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Department of Internal Medicine, University of Erlangen-Nürnberg, 91054 Erlangen, Germany
In
rats, the mechanosensitive cardiorenal baroreflex influencing renal
excretory function might be impaired by serotonin occurring in coronary
arteries, e.g., in hypertension. Because the afferent limb of this
reflex could be affected, we investigated the responses of nodose
ganglion cells (one neuron of reflex) to osmotic, mechanical stress in
presence or absence of the serotonin 5-HT3 receptor agonist
phenylbiguanide (PBG). Current-voltage relationships (from 
100 to +50 mV) were obtained using cell patch recordings while the
cells were exposed to control or hypoosmotic solutions to induce
mechanical stress. This protocol was repeated after low doses of PBG
(10 µM), angiotensin II (10 nM), or the stretch-activated channel
blocker gadolinium (20 µM) were added to the extracellular medium
(EM). Hypoosmotic EM induced significant changes in cellular conductance. The full-range current-voltage relationship allowed for
the calculation of a mean reversal potential of 13 ± 1.2 mV
with respect to this change in cellular conductance (n = 44). This increase in conductance was impaired after addition of
either PBG or gadolinium to the EM,which was statistically evaluated at
a voltage of 80 mV, where influences of voltage-gated channels are
not likely to interfere with the responses recorded. The serotonin 5-HT3 receptor antagonist tropisetron (10 nM) prevented the
PBG effect on conductance responses. Angiotensin II had no influence. Hence, serotonin might decrease the mechanical sensitivity of afferent
cardiac nerves controlling renal sympathetic nerve activity.
mechanosensitivity; renal innervation
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