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Abstract: FR-PO331

Low Doses of Intrarenal Bradykinin Induce a Monophasic Sympathoinhibitory Response

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Hindermann, Martin, Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  • Ditting, Tilmann, Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  • Rodionova, Kristina, Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  • Forray, Christina, Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  • Ott, Christian, Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  • Schmieder, Roland E., Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
  • Amann, Kerstin U., University of Erlangen-Nürnberg, Erlangen, Germany
  • Veelken, Roland, Dept. of Nephrology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany
Background

As recently reported intrarenally administered bradykinin induced a biphasic renal sympathetic nerve response (RSNA) with increases and decreases of RSNA but not uniform sympathoexcitation as previously assumed. The high doses necessary to evoke this biphasic response to bradykinin did not suggest a major physiological role of this observation in renal salt and water handling. Hence, we wanted to test the hypothesis that significantly lower doses of intrarenal bradykinin as previously used will induce a merely monophasic renal sympathoinhibition.

Methods

Groups of anesthetized SD rats (n=6-12) were equipped with femoral catheters (blood pressure (BP) & heart rate (HR) recording, drug application), a renal arterial catheter for one time intrarenal administration (IRA) of Bradykinin (BK 5 nM, 5 µl) or Capsaicin (CAP 1 nM, 10 µl) and a bipolar electrode for RSNA recordings; eventually an intravenous (iv) bolus of the NK1-receptor blocker RP67580 (10*10-3M, 15 µl) was given

Results

IRA Bradykinin and IRA CAP decreased RSNA from baseline 3.8±1.2 µV*sec to 1.3±0.7 µV*sec (5 µl, 5 nM BK, p<0.05) and 4.0±0.6 µV*sec to 1.6±0.4 µV*sec (10 µl, 1 nM CAP, p<0.01). After reaching the lowest point of RSNA activity at 95 min, both groups showed a slight re-increase of RSNA within the following 55 min (from 1.3±0.7 µV*sec up to 2.4±1.3 µV*sec (BK) and from 1.6±0.4 µV*sec up to 1.9±0.4 µV*sec (CAP)). Suppressed RSNA in both groups could be unmasked by systemic (i.v.) administration of the NK1-blocker (1.4±0.4 µV*sec to 5.0±1.9 µV*sec; p<0.05 (BK); 3.5±0.6 µV*sec to 9.7±1.7 µV*sec; p<0.01 (CAP)).

Conclusion

Bradykinin is able to reduce renal sympathetic nerve activity in doses that are significantly lower than doses inducing a biphasic sympathoexcitatory/-inhibitory response suggesting a physiological role of bradykinin in renal sympathetic nerve control and hence in neurogenic salt and water handling.

Funding

  • Government Support - Non-U.S.