1 Endothelium-derived hyperpolarizing factor (EDHF) has recently been identi®ed as potassium released from endothelial cells into the myo-endothelial space. The present study was designed to test this hypothesis. 2 In rat small mesenteric arteries, mounted in a wire myograph, relaxation to acetylcholine or potassium was not signi®cantly changed following incubation with oxadiazolo-quinoxalin-1-one (ODQ, 4 mM) and indomethacin (10 mM, n=9). 3 Maximal relaxations to acetylcholine occurred in all arteries, were maintained and were signi®cantly greater (P50.01, n=9) than the transient relaxations to potassium, which only occurred in 30 ± 40% of vessels. 4 Removal of the vascular endothelium abolished relaxant responses both to potassium and acetylcholine (P50.005, n=9). 5 Compared with responses in 5.5 mM potassium PSS, relaxation responses to added potassium in arteries maintained in 1.5 mM potassium PSS were more marked and were not dependent on the presence of an intact endothelium (n=8). 6 Incubation with BaCl 2 (50 mM) signi®cantly inhibited the maximal relaxant response to potassium in the presence of an intact endothelium in 5.5 mM potassium PSS (P50.05, n=4), but had no eect on relaxation of de-endothelialized preparations in 1.5 mM potassium PSS (n=5). 7 Treatment with ouabain (0.1 mM) abolished the relaxant response to potassium in 1.5 mM potassium PSS (P50.001, n=9), but only partly inhibited the maximal relaxant response to acetylcholine in 5.5 mM potassium PSS (P50.01, n=5). 8 These data show that at physiological concentrations of potassium an intact endothelium is necessary for potassium-induced relaxation in rat mesenteric arteries. Furthermore, the response to potassium is clearly dierent to that from acetylcholine, indicating that potassium does not mimic EDHF released by acetylcholine in these arteries.

Rat models of cardiac hypertrophy are characterised by a shift in left ventricular myosin isoform from V1 (adult) to V3 (foetal), the latter being associated with a slowing of the acto-myosin ATPase rate. The aim of this study was to examine hypertrophy effects on relaxation by investigating a chemically skinned cardiac preparation from the SHR, where all the cellular membranes are rendered non-functional allowing the myofibrils to be studied in isolation. On comparison, following photolysis of the photolabile caged Ca2+ chelator diazo-2, it can be seen that the SHR fibres relax at a slower rate than their age-matched WKY counterparts. We suggest that, since the thin filament regulatory proteins seem not to be affected by cardiac hypertrophy in the rat, this result can be attributed to the shift in left ventricular myosin isoforms. The reduced relaxation rate in the SHR could be the result of a slowing of the dissociation of actin and myosin during the cross-bridge cycle. These results have previously been published in abstract form [1].