Keizo Umegaki

Congenital changes of platelet functions in stroke-prone SHR:Aggregability of gel-filtered platelets, PRP and whole blood, and effects of hypotensive treatment

Platelet aggregation in whole blood, platelet rich plasma, and gel-filtered platelets were markedly attenuated in SHRSP compared with those in age-matched normotensive WKY. The result was consistent with the previous report of washed platelets. Despite prevention of high blood pressure, a long duration of hypotensive treatment only slightly improved aggregability of washed platelets but did not restore it to the range of age-matched WKY platelets. Blood pressure, heart ratios and thrombin-induced washed platelet aggregation were examined in SHRSP, WKY, and the cross (F1: WKY x SHRSP). The higher blood pressure and heart ratios the lower platelet aggregability was observed in the three strains, and there was no overlapping distribution of these values. F1 progeny exhibited intermediate values in blood pressure, heart ratio and platelet aggregability between the parental values. These results suggested that hypofunctions of SHRSP platelet were not secondary changes due to high blood pressure, but primary changes which are genetically linked to high blood pressure.

Defective calcium transport in platelets from stroke-prone spontaneously hypertensive rats

Aggregation and secretion of washed platelets from stroke-prone spontaneously hypertensive rats(SHRSP) were greatly reduced by the development of hypertension in comparison with age-matched normotensive WKY platelets. In an attempt to clarify the mechanism of the defective functions, Ca2+ transport in platelets from SHRSP and WKY were studied. Changes of cytoplasmic free Ca2+ concentration ([Ca2+]i) were examined by using Quin 2. [Ca2+]i increase in response to thrombin(0.028 - 0.11 U/ml) was significantly delayed in SHRSP platelets compared with that of age-matched WKY platelets. The time(sec) to peak in [Ca2+]i was about two times longer in SHRSP platelets than in WKY platelets. [Ca2+]i levels at resting state were significantly lower in SHRSP platelets while there was no difference in maximal [Ca2+]i level in response to thrombin (0.031 - 0.125 U/ml) between the two strains. In addition thrombin-induced 45Ca2+ uptake was significantly delayed in SHRSP platelets. This delay of [Ca2+]i increase following thrombin stimulation might be associated with the hypofunctions of SHRSP platelets.

Antiatherogenic Effects of Tea Polyphenols (Flavan-3-ols) in Humans and ApoE-Deficient Mice

In the subendothelial space, low-density lipoproteins (LDL) are converted to oxidized forms through contact with macrophages, endothelial and smooth muscle cells.1 Oxidatively modified LDL have chemotactic properties and recruit blood monocytes developing into tissue macrophages. In addition, modified LDL are taken up into macrophages through scavenger receptors to convert to lipid-laden foam cells. Thus, the prevention of LDL oxidation is assumed to be one of the initial and critical measures for antiatherosclerosis.