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. Author manuscript; available in PMC: 2022 Jul 12.
Published in final edited form as: Hypertension. 2013 Feb;61(2):e20. doi: 10.1161/hypertensionaha.111.00571

Response to Angiotensin-(1-7) and Bradykinin in Baroreceptor Reflex Sensitivity in Hypertension

Manisha Nautiyal 1, Hossam A Shaltout 2, Daniel C de Lima 3, Kenia do Nascimento 4, Mark C Chappell 5,6, Debra I Diz 7,8
PMCID: PMC9274326  NIHMSID: NIHMS1820746  PMID: 23444463

The letter by Tsuda1 raises the question of whether bradykinin contributes to the effects of chronic intracerebroventricular angiotensin (Ang)-(1-7) to enhance baroreflex function in hypertensive (mRen2)27 rats. Our studies exclusively focused on the effects of Ang-(1-7) on NADPH oxidase and mitogen-activated protein kinase signaling pathways in the brain dorsal medulla relative to baroreflex and blood pressure responses. Thus, we cannot provide additional insight regarding the contribution of bradykinin to these responses. It is well established that there are interactions between bradykinin and Ang-(1-7), as well as other components of the RAS that may reflect an interaction through the common metabolism pathway involving angiotensin-converting enzyme, release of bradykinin by Ang-(1-7), or potential receptor interactions.2–5 In an earlier study, however, we demonstrated that the effects of a peptidic angiotensin-converting enzyme inhibitor injected acutely into the nucleus of the solitary tract were mediated primarily by Ang-(1-7) but not by bradykinin.6 Specifically, the selective Ang-(1-7) antagonist d-Ala7-Ang-(1-7) (A779) blocked the improvement in the baroreflex, but the bradykinin antagonist HOE 140 had no effect in that study.

Footnotes

Disclosures

None.

Contributor Information

Manisha Nautiyal, Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC.

Hossam A. Shaltout, Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC

Daniel C. de Lima, Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC

Kenia do Nascimento, Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC.

Mark C. Chappell, Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC Department of General Surgery, Wake Forest University School of Medicine, Winston-Salem, NC.

Debra I. Diz, Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, NC Department of General Surgery, Wake Forest University School of Medicine, Winston-Salem, NC.

References

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