Prenatal caffeine exposure induces down-regulation of the protein kinase A/ryanodine receptor/large-conductance Ca2+-activated K+ pathway in the cerebral arteries of old offspring rats.

Background/aims: The current study investigated the long-term effects of prenatal caffeine (Caf) exposure on cerebral vessels of old offspring rats.

Methods: Pregnant rats were treated with Caf (20 mg/kg, twice daily) or 0.9% normal saline during gestational days 3.

Prenatal hypoxia plus postnatal high-fat diet exacerbated vascular dysfunction via up-regulated vascular Cav1.2 channels in offspring rats.

Background: This study aimed to examine whether and how postnatal high-fat diet had additional impact on promoting vascular dysfunction in the offspring exposed to prenatal hypoxia.

Methods And Results: Pregnant Sprague-Dawley rats were randomly assigned to hypoxia (10.5% oxygen) or normoxia (21% O ) groups from gestation days 5-21.

Prenatal caffeine damaged learning and memory in rat offspring mediated by ARs/PKA/CREB/BDNF pathway.

Prenatal exposure to caffeine can cause developmental problems. This study determined chronic influence of prenatal caffeine at relatively higher doses on cognitive functions in the rat offspring. Pregnant Sprague-Dawley rats (4-month-old) were exposed to caffeine (20 mg/kg, twice a day) for whole pregnancy from gestational day 4.

Downregulation of L-Type Voltage-Gated Ca, Voltage-Gated K, and Large-Conductance Ca-Activated K Channels in Vascular Myocytes From Salt-Loading Offspring Rats Exposed to Prenatal Hypoxia.

Background: Prenatal hypoxia is suggested to be associated with increased risks of hypertension in offspring. This study tested whether prenatal hypoxia resulted in salt-sensitive offspring and its related mechanisms of vascular ion channel remodeling.

Methods And Results: Pregnant rats were housed in a normoxic (21% O) or hypoxic (10.

Chronic Prenatal Hypoxia Down-Regulated BK Channel Β1 Subunits in Mesenteric Artery Smooth Muscle Cells of the Offspring.

Background/aims: Chronic hypoxia in utero could impair vascular functions in the offspring, underlying mechanisms are unclear. This study investigated functional alteration in large-conductance Ca2+-activated K+ (BK) channels in offspring mesenteric arteries following prenatal hypoxia.

Methods: Pregnant rats were exposed to normoxic control (21% O2, Con) or hypoxic (10.

Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring.

Scope: High sucrose intake during pregnancy is linked to type 2 diabetes mellitus and altered insulin resistance.

Methods And Results: This study attempts to ascertain whether prenatal high sucrose intake (20% sucrose) alleviates the detrimental effects of high postnatal sugar consumption in the offspring, and the molecular mechanisms are investigated using a rat model. High prenatal sucrose exposure increases the body weight of the offspring at 1-3 weeks of age.

Regulation of cerebral arterial BKCa channels by angiotensin II signaling in adult offspring exposed to prenatal high sucrose diets.

Prenatal insults have been shown to affect vascular functions, leading to increased risks of cardiovascular diseases in offspring. The present study determined whether high sucrose (HS) intake in pregnancy affected central vascular functions in middle cerebral artery (MCA) of offspring. Sprague-Dawley rats were fed a standard food and tap water with normal or high (20%) sucrose content during pregnancy.

Maternal high-sucrose diets altered vascular large-conductance Ca2+-activated K+ channels via reactive oxygen species in offspring rats.

Overnutrition during pregnancy could increase risks of cardiovascular diseases in late life. This study investigated whether and how reactive oxygen species (ROS) may influence functions of large-conductance Ca2+-activated K+ channels (BKCa) in the offspring exposed to prenatal high sucrose (HS). We found that prenatal HS diets significantly increased phenylephrine (PE)-induced vessel contractions in mesenteric arteries of the adult offspring.

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia.

The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.

Maternal high salt diet altered Adenosine-mediated vasodilatation via PKA/BK channel pathway in offspring rats.

Scope: High salt (HS) diets are related to cardiovascular diseases, and prenatal HS was suggested to increase risks of coronary artery diseases in the offspring. This study tested the hypothesis that prenatal HS may influence Adenosine-induced vasodilatation via protein kinase A (PKA) pathway in coronary arteries.

Methods And Results: Sprague-Dawley rats were fed with 8% salt diet for gestation, the control was fed with 0.

Antioxidative Effects of Rhodiola Genus: Phytochemistry and Pharmacological Mechanisms against the Diseases.

Rhodiola as one of traditional medicines has been used for clinical treatments due to its strong antioxidant properties. Phytochemical analysis revealed the presence of flavonoids, phenylpropanoids, phenylethanol/benzyl alcohol derivatives, cyanogenic glycosides and terpenoids. The bioactive compounds had been demonstrated to be effective at scavenging reactive oxygen species (ROS).

Roles of ion channels in regulation of acetylcholine-mediated vasoconstrictions in umbilical cords of rabbit/rats.

We recently demonstrated that acetylcholine (ACh) produced reliable vasoconstrictions in the umbilical cords. This study investigated the possible mechanisms with different antagonists. ACh-mediated vasoconstrictions were decreased by voltage-operated calcium (Ca) channels antagonist nifedipine or inositol-1,4,5-trisphosphate-mediated Ca release antagonist 2-aminoethyl diphenylborinate, indicating that both extracellular and intracellular calcium modulated the ACh-stimulated umbilical contraction.