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ABSTRACT
Glucocorticoids are known to regulate the contractility of vascular smooth muscle by increasing its response to noradrenaline. The molecular mechanisms for achieving this remain unclear. Recent results in our laboratory have demonstrated that glucocorticoids affect both α1-adrenoceptor number and coupling to G proteins. Whether this leads to an increase in second-messenger production has to be established. The present experiments, therefore, report the effects of dexamethasone on inositol polyphosphate production in vascular smooth muscle cells in culture. Noradrenaline induced the release of inositol polyphosphates from prelabelled [3H]inositol phosphoinositides in the membrane in a dose-dependent manner. The concentration of noradrenaline which caused half-maximal response was 1·26 μmol/l. Prazosin inhibited noradrenaline-induced inositol monophosphate formation to 10·26 ± 3·67% (mean ± s.e.m.; P < 0·01, n = 5) of control value whereas yohimbine reduced it to only 61·74 ± 11·82% (P < 0·05, n = 5), suggesting an action primarily through α1-adrenergic receptors. Dexamethasone (100 nmol/l, 48 h) enhanced noradrenaline-induced inositol monophosphate, bisphosphate and trisphosphate formation up to twofold (P < 0·001, n = 5). The enhancement of the response occurred despite the fact that dexamethasone reduced [3H]inositol prelabelling of membrane phosphoinositides by 49·5 ± 9·9% (P < 0·05, n = 3). The present results suggest that the potential action of glucocorticoids on vascular smooth muscle contractility is, at least in part, through controlling α1-adrenoceptor-mediated second-messenger production.
Journal of Endocrinology (1992) 133, 405–411
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A method of estimating thyroid function with carrier-free radio-iodine which provides an arbitrary numerical scale of thyroid activity is described. It is suitable for investigating borderline thyroid dysfunction.
The results on over 500 psychiatric patients are given in the form of histograms, and arbitrary limits of normality are defined on the basis of these results.
While there is usually a correlation between the tracer method and the basal metabolic rate, cases exist in which increased thyroid activity, determined by the radio-active method, is associated with normal or subnormal b.m.r. and vice versa. This is explained as a disturbance of the sensitivity of body tissues to thyroid hormone.
The significance of under-sensitivity to thyroid hormone and related problems is discussed, and the importance of considering peripheral sensitivity of the tissues of the body in evaluating an abnormal thyroid activity is emphasized.
