The Contribution of cocoa additive to cigarette smoking addiction

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Page 74 of 207 RIVM report 650270002 Histamine pressure and heart rate during systemic administration of histamine. Histamine, 0.1 – 11.1 µg/kg/min, lowered blood pressure in a similar dose-dependent fashion in all three species. In man and in cat this was accompanied by clear dose-dependent tachycardia whereas in dog the heart rate changes were minimal. Pharmacological analysis of the depressor responses to histamine in all three species and the reduction in total peripheral resistance in cat and dog showed that the immediate responses to histamine in all three species involved H1-receptors and that sustained responses involved H2 -receptors (27). In pithed guinea pigs, the general characteristics and origin of the pressor response to intravenous injection of histamine were examined. Histamine (5-80 µg/kg) produced a rapid, short-lasting, constant, prominent and dose-dependent pressor response, followed by a secondary slight and prolonged depressor response. The vascular response to histamine was accompanied by a marked tachycardia. The pressor effect of histamine (30 µg/kg) was strongly reduced or abolished in animals pretreated with nicotine, reserpine, bretylium or 6-hydroxydopamine. Furthermore, pyrilamine, a histamine H1-receptor antagonist, antagonized in a dose-dependent manner the pressor response to histamine. On the contrary, metiamide, a histamine H2 -receptor antagonist, as well as hexamethonium and atropine, cholinergic antagonists, did not suppress the pressor effect of histamine. Those experiments provide evidence that in guinea-pigs, the pressor component of the vascular response to histamine results predominantly from the activation of histamine H1-receptors in the sympathetic ganglia with consequent release of noradrenaline at postganglionic sympathetic nerve terminals (28). heart rate: Histamine is released into the systemic circulation during anaphylaxis by drugs and by surgical procedures. Studies in animal models have conclusively demonstrated that released cardiac histamine is a major mediator of arrhythmias that occur during anaphylaxis and following the administration of histaminereleasing drugs. Several lines of evidence suggest a similar arrhythmogenic role for cardiac histamine in humans: (1) The human heart is rich in histamine; (2) cardiac histamine can be readily released from human heart in vitro by therapeutic concentrations of drugs; (3) histamine has potent arrhythmogenic effects on the human heart in vitro. Arrhythmogenic effects of histamine include enhancement of normal automaticity, induction of abnormal automaticity, induction of triggered tachyarrhythmias, depression of atrioventricular conduction, and increase in the vulnerability of the ventricles to fibrillation (24, 29). Renal system It is suggested that 1) H1 and H2 receptors are present in the renal vasculature, 2) changes in intrarenal blood flow distribution are not responsible for histamineinduced diuresis, and 3) H1 receptors are primarily postglomerular while H2 receptors exhibit both pre- and postglomerular distribution (30, 31). diuresis: Histamine, when given intracerebroventricularly (i.c.v.), has been reported to produce antidiuresis in the rabbit. Histamine (H), 100 µg/kg i.c.v., produced antidiuresis with decreases in renal plasma flow and glomerular filtration rate in urethane-anesthetized rabbits. With larger doses, a tendency towards increased electrolyte excretion was noted in spite of decreased filtration.
RIVM report 650270002 Page 75 of 207 Histamine In the denervated kidney, marked diuresis and natriuresis were observed following i.c.v. histamine, whereas the contralateral innervated kidney responded with typical antidiuresis. It was suggested that histamine, given i.c.v., influences renal function in dual ways, i.e., antidiuresis by increasing the sympathetic tone to the kidney and diuresis due to some humoral natriuretic factor, the latter becoming apparent only when the former influence has been removed. Further it is suggested that H1-receptors might be involved in the nerve-mediated antidiuresis, whereas H2 -receptors might mediate the humorally induced natriuresis and diuresis (30). The actions of intracerebroventricularly-infused (i.c.v.) (11 – 89 µg/dose) histamine and selective histamine H1, H2 and H3 receptor agonists on urine flow were studied in rats. It was found that both metoprine and thioperamide, which increase histaminergic activity through different mechanisms, also reduced food intake. This finding indicates that the brain histaminergic system is associated with feeding behavior. The same is true for body water homeostasis. Histamine (i.c.v.) caused a long-lasting diuresis. Also H2 agonists dimaprit and metoprine increased urine flow and the blockade of H2 receptors abolished the diuretic responses to histamine and dimaprit. On the other hand, the H3 agonist (R)-alphamethylhistamine elicited drinking and this effect could be prevented by thioperamide pretreatment. The results imply that activation of H3 receptors predominantly provokes drinking, whereas central H2 receptors mediate the diuretic effect of histamine (32). saluresis: see section diuresis Nervous system central nervous system: Histamine receptors are widely distributed in the CNS. (13, 14). The central histamine receptors may regulate the cardiovascular system (24, 26) diuresis (30, 32) and food intake (32, 33). autonomic system: No data available. Other Maximal gastric secretion was induced in 122 control subjects (without peptic ulcer) and 201 preoperative duodenal ulcer patients by intravenous histamine acid phosphate (14.4 µg/kg/h), and measured as gastric secretory volume (ml/h) and maximal acid output (mmol/h). In both groups, men secreted more than women, and smokers secreted more than non-smokers. Significant correlations were found between maximal gastric secretion on the one hand, and height, age, and chronic smoking on the other (34). Critical assessment Histamine is an autacoid that is closely associated with mast cells and functions as a mediator of inflammation. Histamine is a neurotransmitter in the central and peripheral nervous systems. It mediates its effects through three receptor subtypes with differential selectivities for both agonists and antagonists (e.g., mepyramine for H1, ranitidine for H2, and thiperamide for H3). Through these receptors, histamine evokes several physiological effects. Histamine characteristically causes dilatation of the finer blood vessels, resulting in flushing, lowered total peripheral resistance and a fall in systemic blood pressure. The released cardiac histamine is a major mediator of arrhythmias that occur during anaphylaxis and following the administration of
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