Cholinergic regulation of adrenal medullary blood flow
| Autor: | Joseph R. Tobin, J. G. Kennedy, M. J. Breslow, Richard J. Traystman |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
medicine.medical_specialty
Epinephrine Physiology Blood Pressure Vasodilation Hexamethonium Compounds Receptors Nicotinic Hexamethonium Norepinephrine Dogs Physiology (medical) Internal medicine Muscarinic acetylcholine receptor medicine Animals Adrenal cortex business.industry Splanchnic Nerves Receptors Muscarinic Electric Stimulation medicine.anatomical_structure Nicotinic agonist Endocrinology Adrenal Medulla Catecholamine Cholinergic Vascular Resistance Cardiology and Cardiovascular Medicine Adrenal medulla business Blood Flow Velocity Endocrine gland medicine.drug |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 261:H1836-H1841 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.1991.261.6.h1836 |
| Popis: | To determine the relative role of nicotinic and muscarinic mechanisms in splanchnic nerve stimulation (NS)-induced adrenal catecholamine secretion and medullary vasodilation, 12 pentobarbital-anesthetized dogs were subjected to three identical stimulations. The first NS was performed before drug administration and served as a control. The second NS was performed after administration of either the muscarinic antagonist, atropine 0.5 mg/kg (group 1), or the nicotinic antagonist, hexamethonium 20 mg/kg (group 2). The third NS was performed after administration of both drugs. NS in the absence of drug resulted in 4-fold and greater than 200-fold increases in medullary blood flow (Q, measured with radiolabeled microspheres) and catecholamine secretion (assayed by high-pressure liquid chromatography), respectively. Atropine, when administered alone (group 1), had no effect on these responses. Subsequent administration of hexamethonium to group 1 animals resulted in complete blockade of NS-induced changes in medullary Q and secretion. Hexamethonium alone (group 2) reduced the catecholamine response to NS by 95% but had no effect on the medullary Q response. Addition of atropine further attenuated the increase in catecholamine secretion induced by NS and completely blocked the medullary Q increase. These data suggest the presence of redundant mechanisms to increase medullary Q during NS. One mechanism likely involves neurally released acetylcholine-stimulating vascular muscarinic receptors, whereas the second requires either chromaffin cell degranulation or nicotinic ganglionic transmission. |
| Databáze: | OpenAIRE |
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