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Research Article Free access | 10.1172/JCI106695
Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52240
Veterans Administration Hospital, Iowa City, Iowa 52240
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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52240
Veterans Administration Hospital, Iowa City, Iowa 52240
Find articles by Abboud, F. in: JCI | PubMed | Google Scholar
Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52240
Veterans Administration Hospital, Iowa City, Iowa 52240
Find articles by Ballard, D. in: JCI | PubMed | Google Scholar
Published October 1, 1971 - More info
Experiments were done to study the effects of acute changes in plasma sodium concentration [Na] on vasoconstrictor responses to norepinephrine and to reflex sympathetic stimulation in man. [Na] in the venous return from the forearm of each of 21 normal subjects was reduced (to an average of 118 mEq/liter), increased (147 mEq/liter), and maintained within the normal range (140 mEq/liter) by means of infusions into the brachial artery of three solutions containing different [Na]. Mannitol or sucrose and disodium sulfate were substituted for sodium chloride to produce the desired changes in [Na] without changing blood osmolarity.
Blood flow to the forearm (plethysmograph) increased during infusion of the three solutions, but the increase in flow was not related to [Na]. Vasoconstrictor responses to injections of norepinephrine and angiotensin into the brachial artery were reduced at low [Na] and augmented at high [Na]. Reflex vasoconstriction, activated by lower body negative pressure, was similarly affected by changes in [Na]. In the isolated, perfused gracilis muscle of dog vasoconstrictor responses to norepinephrine and to nerve stimulation were attenuated, and the extraction of norepinephrine by this muscle was smaller when plasma [Na] was reduced.