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Changes in vagal reactivity to the sympathicotonia during the progression of heart failure: From self-suppression to counteraction (CROSBI ID 194842)

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Miličević, Goran ; Udiljak, Nikola ; Miličević, Tena Changes in vagal reactivity to the sympathicotonia during the progression of heart failure: From self-suppression to counteraction // Medical hypotheses, 81 (2013), 2; 254-267. doi: 10.1016/j.mehy.2013.04.033

Podaci o odgovornosti

Miličević, Goran ; Udiljak, Nikola ; Miličević, Tena

engleski

Changes in vagal reactivity to the sympathicotonia during the progression of heart failure: From self-suppression to counteraction

Activities of both autonomic nervous system divisions, sympathetic and parasympathetic, are dual – continuous, tonic and changing, modulating. Tonic activity domination accompanies stationary (patho)physiological conditions, while modulating activity occurs with the change of stimuli. The intensity of the two activities is inversely proportional. In patients with heart failure, spectral analysis of heart rate variability displays reduced sympathetic modulation activity during illness, as a logical consequence of an increased sympathetic tone. On the other hand, vagal modulation activity slightly decreases or does not change at the very early stage of disease, soon afterwards it increases, and after a certain period of time, with the progression of the disease, vagal modulation decreases, and finally disappears. These changes reveal sequential response of vagal tone to the progression of heart failure and consequent sympathicotonia ; slight initial oscillation or unresponsiveness, soon followed by self-suppression, and then, in an advanced heart failure, by counteraction to the sympathicotonia. This model of polyphasic reaction of vagal system, dependent on the stage of heart failure, challenges traditional concept of sympathovagal interaction. By this hypothesis, the self-suppression of vagal tone occurs in order to enable full sympathetic activation of compensatory mechanisms which aim to correct hemodynamic deterioration. Once the sympathicotonia becomes inefficient and even harmful, counter-regulatory increase in vagal tone develops, in order to decrease oxygen consumption and preserve or possibly enhance residual systolic and diastolic cardiac function. Decreased vagal tonic activity is probably mediated centrally. Later increase of vagal tone is probably triggered by an increased concentration of natriuretic peptides. The existence of predominantly adrenergic IL, Ca and predominantly cholinergic IK, Ach currents and of a common If current in sinoatrial nodal cells enables such dual – synergistic and antagonistic – sympatho-vagal relationship. In conclusion, a complex, polyphasic vagal reaction to the sympathicotonia and heart failure progression is suggested by the hypothesis. Clinical and experimental studies based on this hypothesis will probably allow better insight into autonomic functions.

autonomic nervous system; heart failure

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Podaci o izdanju

81 (2)

2013.

254-267

objavljeno

0306-9877

10.1016/j.mehy.2013.04.033

Povezanost rada

Temeljne medicinske znanosti, Kliničke medicinske znanosti, Biologija

Poveznice
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