Brain vascular function

Analysis of ESRB 7 mice showed fewer and smaller litters than wild type mice as well as abnormal vascular function and hypertension. The reduction in fertility was attributed to reduced ovarian efficiency. Mutant females had normal breast development and lactated normally. Older mutant males displayed signs of prostate and bladder hyperplasia. s -2-deficient mice furthermore display diverse regulatory defects in the function of brain, lung, and white blood cells. The results indicated that ESRB is essential for normal ovulation efficiency but is not essential for lactation, female or male sexual differentiation, or fertility. 

Michenfelder J. D. (1988) The hypothermic brain. In Anesthesia and the Brain Clinical, Functional, Metabolic and Vascular Correlates (Michenfelder J. D., ed.), Churchill Livingstone, New York. 

Lin AL, Zheng W, Halloran JJ, Burbank RR, Hussong SA, Hart MJ et al (2013) Chronic rapamycin restores brain vascular integrity and function through NO synthase activation and improves memory in symptomatic mice modeling Alzheimer s disease. J Cereb Blood Flow Metab 33 1412-1421... 

Owman, C., Fuxe, K., Jason, A., Kahrstrom, J., 1989. Studies of the protective actions of nicotine on neuronal and vascular functions in rats comparison between sympathetic noradrenergic and mesostriatal dopaminergic fiber system and the effect of a dopamine agonist. Prog. Brain Res. 79, 267-276. 

Epoxygenase metabolites of arachidonic acid have potent pharmacological effects on kidney and vascular functions. Particularly well studied is the ability of some of these products to inhibit ion transport, reduce renin activity, and increase water and electrolyte excretion in kidney. Epoxygenase metabolism of arachidonic acid has also been demonstrated in brain,where it could participate in mediating certain intracellular responses of hypothalamic neurons to the modulatory neurotransmitter, dopamine. ... 

The proposal that NO or its reactant products mediate toxicity in the brain remains controversial in part because of the use of non-selective agents such as those listed above that block NO formation in neuronal, glial, and vascular compartments. Nevertheless, a major area of research has been into the potential role of NO in neuronal excitotoxicity. Functional deficits following cerebral ischaemia are consistently reduced by blockers of NOS and in mutant mice deficient in NOS activity, infarct volumes were significantly smaller one to three days after cerebral artery occlusion, and the neurological deficits were less than those in normal mice. Changes in blood flow or vascular anatomy did not account for these differences. By contrast, infarct size in the mutant became larger... 

An increase in plethora and focal dystrophic changes in the endocrine system matches clinical observations of changes in adrenal and thyroid function, as well as changes in local and general vascular dystonia, all detected in humans poisoned by OCP. Morphological changes in the brain s nerve cells conform to information on the disruption of reflex activity in the early stages of OCP exposure. 

---