Angiotensin II (AngII) constricts isolated descending vasa recta (DVR), apparently by contracting surrounding pericytes, at least partly by stimulating chloride currents (Turner et al. 2001; Zhang et al. 2001; Pallone & Huang, 2002). Such vasoactivity suggests that DVR may regulate the distribution of blood flow within the renal medulla. Blocking AngII receptor subtypes indicates that AT₁ stimulation constricts DVR, whereas AT₂ stimulation opposes constriction (T.L. Pallone, personal communication). I have looked for effects of selective AT₁ or AT₂ antagonists, losartan and PD123,319, respectively, upon pericyte currents stimulated by AngII, during whole-cell permeabilised patch-clamp recording from DVR.

Individual DVR were dissected from renal tissue kept at 4 °C (Zhang et al. 2001), after removal from rats humanely killed by stunning and cervical dislocation. DVR were incubated in collagenase and hyaluronidase (0.4 mg ml^-1 of each) at room temperature for 8Ð9 min, stored at 4 °C and transferred at intervals to solution at room temperature, containing (mM): Na⁺ 150, K⁺ 5, Mg²⁺ 1, Ca²⁺ 1, Cl^– 159, Hepes 10 and glucose 10, plus 18β-glycyrrhetinic acid (40 mM), a gap junction blocker (Yamamoto et al. 1998). Heat-polished pipettes filled with solution containing Na⁺ 10, K⁺ 140, Cl^– 150 and Hepes 10, plus gramicidin (0.4 mg ml^-1), were applied to pericyte cell bodies to form gigaohm seals and AngII was added once to each microvessel.

AngII stimulated repetitive transient inward currents in pericytes at -50 mV (Turner et al. 2001; Pallone & Huang, 2002). Losartan (10^-6 M) reduced the amplitude and frequency of transients between 40 and 180 s of exposure to AngII (10^-8 M), but PD123,319 (10^-6 M) did not modify them significantly (Fig. 1). This is evidence that AngII acts via AT₁, but not AT₂, receptors to modulate these currents.

This work was supported by British Heart Foundation grant PG/2000105. Losartan was provided by Merck, USA.

All procedures accord with current UK legislation.