From the abstract is hard to tell how they reached the conclusion. In vitro? On Rats? Hopefully it's true and it also work on big rats. Anyway, more EGCG will be, there isn't danger in that.100/65 gives you a pulse pressure of 35. Pulse pressure has to do with the stiffness of the vasculature (I think). How can one decrease the stiffness without an effective cross link breaker?New guidelines term systolic over 115 "pre-hypertension." I'd aim for 100/65.
I'd speculate that green tea (EGCG) and possibly resveratrol could do that.J Cardiovasc Pharmacol. 2004 Feb;43(2):200-8. Links
Inhibitory effect of epigallocatechin 3-O-gallate on vascular smooth muscle cell hypertrophy induced by angiotensin II.Zheng Y, Song HJ, Kim CH, Kim HS, Kim EG, Sachinidis A, Ahn HY.
Department of Pharmacology, College of Medicine, Chungbuk National University, Cheongju, South Korea.
Recent evidence indicates that epigallocatechin 3-O-gallate (EGCG), the major catechin derived from green tea leaves, lowers the risk of cardiovascular diseases such as atherosclerosis and hypertension. However, a precise mechanism for this biologic function has not yet been clearly delineated. Angiotensin II (Ang II) stimulates vascular smooth muscle cell (VSMC) hypertrophy, which is a critical event in the development of atherosclerosis, hypertension, and angioplasty-induced restenosis. In the present study, we show that EGCG inhibits Ang II-stimulated VSMC hypertrophy, as determined by [3H]leucine incorporation into VSMC. Since mitogen-activated protein kinase (MAPK) families are involved in cell growth, we determined whether EGCG affects them. EGCG pretreatment did not exert any significant changes in Ang II-stimulated activation of extracellular signal-regulated kinase (ERK) and p38 MAPK. EGCG only inhibited Ang II-stimulated activation of c-Jun N-terminal kinase (JNK). Moreover, EGCG suppressed Ang II-induced c-jun mRNA expression. In contrast, EGC, a structural analogue of EGCG, did not inhibit the JNK activity or c-jun mRNA expression. In addition, a specific JNK inhibitor, SP600125, dose-dependently suppressed Ang II-stimulated VSMC hypertrophy. These results suggest that the effect of EGCG on Ang II-induced VSMC hypertrophy is due to specific inhibition of the JNK signaling pathway at both transcriptional and posttranslational levels, which may underlie its beneficial effect on the cardiovascular diseases.
PMID: 14716206
Thanks.
Caveat.- Some red flags sprung up recently as far as research coming out of Korea. They are turning into the Nigerians of Science.