A single dose of guanethidine produces a substantial, long-lasting depletion of tissue catecholamines in the rat, whereas a similar dose of bretylium has no effect. Both drugs produce block of the eserine-induced sympathetic pressor effect. Block by guanethidine is induced more rapidly than is amine depletion. When amine depletion is maximal, a noradrenaline infusion is capable of restoring the response to eserine, but no restoration of the response to eserine occurs after noradrenaline infusion into bretylium-treated rats. Catecholamine levels in isolated tissues are not reduced when complete block of sympathetic nerve stimulation has been produced by guanethidine. It is suggested that guanethidine possesses a primary bretyliumlike, and a secondary reserpine-like, blocking action. Guanethidine produces a transient lowering of intestinal 5-hydroxytryptamine, and this coincides with increased intestinal motility.

Available information suggests that currently over 47% of males and 59% of females use dietary supplements for health benefits, and the number of users is rapidly increasing. However, numerous studies published over more than a decade have linked some supplements (including vitamins E, C, D, A, and B, as well as selenium) to no health benefits or even to adverse health effects. Recent studies with negative results, which drew media attention, include the following: a 2008 study on the ability of vitamin E and selenium to lower the risk of prostate cancer was halted amidst fear of potential harm; vitamin C may do more harm than good as it may protect cancer cells; intake of vitamins E and C by 15,000 male physicians for 10 years had no health benefits. In contrast, there are compelling cause and effect data linking the use of folic acid with consistent and significant reductions in fetal adverse pregnancy outcomes, demonstrating no beneficial effects of calcium and vitamin D supplements in improving bone strength and reducing fractures. These equivocal and conflicting findings on the effects of supplements on health outcomes have left consumers confused about their benefits and wary of the possible adverse effects of vitamin and mineral supplementation. The objectives of this session are to characterize the current state of the science as it relates to the impact of vitamin and mineral supplementation on human health, review the statutory and regulatory perspective of vitamin use from a safety perspective, assess the credibility of meta-analysis in the safety assessment of vitamins, and elicit the mechanisms of these interactions-pro-oxidant versus antioxidant effects and beneficial versus adverse effects.

1 The effects of the putative alB-adrenoceptor antagonist, chloroethylclonidine (CEC) 4 We suggest that the putative L1B-adrenoceptors may be functionally confined to the synaptic region whereas the putative olA-adrenoceptors are excluded from this region. Trains of pulses would allow NA to accumulate and spill out beyond the synaptic region to reach and activate the putative alA-adrenoceptors.

Enzyme histochemical and autoradio graphic methods provided evidence for adrenergic and cholinergic innervation of both alpha and beta cells in the islets of Langerhans of the cat. DIABETES 17:33-36, January, 1968.

A comprehensive investigation of the innervation of the vas deferens of the mouse was made using pharmacological, histochemical and electronmicroscopical techniques. Guanethidine inhibited the response of the vas to transmural stimulation and potentiated the response to noradrenaline (NA). Phentolamine abolished responses to NA and to transmural stimulation. After chemical sympathectomy degenerative changes were seen in presumptive noradrenergic axons; histochemical fluorescence due to catecholamines was absent. The vas failed to respond to transmural stimulation, and a 10‐fold increase in sensitivity of the vas to exogenous NA was observed. NA is shown to diffuse slowly through this tissue whose muscle cells are densely packed. This is discussed in relation to the apparent ‘insensitivity’ of the vas to exogenous NA. A cholinergic component was identified histochemically which did not contribute significantly to the motor response of the vas as chemical sympathectomy abolished completely the motor response elicited by transmural stimulation. It is concluded that NA is the motor transmitter for the smooth muscle of the vas deferens of the mouse.