Enhanced blood pressure sensitivity to deoxycorticosterone in mice with disruption of bradykinin B2 receptor gene

Costanza Emanueli, Edwin Fink, Anna Franca Milia, Maria Bonaria Salis, Milena Conti, Maria Piera Demontis, Paolo Madeddu

Research output: Contribution to journalArticlepeer-review

Abstract

The renal kallikrein-kinin system is activated under conditions of mineralocorticoid excess. To evaluate whether endogenous kinins exert a protective role against the development of mineralocorticoid-induced hypertension, we studied the cardiovascular effects induced by long-term administration of deoxycorticosterone (DOC; 0.3 μmol/g body wt SC once per week for 6 weeks) or vehicle in transgenic mice (Bk2r(-/-)) lacking the bradykinin B2 receptor gene and in wild-type controls (Bk2r(+/+)). Under basal conditions, Bk2r(-/-) mice showed higher systolic blood pressure (tail- cuff plethysmography) than wild-type Bk2r(+/+) and heterozygous Bk2r(+/-) mice (121 ± 2 versus 114 ± 2 and 115 ± 2 mm Hg, respectively; P2 receptor is essential for regulation of blood pressure and heart rate under basal conditions. In addition, they indicate that activation of the kallikrein-kinin system represents a compensatory response against the development of hypertension induced by mineralocorticoid excess.

Original languageEnglish
Pages (from-to)1278-1283
Number of pages6
JournalHypertension
Volume31
Issue number6
Publication statusPublished - 1998

Keywords

  • Blood pressure
  • Kallikrein-kinin system
  • Mineralocorticoids

ASJC Scopus subject areas

  • Internal Medicine

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