Document Detail

Angiotensin (1-7) receptor antagonism equalizes angiotensin II-induced hypertension in male and female spontaneously hypertensive rats.
MedLine Citation:
PMID:  20713916     Owner:  NLM     Status:  MEDLINE    
Females are less sensitive to the hypertensive effects of angiotensin II compared with males, although the molecular mechanisms responsible are unknown. We hypothesize that differential activation of angiotensin II, angiotensin (1-7), angiotensin II type 1, angiotensin II type 2, and mas levels in the renal cortex of male and female spontaneously hypertensive rats contribute to sex differences in the blood pressure response to angiotensin II infusion. Males had a greater increase in blood pressure after angiotensin II infusion than females (males: 150±2 to 186±3 mm Hg; females: 137±3 to 160±4 mm Hg; P<0.05). Angiotensin II infusion resulted in comparable increases in plasma and renal cortical angiotensin II levels in both sexes. Renal cortical angiotensin (1-7) levels were higher in female rats under basal conditions (195±10 versus 67±11 ng/g of cortex; P<0.05) and after angiotensin II infusion (281±25 versus 205±47 ng/g of cortex; P<0.05) compared with male rats. In the renal cortex of male rats, angiotensin II infusion decreased angiotensin II type 1 protein expression and increased angiotensin II type 2 expression with no change in mas expression. In female rats there was an increase in mas receptor protein expression with angiotensin II infusion, although angiotensin II type 1 and angiotensin II type 2 expressions were unchanged. Male and female rats were then treated with the angiotensin (1-7) mas receptor antagonist A-779 in the absence and presence of angiotensin II. A-779 equalized the blood pressure response to angiotensin II in males and females (blood pressure at the end of treatment: males, 166±4 mm Hg; females, 164±5 mm Hg). In conclusion, angiotensin (1-7) contributes to the sex difference in angiotensin II-induced increases in blood pressure in spontaneously hypertensive rats.
Jennifer C Sullivan; Kanchan Bhatia; Tatsuo Yamamoto; Ahmed A Elmarakby
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-08-16
Journal Detail:
Title:  Hypertension     Volume:  56     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-16     Completed Date:  2010-10-29     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  658-66     Citation Subset:  IM    
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MeSH Terms
Angiotensin I / metabolism*
Angiotensin II / analogs & derivatives,  blood,  metabolism,  pharmacology,  toxicity*
Blood Pressure / drug effects*,  physiology
Blotting, Western
Hypertension / chemically induced,  physiopathology*
Kidney Cortex / drug effects,  metabolism
Peptide Fragments / metabolism*,  pharmacology
Proto-Oncogene Proteins / antagonists & inhibitors,  genetics,  metabolism*
Rats, Inbred SHR
Receptor, Angiotensin, Type 1 / genetics,  metabolism
Receptor, Angiotensin, Type 2 / genetics,  metabolism
Receptors, G-Protein-Coupled / antagonists & inhibitors,  genetics,  metabolism*
Reverse Transcriptase Polymerase Chain Reaction
Sex Factors
Vasoconstrictor Agents / blood,  metabolism,  toxicity
Grant Support
1R01HL093271-01A1/HL/NHLBI NIH HHS; R01 HL093271/HL/NHLBI NIH HHS; R01 HL093271-01A1/HL/NHLBI NIH HHS; R01 HL093271-02/HL/NHLBI NIH HHS; R01 HL093271-03/HL/NHLBI NIH HHS
Reg. No./Substance:
0/7-Ala-angiotensin (1-7); 0/Peptide Fragments; 0/Proto-Oncogene Proteins; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2; 0/Receptors, G-Protein-Coupled; 0/Vasoconstrictor Agents; 0/angiotensin I (1-7); 0/proto-oncogene proteins c-mas-1; 11128-99-7/Angiotensin II; 9041-90-1/Angiotensin I

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