Norepinephrine (medication)

About: Norepinephrine (medication) is a research topic. Over the lifetime, 12189 publications have been published within this topic receiving 371139 citations. The topic is also known as: Norepinephrine bitartrate & Norepinephrine (drug).

Neuropeptide Y injected in the paraventricular hypothalamus: a powerful stimulant of feeding behavior.

Abstract: Neuropeptide Y (NPY) was injected directly into the paraventricular nucleus of the hypothalamus (PVN) of satiated, brain-cannulated rats, and food and water intake were measured 0.5, 1, 2, 4, and 22 hr postinjection. NPY (24, 78, 235, 783, and 2351 pmol/0.3 mul) produced a large, dose-dependent increase in food intake as well as small increase in water intake. The latency to eat was about 10 min, with substantial feeding occurring in the first 30 min. At dose below 78 pmol, the eating generally occurred only within the first hour. At doses above 235 pmol, however, the subjects' food intake continued to increase such that by 4 hr postinjection they had consumed the equivalent of normal 22-hr intake, and 22 hr postinjection they had also eaten significantly more than control subjects. Previous studies have shown that norepinephrine injected into the PVN stimulates feeding through alpha-adrenergic receptors. To investigate a possible interaction, subjects were given PVN injections of phentolamine (60 nmol) prior to injections of either NPY (78 pmol) or norepinephrine (20 nmol). Phentolamine pretreatment significantly decreased feeding elicited by norepinephrine without affecting feeding elicited by NPY. This suggests that NPY does not stimulate feeding through the release of endogenous norepinephrine. The powerful stimulation of feeding elicited by this neuropeptide suggests an important role for hypothalamic NPY, or a structurally related peptide, in the regulation of feeding behavior.

Physiology and Pathophysiology of the Human Sympathoadrenal Neuroendocrine System

Abstract: THE sympathoadrenal system is the prototype neuroendocrine system. Epinephrine is a hormone in the traditional sense. It is secreted from the adrenal medullae into the circulation and transported to its various target cells. In contrast, norepinephrine is primarily a neurotransmitter. It is released from axon terminals of sympathetic postganglionic neurons and deposited directly at innervated target cells. The adrenal medullae also release some norepinephrine1 and can become major sources of norepinephrine in plasma under certain conditions such as hypoglycemia. Since plasma norepinephrine concentrations occasionally rise to levels that produce biologic effects, 2 norepinephrine may also act as a hormone. The catecholamines . . .

Assessment of human sympathetic nervous system activity from measurements of norepinephrine turnover.

Abstract: SINCE the sympathetic nervous system has such a central place in homeostasis in general, and in circulatory adaptation in particular, it is paradoxical that so little is known about the possible contribution of disturbed sympathetic nervous function to the development of human diseases. Clinical tests of sympathetic nervous system activity have, by and large, been routinely applied in one setting only: the detection of sympathetic nervous failure, from autonomic insufficiency syndromes, in patients with postural hypotension. A list of \"candidate\" diseases for sympathetic nervous system dysfunction might include, for example, essential hypertension, cardiac failure, coronary artery spasm, cirrhosis, mitral valve prolapse, and Raynaud's syndrome. Until very recently, the picture of sympathetic nervous pathophysiology for conditions such as these was particularly sketchy, mainly because of the rudimentary nature of the tests of sympathetic nervous system function available to investigative clinical medicine. Pertinent questions have gone incompletely answered at best — questions such as: Is the sympathetic nervous system directly involved in the early pathogenesis of essential hypertension? Is increased renal sympathetic activity a common cause of sodium retention in edematous states? Is increased cardiac sympathetic nerve firing an important element in the development of cardiac arrhythmias in humans?