Publications by authors named "M A Kowatch"

Cutaneous wounds close more slowly in rats and monkeys as age increases. Caloric restriction of 40% in rats and 30% in monkeys did not significantly affect healing rates, although it did exert a trend toward faster closure. Similarly, voluntary exercise did not significantly alter healing rates in rats.

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The age related decrease in alpha 1-adrenergic stimulated inositol 1, 4, 5 trisphosphate (IP3) production in parotid cells of aged rats can be partially restored by treatment with S-adenosylmethionine (SAM). This effect is completely blocked by S-adenosyl homocysteine (SAH) and occurs in association with an increase in the conversion of phosphatidylethanolamine to phosphatidylcholine and a decrease in membrane viscosity. In contrast, SAM treatment actually inhibits stimulated IP3 production in cells of young rats.

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Alpha 1-adrenergic and muscarinic-cholinergic stimulated IP3 production and calcium mobilization are inhibited by treatment of parotid cell aggregates with methanol, hydrogen peroxide and saponin. Only methanol exerts an effect on binding to receptors. In most cases a close correspondence exists between inhibition of alpha 1-adrenergic and muscarini-cholinergic responses as well as inhibition of IP3 production and calcium mobilization.

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We measured basal and dopamine-inhibited pituitary cell prolactin (PRL) release in vitro, and dopamine receptor binding in pituitary homogenates, from intact male and female Wistar rats of varying ages. During 48-72 hours in culture, the baseline secretion rate of PRL from pituitary cells of old (24 months) male rats was less than one-half that from cells of mature (6 months) male rats, whereas the corresponding basal secretion rate of PRL from cells of old female rats was nearly 3-fold greater than that from cells of mature female rats (p < 0.001).

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The effects of the nonionic detergent saponin on alpha 1-adrenergic signal transduction were investigated using rat parotid cells and membrane preparations. Fifty microM epinephrine-stimulated 45Ca2+ efflux and inositol 1,4,5-triphosphate (Ins[1,4,5]P3) production in adult parotid cells were significantly decreased after saponin treatment. Saponin did not alter the concentration of alpha 1-adrenergic receptors labeled by [3H]prazosin, but significantly reduced the guanosine imido diphosphate (GppNHp)-induced shift from high to low affinity sites.

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