17β-estradiol reduces Ca 1.2 channel abundance and attenuates Ca -dependent contractions in coronary arteries.

One mechanism by which the female sex may protect against elevated coronary vascular tone is inhibition of Ca entry into arterial smooth muscle cells (ASMCs). In vitro findings confirm that high estrogen concentrations directly inhibit voltage-dependent Ca 1.2 channels in coronary ASMCs.

Using three-point bending to evaluate tibia bone strength in ovariectomized young mice.

It is well known that estrogen deficiency induces a deterioration of bone strength in aged females. The aim of this study is to determine the effect of estrogen depletion on tibia bone strength in sexually mature mice that are still undergoing skeletal maturation. At 8 weeks of age, C57BL/6 female mice underwent an ovariectomy (OVX) or sham (SHAM) surgery.

Oestrogen upregulates the sarcoplasmic reticulum Ca(2+) ATPase pump in coronary arteries.

The presence of circulating plasma 17β-oestradiol (E2) is beneficial in women against abnormal vascular tone development, such as coronary arterial vasospasms. Several vascular diseases have demonstrated that increased expression of the sarcoplasmic reticulum Ca(2+) -ATPase pump (SERCA2b) serves to limit the excessive accumulation of intracellular Ca(2+) . Therefore, the hypothesis of the present study was that E2 would increase SERCA2b expression in the coronary vasculature.

Nongenomic inhibition of coronary constriction by 17ß-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol.

The cardioprotective effects of 17beta-estradiol (E2) in women are hypothesized to be partially mediated by the E2 metabolites 2-hydroxyestradiol (2-HOE) and 2-methoxyestradiol (2-MeOH). Therefore, the purpose of our study was to determine the acute effects of E2, 2-HOE, and 2-MeOH on inhibition of coronary arterial constriction. Right coronary arteries obtained from breeding sows were cut into 4 mm rings and suspended in organ baths.

The enhanced endothelin-1-induced contraction in cultured coronary arteries from mature female pigs is not antagonized by 17beta-estradiol.

We have previously reported that organ cultured coronary arteries from market-age pigs (6-9 months of age) exhibit an enhanced contraction to the atherosclerotic-associated peptide, endothelin-1 (ET-1). The objective of this study was to investigate the interaction of 17beta-estradiol with ET-1 in organ cultured coronary arteries from older female pigs (3-4 years old). A cumulative concentration-response relationship (1 x 10(-9) M to 3 x 10(-7) M) was generated to ET-1, and the isometric tension measured in fresh and organ cultured (4 days at 37 degrees C) arterial rings that were each pre-incubated for 50 min in different concentrations (1 x 10(-9) M to 1 x 10(-5) M) of 17beta-estradiol.

A simple classroom teaching technique to help students understand Michaelis-Menten kinetics.

A new, simple classroom technique helps cell biology students understand principles of Michaelis-Menten enzyme kinetics. A student mimics the enzyme and the student's hand represents the enzyme's active site. The catalytic event is the transfer of marbles (substrate molecules) by hand from one plastic container to another.

Increased calcium buffering in coronary smooth muscle cells from diabetic dyslipidemic pigs.

No studies exist concerning the ability of the plasma membrane Ca(2+) pump (PMCA), sarcoplasmic reticulum Ca(2+) pump (SERCA) and Na(+)-Ca(2+) exchanger (NCX) to regulate myoplasmic Ca(2+) (Ca(m)) in vascular smooth muscle cells from diabetic individuals with dyslipidemia. We tested the hypothesis that diabetic dyslipidemia would increase vascular smooth muscle cells to buffer Ca(m). Cells were isolated from the coronary artery of male Yucatan pigs treated for 20 weeks with: (1) a low fat diet (control group); (2) a high fat/cholesterol diet (F group); or (3) alloxan-induced diabetic pigs fed the high fat diet (DF group).

Pharmacological characterization of a UTP-sensitive P2Y nucleotide receptor in organ cultured coronary arteries.

Our lab has previously demonstrated that organ cultured coronary smooth muscle cells express a nucleotide receptor that is dramatically more responsive to UTP than non-organ cultured cells. Thus, the purpose of this study was to pharmacologically characterize this UTP-sensitive nucleotide receptor. Porcine coronary arteries were organ cultured (serum-free media, 37 degrees C) for 4 days, and fura-2 imaging of single cells was used to measure myoplasmic Ca2+ (Cam) in response to several nucleotide agonists.