Summary Uterine vascular tone significantly decreases while uterine blood flow dramatically increases during pregnancy. However, the complete molecular mechanisms remain elusive. We hypothesized that increased BKCa channel activity contributes to the decreased myogenic tone of uterine arteries in pregnancy. Resistance-sized uterine arteries were isolated from nonpregnant and near-term pregnant sheep. Electrophysiological studies revealed a greater whole-cell K+ current density in pregnant than nonpregnant uterine arteries. Tetraethylammonium and iberoitoxin inhibited K+ currents to the same extent in uterine arterial myocytes. The BKCa channel current density was significantly increased in pregnant uterine arteries. In accordance, tetraethylammonium significantly increased pressure-induced myogenic tone in pregnant uterine arteries and abolished the difference in myogenic responses between pregnant and nonpregnant uterine arteries. Activation of protein kinase C produced a similar effect to tetraethylammonium by inhibiting BKCa channel activity and increasing myogenic tone in pregnant uterine arteries. Chronic treatment of nonpregnant uterine arteries with physiologically relevant concentrations of 17β-estradiol and progesterone caused a significant increase in the BKCa channel current density. Western blot analyses demonstrated a significant increase of the β1, but not α, subunit of BKCa channels in pregnant uterine arteries. In accordance, steroid treatment of nonpregnant uterine arteries resulted in an upregulation of the β1, but not α, subunit expression. The results indicate that the steroid hormone-mediated upregulation of the β1 subunit and BKCa channel activity may play a key role in attenuating myogenic tone of the uterine artery in pregnancy.

Abstract-Epidemiological studies suggest that maternal cigarette smoking is associated with an increased risk of elevated blood pressure (BP) in postnatal life. The present study tested the hypothesis that prenatal nicotine exposure causes an increase in BP response to angiotensin II (Ang II) in adult offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps throughout the gestation. BP and vascular responses to Ang II were measured in 5-month-old adult offspring. Prenatal nicotine had no effect on baseline BP but significantly increased Ang II-stimulated BP in male but not female offspring. The baroreflex sensitivity was significantly decreased in both male and female offspring. Prenatal nicotine significantly increased arterial media thickness in male but not female offspring.In male offspring, nicotine exposure significantly increased Ang II-induced contractions of aortas and mesenteric arteries. These responses were not affected by inhibition of endothelial NO synthase activity. Losartan blocked Ang II-induced contractions in both control and nicotine-treated animals. In contrast, PD123319 had no effect on Ang II-induced contractions in control but inhibited them in nicotine-treated animals. Nicotine significantly increased Ang II type 1 receptor but decreased Ang II type 2 receptor protein levels, resulting in a significant increase in the ratio of Ang II type 1 receptor/Ang II type 2 receptor in the aorta. Furthermore, the increased contractions of mesenteric arteries were mediated by increases in intracellular Ca 2ϩ concentrations and Ca 2ϩ sensitivity. These results suggest that prenatal nicotine exposure alters vascular function via changes in Ang II receptor-mediated signaling pathways in adult offspring in a gender-specific manner, which may lead to an increased risk of hypertension in male offspring. Key Words: nicotine Ⅲ fetal programming Ⅲ gender Ⅲ angiotensin II Ⅲ vascular contractility M aternal cigarette smoking probably is the single most widespread prenatal insult in the world. Recent epidemiological studies have demonstrated that in utero exposure to maternal smoking is associated with elevated blood pressure (BP) and/or cardiovascular disease in offspring later in life. 1,2 As one of the major components in cigarette smoking, nicotine is likely to contribute to the developmental programming of cardiovascular disorders. Nicotine readily crosses the placenta, and maternal cigarette smoking produces higher nicotine concentrations in fetal circulation than that experienced by the mother. 3,4 In the developing fetus, chronic nicotine exposure resulted in permanent changes in nicotinic receptors and alterations in the activity of the central and peripheral nervous systems. 5 Our recent studies in the rat have demonstrated that fetal nicotine exposure causes reprogramming of vascular reactivity and produces genderdependent alterations in both ␣ 1 -adrenoceptor-mediated contractions and endothelial NO synthase (eNOS) activity of arteries in adult offspring. 6 In additi...

Water-storage capacity was measured inThuja occidentalis L.,Tsuga canadensis (L.) Carr., andAcer saccharum Marsh. during the dehydration of stem segments 1.5-2.5 cm in diameter. Stem water potential was measured with a temperature-corrected stem hygrometer and cavitations were detected acoustically. Water loss was measured by weight change. Dehydration isotherms consistently displayed three phases. The first phase, from water potential (Ψ) 0 to about -0.2 MPa, had a high capacitance (C>0.4kg water lost· (1 of tissue)(-1)· MPa(-1)) and we have attributed this high C to capillary water as defined by Zimmermann (1983, Xylem structure and the ascent of sap, Springer-Verlag). The second phase from Ψ=-0.5 to about -2.0 had the lowest C values (<0.02 kg·l(-1)·MPa(-1)) and was accompanied by a few cavitation events. This phase may have been a transition zone between capillary storage and water released by cavitation events as well as water drawn from living cells of the bark. The third phase also had a high C (about 0.07-0.22kg·l(-1)·MPa(-1)) and was associated with many cavitation events while Ψ declined below about -2.5 MPa; we presume the high capacitance was the consequence of water released by cavitation events. We discuss the ecological adaptive advantage of these three phases of water-storage in trees. In moist environments, water withdrawn from capillary storage may be an important fraction of transpiration, but may be of little adaptive advantage. For most of the growth season trees draw mainly on elastic storage, but stem elastic storage is less than leaf elastic storage and therefore unlikely to be important. In very dry environments, water relased by cavitation events might be important to the short-term survival of trees.

Corticosteroid hormones play an important role in the control of vascular smooth muscle tone by their permissive effects in potentiating vasoactive responses to catecholamines through glucocorticoid receptors. Increased cortisol response has been associated with an increase in arterial contractile sensitivity to norepinephrine and vascular resistance. Glucocorticoids regulate vascular reactivity by acting on both endothelial and vascular smooth muscle cells. Both glucocorticoid receptor protein and mRNA have been identified in endothelial and vascular smooth muscle cells. In endothelial cells. glucocorticoids suppress the production of vasodilators. such as prostacyclin and nitric oxide. In vascular smooth muscle cells. glucocorticoids enhance agonist-mediated pharmacomechanical coupling at multiple levels. The effect of glucocorticoids on vascular reactivity is regulated by 11 beta-hydroxysteroid dehydrogenase (11beta-SD). The presence of 11beta-HSD in many tissues suggests that it modulates the access of corticosteroids to their receptors at both renal and extra-renal sites. The two 11beta-HSD isozymes catalyze the interconversion of cortisol and cortisone. Type 11beta-HSD has bidirectional activity, while the type 2 mainly converts cortisol into cortisone, the biologically inactive form. Both type 1 and type 2 11beta-HSD have been found in vascular endothelial and smooth muscle cells, suggesting that abnormal 11B-HSD expression may play a pathogenic role in the common forms of hypertension. In this article, we review possible mechanisms involved in the glucocorticoid-mediated potentiation of vascular reactivity, its regulation by 11beta-HSD, and their physiological and pathophysiological significance.

A theoretical model of bubble dissolution in xylem conduits of stems was designed using the finite differential method and iterative calculations via computer. The model was based on Fick's, Henry's and Charles' laws and the capillary equation. The model predicted the tempo of recovery from embolism in small diameter branches of woody plants with various xylem structures under different xylem water pressures. The model predicted the time required to recover conductivity in any position in the stem. Repeated iterative solution of the model for different situations yielded an empirical formula to calculate the time for complete recovery of conductivity in stems from a fully embolised initial state. The time, tp, is given by: a (1-95X 9 (rcs+0046) where a is a temperature coefficient; D is the coefficient of diffusion of air in wood at 25 °C; res is the ratio of the area of total conduit cross section to the stem cross section; t|fxp is the stem xylem pressure potential (Pa, where 0 Pa equals atmospheric pressure); T is solution surface tension (0-072N m"^); and Do and Dg are diameters of the conduits and the stem, respectively (m). The equation is valid only when V()^>-4T/DC-The model predicts no recovery of conductivity when \\)XP^-4T/DC-The model agreed with experiments.