Plasticity of cerebral microvascular structure and mechanics during hypertension and following recovery of arterial pressure.

Changes in vascular structure contribute to vascular events and loss of brain health. We examined changes in cerebral arterioles at the onset of hypertension and the hypothesis that alterations during hypertension would recover with the return of mean arterial pressure (MAP) to normal. MAP was measured with radiotelemetry in awake male C57BL/6J mice at baseline and during infusion of vehicle or angiotensin II (ANG II, 1.

Interference with PPARgamma signaling causes cerebral vascular dysfunction, hypertrophy, and remodeling.

The transcription factor PPARgamma is expressed in endothelium and vascular muscle where it may exert antiinflammatory and antioxidant effects. We tested the hypothesis that PPARgamma plays a protective role in the vasculature by examining vascular structure and function in heterozygous knockin mice expressing the P465L dominant negative mutation in PPARgamma (L/+). In L/+ aorta, responses to the endothelium-dependent agonist acetylcholine (ACh) were not affected, but there was an increase in contraction to serotonin, PGF(2alpha), and endothelin-1.

A comparison of the effect of halothane on N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor-mediated excitatory synaptic transmission in the hippocampus.

Halothane depresses synaptic transmission in the rat brain. First we determined the concentration of halothane which decreased the amplitude of the population spike recorded in the CA1 region of the hippocampus to 50% of the control value (105 +/- 4.9 micrograms/mL [0.