Biomedical subjects
Publications and source records attributed to L Landsberg.
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In the spontaneously hypertensive rat (SHR), caloric restriction without sodium restriction is associated with reduced blood pressure. Four days of fasting lowered blood pressure 19% while 4 days of eating 50% of ad lib intake reduced blood pressure 10%. Similar dietary changes had less effect on blood pressure in normotensive rats of the same strain (Wistar-Kyoto--WKY). These data are consistent with the hypothesis that caloric restriction lowers sympathetic activity.
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Two days of fasting in rats significantly reduces the turnover of norepinephrine in the heart. In contrast to the effects of ganglionic blockade in fed controls, similar blockade in fasted animals is without significant effect on [3H]-norepinephrine retention or endogenous norepinephrine in the heart. These data are consistent with suppression of centrally mediated sympathetic activity in the fasted state. The decrease in norepinephrine turnover during fasting is completely reversed by 1 day of refeeding.
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Addition of norepinephrine or epinephrine to the isolated rat kidney perfused at constant pressure resulted in an increase in sodium reabsorption and the excretion of a dilute urine with an increase in free water clearance. Vasopressin reversed the fall in urinary osmolarity but not the diminution in sodium excretion. The urinary changes produced by catecholamines were blocked by propranolol but not by phenoxybenzamine, suggesting that they were mediated, at least in part, by beta receptors. Similar though less pronounced changes in sodium excretion and urinary osmolarity were produced by isoproterenol and phenylephrine, while the combination of these drugs induced marked dilution of the urine. The results suggest that circulating catecholamines or adrenergic nerves innervating the kidney directly influence renal tubular function and might, therefore, participate in the regulation of sodium and water excretion by the kidneys.
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We have evaluated intravenous glucagon as pharmacologic stimulus to adrenal catecholamine secretion in normal human subjects. Urinary epinephrine and norepinephrine were measured at two hourly intervals before and after the intravenous injection of saline, 4 mg glucagon, or 0.1 mu/kg crystalline insulin. Urinary epinephrine was increased 2.3-fold over baseline after both saline and glucagon. By contrast, insulin hypoglycemia produced a 24-fold rise in urinary epinephrine. No rise in urinary norepinephrine was detected in any test. Under the conditions of this study, we conclude that epinephrine excreted after glucagon injection is due to the stress of the test itself. In normal man, glucagon either does not stimulate adrenal catecholamine secretion, or the effect is too small to measure. By contrast, in pheochromocytoma, glucagon may be specific for catecholamine secretion, based on data from the literature. In normal subjects, insulin hypoglycemia remains the only proved method for assessing adrenal catecholamine reserve.
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The endogenous noradrenaline concentration, fractional turnover, half-life, and turnover rate of tritiated ((3)H) noradrenaline were determined in the oesophagus, non-glandular and glandular portions of the stomach, duodenum, jejunum, ileum, and colon of the rat. The highest concentration of endogenous noradrenaline was present in the duodenum and colon. The (3)H-noradrenaline fractional turnover rates and half-lives were significantly greater in the small and large intestines as compared with the oesophagus and stomach. The noradrenaline turnover rate, which is an estimate of the level of sympathetic activity, was greatest in the colon and duodenum. This method of assessing sympathetic activity in various tissues by direct measurement of the noradrenaline turnover rate may be applied to the study of the adrenergic nervous system in the physiology and pathophysiology of the gastrointestinal tract.