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Regulation of sympathetic nerve traffic to skeletal muscle in resting humans.

Forskningsöversiktsartikel
Författare Gunnar B Wallin
Publicerad i Clinical autonomic research : official journal of the Clinical Autonomic Research Society
Volym 16
Nummer/häfte 4
Sidor 262-9
ISSN 0959-9851
Publiceringsår 2006
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 262-9
Språk en
Länkar dx.doi.org/10.1007/s10286-006-0357-...
Ämnesord Blood Pressure, physiology, Humans, Muscle, Skeletal, innervation, Rest, physiology, Sympathetic Nervous System, physiology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

An overview is given of microneurographic studies of resting vasoconstrictor traffic in human muscle nerves (muscle sympathetic nerve activity = MSNA). In multiunit recordings, the activity consists of synchronized bursts of vasoconstrictor impulses, the outflow of which is under potent arterial baroreflex control. In agreement with this, the bursts always display cardiac rhythmicity and occur during temporary reductions of blood pressure. Burst occurrence shows a close inverse correlation to variations of diastolic blood pressure whereas the correlation to the strength of the bursts is weak or absent, suggesting that the mechanisms controlling the two parameters are not identical. These dynamic characteristics are similar in all subjects despite large, reproducible, interindividual differences in number of bursts. Such interindividual differences probably have a genetic origin, and since discharge frequencies in single vasoconstrictor fibers are similar in subjects with few and many bursts, the differences in multiunit activity are likely to be due to a higher number of active fibers in subjects with many bursts. The interindividual differences in multiunit activity are not associated with differences in resting blood pressure levels. Recent studies have revealed (a) an inverse relationship between resting levels of cardiac output and MSNA and (b) evidence of reduced vascular responsiveness to noradrenaline in subject with many sympathetic bursts at rest. These findings suggest that the vasoconstriction induced by the sympathetic impulses is balanced or reduced by these factors, which thereby contribute to the poor relationship between the mean number of sympathetic bursts and the blood pressure level.

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