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Intra Renal Bradykinin Blunted the Baroreflex Control of Renal Sympathetic Nerve Activity in Anaesthetized Rats
Author(s) -
Akhtar Safia,
Sattar Munavvar Zubaid Abdul,
Rathore Hassaan Anwer,
Ahmad Ashfaq,
Abdullah Nor Azizan,
John Edward James
Publication year - 2016
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.30.1_supplement.lb718
Subject(s) - baroreflex , bradykinin , phenylephrine , medicine , blood pressure , baroreceptor , endocrinology , saline , kidney , anesthesia , heart rate , receptor
There is evidence that bradykinin (BK) results in increased afferent renal nerve activity (ARNA) which leads to sympathetic over activity. This study investigates whether bradykinin supresses high and low‐pressure baroreceptor regulation of renal sympathetic nerve activity (RSNA) in rats. Rats were anaesthetized by means of the administration of 1 mL (i.p.) of a chloralose–urethane mixture (16.5 and 250 mg mL −1 respectively). BK or saline were infused into the cortico‐medullary border of the ipsilateral kidney and RSNA recordings were made from the contralateral (left) kidney. Baroreflex gain curves for RSNA were generated by increasing and decreasing blood pressure using i.v. doses of phenylephrine and sodium nitroprusside (50 μg in a volume of 0.2 mL for each) while the low‐pressure or cardiopulmonary receptors were stimulated by infusing an acute saline volume load for 30 mins. Intrarenal infusion of BK reduced high pressure baroreflex sensitivity for RSNA by 32% (P < 0.05) compared with that of saline infused animals. Volume expansion resulted in greater renal sympatho‐inhibition by 43% (P < 0.05) in rats with saline infusion, whereas BK infused rats shows non‐significant renal sympatho‐inhibition by 12%. Intrarenal infusion of BK causes dysregulation of the arterial and cardiopulmonary baroreflexes. These findings reveal a significant role of the inflammatory mediator, BK which would blunt the normal cardiovascular homeostasis and can contribute to a deranged autonomic control. Support or Funding Information The authors fully acknowledge the Universiti Sains Malaysia Research Undergraduate (USM‐RU) grant (1001/PFARMASI/815078) provided by Universiti Sains Malaysia, Malaysia.Safia Akhtar is a recipient of a USM Fellowship [P‐FD0091/11(R)] from the Institute of Post‐Graduate Studies (IPS), Universiti Sains Malaysia (USM), Penang, Malaysia