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Low doses of Intrarenal Bradykinin induce a Monophasic Sympathoinhibitory Response
Author(s) -
Hindermann Martin,
Ditting Tilmann,
Rodionova Kristina,
Loosen Sonja,
Ott Christian,
Schmieder Roland,
Amann Kerstin,
Veelken Roland
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.851.2
Subject(s) - bradykinin , medicine , endocrinology , blood pressure , bolus (digestion) , bradykinin receptor , chemistry , anesthesia , receptor
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. Material and 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 NK 1 ‐receptor blocker RP67580 (10*10 −3 M, 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 NK 1 ‐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. Support or Funding Information DFG, German Research Foundation Interdisciplinary Center for Clinical Research ‐ University of Erlangen, Erlangen, Germany This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .