:Carrier Proteins; D007473:Ion Channels; D019831:Sodium-Calcium Exchanger; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium