This study demonstrates that phytoestrogens induce endothelium-independent relaxation of coronary arteries; the mechanism involves calcium antagonism. These mechanisms may contribute to the potential long-term cardiovascular protective effect of these substances.

The putative voltage-sensitive release mechanism (VSRM) was investigated in rabbit cardiac myocytes at 37°C with high resistance microelectrodes to minimize intracellular dialysis. When the holding potential was adjusted from −40 to −60 mV, the putative VSRM was expected to operate alongside CICR. Under these conditions however, we did not observe a plateau at positive potentials of the cell shortening versus voltage relationship. The threshold for cell shortening changed by −10 mV, but this resulted from a similar change of the threshold for activation of inward current. Cell shortening under conditions where the putative VSRM was expected to operate was blocked in a dose dependent way by nifedipine and CdCl2 and blocked completely by NiCl2. “Tail contractions” persisted in the presence of nifedipine and CdCl2 but were blocked completely by NiCl2. Block of early outward current by 4-aminopyridine and 4-acetoamido-4′-isothiocyanato-stilbene-2,2′-disulfonic acid (SITS) demonstrated persisting inward current during test depolarizations despite the presence of nifedipine and CdCl2. Inward current did not persist in the presence of NiCl2. A tonic component of cell shortening that was prominent during depolarizations to positive potentials under conditions selective for the putative VSRM was sensitive to rapidly applied changes in superfusate [Na+] and to the outward Na+/Ca2+ exchange current blocking drug KB-R7943. This component of cell shortening was thought to be the result of Na+/Ca2+ exchange–mediated excitation contraction coupling. Cell shortening recorded under conditions selective for the putative VSRM was increased by the enhanced state of phosphorylation induced by isoprenaline (1 μM) and by enhancing sarcoplasmic reticulum Ca2+ content by manipulation of the conditioning steps. Under these conditions, cell shortening at positive test depolarizations was converted from tonic to phasic. We conclude that the putative VSRM is explained by CICR with the Ca2+ “trigger” supplied by unblocked L-type Ca2+ channels and Na+/Ca2+ exchange.

The flagella in Cryptomonas ovata Ehrenberg and two other un-named strains of Cryptomonas both bear stiff hairs with fine distal filaments of the same type as those found in the Xanthophyceae, the Chrysophyceae sensu stricto, the Phaeophyceae, the Bacillariophyceae, the Eustigmatophyceae and the Oomycetes. On the longer of the two flagella the hairs are 2.5 ~m long and in two opposite rows whereas on the shorter flagellum they measure only 1 p.m, are arranged in a single row and are more closely spaced. The long flagellum also bears a characteristic lateral swelling with a tuft of hairs of the same type as on the remainder of the flagellum, at approximately the level at which it emerges from the gullet. The hairs on the flagella of Hemiselmis rufescens Parke are distributed in a similar manner to those in Cryptomonas but they are more flexible and the swelling and tuft of hairs appear to be absent from the long flagellum. Hairs are apparently absent from the short flagellum of Chroomonas sp. The periplast in Cryptomonas ovata shows a hexagonal pattern in surface view and in sections of all three Cryptomonas strains appears as a typical plasmalemma underlain by a discontinuous layer of electron-dense material with variable substructure. The distribution of flagellar hairs and the structure of the periplast appear to be characters unique to the Cryptophyceae and these features emphasise the isolated position of this class of algae.

No abstract