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Thromb Haemost 1986; 56(02): 120-123
DOI: 10.1055/s-0038-1661623
Original Article
Schattauer GmbH Stuttgart

Increased Plasma Noradrenaline During Severe Sodium Restriction Does Not Stimulate Platelet Release in Essential Hypertension

S E Kjeldsen
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
K Lande
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
K Gjesdal
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
M B Jackson
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
A Westheim
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
P Frederichsen
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
P Leren
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
,
I Eide
Departments of Internal Medicine, Clinical Physiology and Clinical Chemistry, Oslo University School of Medicine, Ullevaal Hospital, Oslo, Norway
› Author Affiliations
Further Information

Publication History

Received 23 April 1986

Accepted 12 June 1986

Publication Date:
20 July 2018 (online)

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Summary

Seventeen 50-year old hypertensive men, previously untreated with blood pressure 157 ± 4/110 ± 2 mmHg (means ± SE) were given a low sodium diet for 2 weeks. During the second week, the diet was supplemented with potassium. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:4 and 1:11, respectively.

Sympathetic noradrenergic tone increased considerably during the first week. Thus, venous plasma noradrenaline increased from 254 ± 22 to 347 ± 28 pg/ml (p <0.001) and arterial concentration from 253 ± 36 to 317 ± 42 pg/ml (n = 10, p <0.001). No significant change was observed in sympathetic adrenal tone as reflected by normal plasma adrenaline in venous (42 ± 5 vs 43 ± 6 pg/ml, ns) or arterial blood (71 ± 10 vs 82 ± 15 pg/ml, n = 10, ns) or in venous plasma concentration of the blood platelet release product beta-thromboglobulin (BTG) (50 ± 8 vs 43 ± 5 ng/ml, ns). During the second week sympathetic noradrenergic tone remained highly significantly elevated compared to baseline but still no change in plasma adrenaline or plasma BTG was found.

Thus, whereas sodium depletion did increase plasma noradrenaline concentration markedly in these hypertensive men, no change in adrenaline concentration was observed, and blood platelet release reaction was unchanged. Plasma noradrenaline within the physiological concentration range does not seem to serve as a regulator of in vivo platelet function.

Key words

Adrenaline - Beta-thromboglobulin - Catecholamines - Platelet function - Salt
 

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