Abstract: SA-PO326
Different Forms of Afferent Nerve Input in Cardiac and Renal Disease in Rats?
Session Information
- Hypertension and CVD: Mechanisms
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1403 Hypertension and CVD: Mechanisms
Authors
- Rodionova, Kristina, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Ditting, Tilmann, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Pickny, Lisa, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Ott, Christian, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Schmieder, Roland E., Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Schiffer, Mario, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Amann, Kerstin U., Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Veelken, Roland, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
Background
Afferent nerve pathways form kidney and heart likely control sympathetic renal nerve activity. In renal disease (anti Thy1 nephtitis) the responsiveness of afferent renal nerve units was shifted from units with highly active primary neurons (tonic response pattern) to units with neurons of very low activity upon stimulation (phasic response pattern). Afferent renal nerve activity was likely decreased. Likewise, afferent vagal nerve activity in congestive heart failure (CHF) had a lower frequency at saturation than controls. Hence we wanted to test the hypothesis that in CHF the vagal afferent nerve pathway consists of a decreased number of highly active tonic sensory neurons in the nodose ganglion.
Methods
CHF was induced by coronary artery ligature, nephropathy by injections of an anti Thy1.1 antibody (OX7, 1.2mg/kg). After a respective time (CHF 21 days, nephropathy 7 days after induction) nodose ganglion neurons with cardiac vagal afferents from CHF rats or neurons form dorsal root ganglia with renal afferents from rats with nephropathy were cultured. Current clamp was used to characterize neurons as “tonic”, i.e. sustained action potential (AP) firing or “phasic”, i.e. <5 APs upon current injection. Electrophysiological parameters and AP properties were determined in neurons from animals with CHF or nephropathy.
Results
In CHF rats, the number of neurons with a tonic , more active response pattern from CHF animals did not differ from controls (64% vs. 70 %, ns). However, tonic cardiac neurons from CHF rats exhibited an increased production of action potentials compared to controls (24.4+/-5.0 vs. 14.7+/-1.8 APs/10s; p<0.05; mean+/-SEM). In nephropathic rats, the number of neurons with a tonic response pattern decreased significantly (43% vs. 64 %, p<0.05) , but there was no difference in action potential production as compared to controls.
Conclusion
In contrast to our hypothesis, in CHF the number of afferent neurons with a tonic response pattern was not altered, instead the action potential production of these neurons increased increased upon stimulation. Hence, in congestive heart failure vagal afferent neurons increase their sensitivity in the presence of impaired intracardiac receptors whereas in renal disease the responsiveness of the first part of the afferent pathway is impaired as a whole