Possible Role of Chitin-Like Proteins in the Etiology of Alzheimer's Disease.

Chitin is a β-linked straight chain carbohydrate matrix monopolymer prominent in invertebrates, from fungi to arthropods. Surprisingly, chitin is now documented in vertebrates, including humans, a component of vertebrate physiology that has been neglected until now. Chitin levels are elevated in Alzheimer's disease (AD) patients, not only in the central nervous system but also in the cerebrospinal fluid and plasma.

[Mechanism of primary hypertension].

We review various theories of the pathogenetic mechanisms of steroid-induced and essential hypertension. We investigated the possibility that a pathogenetic mechanism leading to glucocorticoid (GC)-induced hypertension or to mineralocorticoid (MC)-induced hypertension, or both, may be of critical importance in primary hypertension. We studied plasma levels of corticosterone (BK) and aldosterone (Aldo), and their concentrations in arterial and renal tissues of spontaneously hypertensive rats (SHR), a model of primary hypertension, and in the antecedent strain WKY rats as a normotensive control.

Study on the mechanisms of glucocorticoid-induced hypertension: glucocorticoids increase transmembrane Ca2+ influx in vascular smooth muscle in vivo.

Blood pressure (BP) and ex vivo influx rate of Ca2+ in excised aortae were measured in rabbits implanted with silastic rubber strips impregnated with glucocorticoids (GC) [dexamethasone (DEX) or cortisol (FK)], or carbenoxolone (CX) [inhibitor of 11 beta-hydroxysteroid dehydrogenase (11-HSD), in a large (lg) or a small (sm) (10 times smaller) concentration], or FK plus CX (sm), or DEX plus RU 38486 (a specific GC-receptor blocker). After 4-6 weeks rabbits implanted with DEX, CX (lg), and FK+CK (sm) developed hypertension. Those implanted with FK alone (yielding physiological serum concentration of FK), CX (sm), and DEX+RU 38486 did not develop hypertension.

Alpha adrenergic antagonism by cyclosporine.

Cyclosporine has been shown to exert antiadrenergic actions in previous studies from this laboratory. Interactions of CsA with the alpha-one and alpha-two receptor were studied in rabbits. Blood pressure studies revealed that CsA exerts a competitive, reversible antagonism against norepinephrine, epinephrine, and phenylephrine.

Cyclosporine-induced hypotension.

The cardiovascular effects of i.v. infusion of cyclosporine were studied in pentobarbital-anesthetized rabbits.