Effects of angiotensin II on ionic fluxes in rat myometrium.
1. The action of angiotensin II (At II) on 24Na, 42K and 36 Cl fluxes was examined using longitudinal strips of rat myometrium as an experimental model. 2. In normally polarized muscles, At II 3.3 x 10(-6)M, a concentration 10 times higher than necessary to produce a maximal contraction of the muscle, increases 42K and 36 Cl efflux rates as well as 42K uptake. The action of At II on 42K and 36Cl effluxes is concentration-dependent. Under the same conditions 24Na efflux is not affected by At II, but a significant increase of 24Na uptake is obtained. In order to know whether the observed effects were membrane potential dependent, we reexamined the action of the peptide in preparations previously depolarized by a 101 mM K+ solution (K+ replacing Na+). In depolarized preparations, At II 3.3 x 10(-6)M still increases 24Na uptake, but the effects previously observed on 42K and 36Cl fluxes in normally polarized preparations are suppressed. It is concluded that At II produces a primary increase in the membrane permeability to Na+ and that the stimulation of 42K and 36Cl fluxes induced by At II in myometrial strips appears to be mainly potential dependent.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D002712:Chlorides / Q000378:metabolism; D005260:Female; D007477:Ions / Q000378:metabolism*; D008566:Membranes / Q000378:metabolism; D009215:Myometrium / Q000187:drug effects* / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D014599:Uterus / Q000187:drug effects*
D002712:Chlorides; D007477:Ions; D000804:Angiotensin II; D012964:Sodium; D011188:Potassium