Effect of a low concentration of angiotensin II on vascular smooth muscle tone.
We have previously found that long-term blockade of angiotensin II (AII) formation by captopril suppresses the "leakiness" of vascular smooth muscle membrane from spontaneously hypertensive rats. The present study was undertaken to examine whether a subpressor concentration of AII alters the membrane permeability and the tension of vascular smooth muscle of rats. The isometric tensions of rat aortic strips were recorded and the cellular Na contents in the muscles were measured by the "cold Li-exchange method." Lowering external K+ concentration to 0 or 0.5 mM produced slowly developing contractions in the muscles. These contractions were significantly enhanced by 4 h of pretreatment with 3 X 10(-10) M AII, whereas there were no contractions in normal Tyrode solution. Increase in cellular Na during incubation in K+-free solution was greater in AII-pretreated muscles and the cellular Na in these muscles leaked out more rapidly into cold Li solution than it did in untreated muscles. These findings suggest that the subpressor concentration of AII increases the passive permeability of vascular smooth muscles to Na and, if the Na pump activity is partially impaired, elevates the vascular tone.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic; D002463:Cell Membrane Permeability / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006973:Hypertension / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism
D000804:Angiotensin II; D012964:Sodium; D011188:Potassium