Phenolic compounds in Commander, Majak, and Valley sunflowers varied between 3.0 and 3.5 g of chlorogenic acid per 100 g of flour. Under neutral and alkaline conditions, sunflower protein solutions develop dark green and brown colors because of bonding with oxidation products of polyphenolic compounds, especially chlorogenic acid. Therefore, a reducing agent was utilized in the present study to inhibit the formation of covalent bonds but 30% of the chlorogenic acid was nondialyzable and remained bound to the flour constituents. About one-half of the phenolic constituents were extracted with the soluble sunflower proteins by neutral salt solutions and about onethird o:: this fraction was also nondialyzable.Fractionation of the neutral salt extracts revealed that all of the soluble chlorogenic acid was associated with the low molecular weight components (mol wt <5000) in the third fraction on Sephadex G-25 and fraction V in Sephadex G-200 chromatography. The elution behavior on Sephadex gels, the low nitrogen contents, and the low amino acid recoveries demonstrated that these fractions were polypeptides and oligonucleotides. Rechromatography of fraction V on Sephadex G-200 in the presence of a strong hydrogen bonding agent, 7 M urea, revealed that 68% of the salt-soluble polypeptides were hydrogen bonded and about 32% were apparently covalent bonded to chlorogenic acid in Commander sunflower.Sunflower is one of the fastest developing oilseed crops and ranks second in importance as a world source of vegetable oil. The fibrous by-product of oil extraction is uti-

Eight of the ten phenolic compounds in the aqueous methanolic extracts from three varieties of sunflower were tentatively identified and quantitated by their spectrophotometric and chromatographic characteristics. Chlorogenic acid, one of its isomers, and caffeic acid constituted 70% of the total phenolic compounds in the flour of each variety. Compounds related to p-coumaric, iso-ferulic, and sinapic acids and a hydroxycinnamic acid-sugar ester were also detected by tic and glc analyses. The sinapic acid like compound represented 15% of the total phenolic compounds in the three flours. Two minor components with long retention times were also present in the neutral fraction.Sunflower ranks as second in importance among world sources of vegetable oils and there is considerable interest in utilizing the light-colored defatted flour for food purposes. The utilization of the high protein by-product from oilseed crushing in foods has been limited by the presence of phenolic constituents which are readily oxidized into dark green and brown compounds. A number of extraction procedures have been devised to remove the phenolic compounds from sunflower kernels and flours (Gheyasuddin et al., 1970;Sosulski et al., 1972) but the economic feasibility of these processes is unknown.Chlorogenic acid has been identified as the major phenolic compound in sunflower kernels with minor constituents being caffeic acid, 3,5-dicaffeoylquinic acid, and a disubstituted cinnamic acid (Mikolajczak et al., 1970;

Smooth muscle cells were cultured from rat thoracic aorta and labeled to a stable specific activity with 45Ca2+, myo-[2-3H]inositol, or 32p;. The efflux of 45Ca2+ was monitored over 10-sec intervals. Angiotensin II (All) increased the amount off5Ca21 lost by 5-fold in the first 10-sec interval after the addition of All and by 10-fold in the second 10-sec interval. AII-stimulated 45Ca2+ release was blocked by the angiotensin antagonist [1-sarcosine, 8-leucine]AII and byLa3+. The removal of external Ca2' had no effect on All-stimulated 45Ca2+ release. Depolarization with high external K+ only slightly increased 45Ca2' efflux and had no effect on Allinduced 45Ca2+ release. All had no effect on the initial rate of 45Ca2+ influx. These results indicate that the rapid 45Ca2+ efflux evoked by All is probably due to the release of 45Ca2+ sequestered intracellularly rather than to an increase in the Ca2+ permeability of the plasma membrane. All provoked rapid increases in the levels of phosphatidic acid and phosphoinositides in the cells. These increases in phospholipids were associated with increases in phospholipase C-generated inositol phosphates (tri-, di-, and mono-). It appears that All simultaneously increases phosphoinositide hydrolysis and synthesis in vascular smooth muscle, and both phospholipid effects may contribute to inositol triphosphate generation, which was sufficiently rapid to have a role in intracellular Ca2+ mobilization.Angiotensin II (All) is a potent vasoconstrictor that acts directly on vascular smooth muscle (1, 2). The binding of the hormone to a receptor on the surface of the smooth muscle cell (SMC) (3-6) somehow increases cytoplasmic calcium activity, which evokes a contractile response. The initial phase of the contractile response to AII (7) and other agonists (7-11) appears to be dependent on intra-rather than extracellular Ca2 . In contrast, the slow tonic component of agonist-induced contraction depends on extracellular Ca2+ (7-11). SMC cultured from rat aorta respond to AII by increasing the cycling of Na+ in and out of the cell (12-14). AII stimulates Na+ entry via an amiloride-inhibitable transporter, which results in an increased supply of Na+ to the Na+/K+ pump. Na+/K+ pump activity is thereby increased because cellular Na+ is the rate-limiting substrate for the pump in mammalian cells including vascular smooth muscle in vivo and in culture (15-17). AII depolarizes cultured aortic SMC by 10-15 mV as indicated by reciprocal changes in the steady-state distributions of [ H]tetraphenylphosphonium+ and 35SCN- (18).Recent evidence has suggested that inositol 1,4,5-(PO4)3 (Ins-P3), which is generated by agonist-induced hydrolysis of triphosphoinositide (19,20), releases calcium from a nonmitochondrial site, presumably the endoplasmic reticulum (21-23). All has been shown to provoke TPI breakdown in rat liver (24) and adrenal glomerulosa cells (25), and the effect of All in the latter tissue is apparently associated with an increase in de novo synthesis of phosphoinositides (26)....

No abstract

a company or product name by the department does not imply approval or recommendation of the product to the exclusion of others which may also be suitable.