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Role of the kallikrein‐kinin system on the hypotensive and hypoglycemiant effects of exercise in type 2 diabetics
Author(s) -
Arsa Gisela,
Lima Laila Jesus,
Motta Daisy Fonseca,
Almeida Wesley Salazar,
Campbel Carmen Silvia Grubert,
Araujo Ronaldo Carvalho,
Pesquero Jorge Luiz,
Casarini Dulce Elena,
Carmona Adriana Karaoglanovic,
Simões Herbert Gustavo
Publication year - 2011
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.25.1_supplement.1027.20
Subject(s) - medicine , bradykinin , endocrinology , kallikrein , ingestion , kinin , blood pressure , chemistry , enzyme , biochemistry , receptor
We evaluated the possible role of plasma of kallikrein activity (PKA) and bradykinin (BK) on blood glucose (BG) and blood pressure (BP) responses to exercise and to post‐exercise carbohydrate (CHO) ingestion in diabetics (D) and non‐diabetics (ND) individuals. Ten diabetics (53±2 years; fasting BG 167±11mg.dL‐ 1 ) and ten non‐diabetics (48±2 years; fasting BG 92mg.dL‐ 1 ) underwent incremental maximal exercise test (IT); a submaximal exercise at 90% of lactate threshold (90L); and a control session (C). Data was recorded at rest and 135min of post‐exercise recovery (R15‐R135). CH was administered at R45. In D, PKA increased after IT compared to C (74%, p<0.05) and 90L (47%, p<0.05). In ND, PKA increased after 90L compared to rest (53%, p<0.05). At R15 (IT), PKA was higher in D compared to ND. BK levels were lower in D. Exercise‐induced reductions in BG and BP were more accentuated after IT for D and after 90L for ND. In D, CH‐induced increase in BG was attenuated after IT compared to C. PKA and BK may be among the mechanisms responsible for post‐exercise hypotension and exercise induced changes in BG for D and ND individuals.