Insulin bladder

More recent analysis of tissue specific gene deletions showed that the Cav1.2 channel is involved in a wide variety of function including hippocampal learning, insulin secretion, intestine and bladder motility. Further analysis will be required to unravel the functional significance of voltage-dependent calcium channels for specific cellular functions. 

Congestive heart failure Hypertension Deep vein thrombosis Coronary artery disease Stroke Diabetes Insulin resistance Glucocorticoid imbalance Gall bladder disease Hypercholesterolemia Hypertriglyceridemia Gout Pancreatitis Liver disease Osteoarthritis Rheumatoid arthritis Bone fractures Lower back pain Carpal tunnel syndrome Depression Pain... 

FIGURE 7 Phosphorus NMR spectra of isola ted. perfused rabbit bladder before (B) and after (A) the addition of insulin. A-B is the difference spectrum showing large changes in PPA at 13 ppm and PCr at —2.5 pp. Other peak size changes were not significant over multiple tissue experiments. From Fisher and Dillon (1989 Fig 2 p. 59). 

The increased plasma kynuremne pool and the induced xanthurenic acid urinary excretion have several implications in the assessment of diazinon noncholinergic toxicity. An increase in xanthurenic acid formation may alter glucose metabolism. Xanthurenic acid has been reported to form a complex with insulin and damage pancreatic P cells. Elevated plasma kynurenin may alter kynurenin transport into the brain. Since more than 40% of brain kynurenin originates from the systemic circulation, cerebral biosynthesis of neuroactive kynurenin metabolites such as quinolinic acid and kynurenic acid may change. Finally, the availability of L-iryptophan for other L-lryptophan-dependent processes may be reduced. Tryptophan is the metabolic precursor for. serotonin and nicotinic adenine dinucleotidc. Diabetes, bladder cancer, and neurological disorders may be the toxic consequences of diazinon-altered L-tryptophan metaboli.sm (Seifert and Pewnim, 1992 Pewnim and Seifert, 1993). 

S 35 (d id 0 V 1 I Broncnodilation (B), vasoconstriction (a), and decreased secretions (a). Used therapeutically as bronchodilator (Table 5.1). Glycogenolysis and gluconeogenesis (B2), lipolysis (Pl), predominant insulin release (u2) but also T insulin release (P2), T renin secretion (pi) Gut relaxation (a,P2) bladder sphincter contraction (a) uterus contraction in non-pregnant women (a1), uterus relaxation in near-term women (p2). ... 

Table 1 Stimulation of Active Sodium Transport by Toad Bladder, Colon and Skin after Treatment of the Animal with Insulin...

Since sodium-transporting epithelia such as toad bladder and colon, seemed to react like toad skin when insulin was injected into the animal, and since toad skin proved capable of direct stimulation, the in-vitro approach was attempted with toad bladder and colon. In the case of urinary bladder of Bufo marinus, a stimula-... 

There are arguments for interpreting the action of aldosterone on active sodium transport by toad bladder, colon and skin as due to a hormone-induced multiplication of the sites of penetration of sodium into the cell, across its apical border (Crabbe, 1967) this requires the intervention of nucleic acid metabolism and the effect of aldosterone is blocked by actinomycin D. This drug actually fails to interfere significantly with the reaction of toad skin to insulin before paired preparations were stimulated with insulin, short-circuit current (uk/cm S.E.) averaged 42.4 + 2.6 for the control, 36.1 1.4 for the matched fragments exposed for 2 hours to actinomycin D, 10 2 hours after addition of insulin to both... 

The effects of aldosterone and insulin on toad skin potentiate each other (Andre and Crabbe, 1966) this was taken as an argument for locating the action of insulin at, or close to, the sodium pump , at the basal cell membrane. Herrera (1965) had formulated the same conclusion after a study of the kinetics of sodium transport across toad bladders stimulated by insulin. 

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