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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Acta Physiol (Oxf). 2012 Nov 26;207(2):358–368. doi: 10.1111/apha.12025

Table 2.

Maximum response (Emax) and sensitivity (logEC50) to angiotensin II (ANGII)-, phenylephrine (PE)-, and KCl-mediated vasoconstriction in aortas from SS-13BN rats and SS rats on normal diet or hyper-caloric diet.

SS-13BN
SS
Normal Hyper-caloric Normal Hyper-caloric
Emax, % Increase in Force
AngII 71±10 (10) 53±11(10) 133±11 (8)* 43±5 (14)
+PEG-SOD 55±6 (6) 27±7 (3) 53±17 (6) 16±2 (9)
+CATALASE 88±13 (4) 25±5 (4) 73±21 (5) 46±6 (12)
+L-NAME 114±15 (6) 51±6 (5) 117±13 (5) 91±11 (11)
KCl 140±4 (12) 114±9 (10)* 156±9 (9) 148±6 (14)

logEC50, [M] for AngII; EC50, [mM] for KCl

AngII −8.1±0.01 (11) −8.2±0.1 (10) −8.4±0.1 (11) −8.1±0.1 (14)
+PEG-SOD −7.8±0.2 (6) −7.7±0.1 (3) −8.0±0.2 (5) −7.9±0.1 (9)
+CATALASE −8.2±0.1 (4) −8.1±0.2 (4) −8.3±0.4 (5) −8.1±0.1 (11)
+L-NAME −8.4±0.1 (6) −7.9±0.1 (5) −8.7±0.3 (6) −8.2±0.04 (11)
KCl 17.6±1.1 (10) 28.8±3.1 (6)* 20.3±1.3 (13) 25.9±1.4 (8)
*

P<0.05 vs. untreated aortas from SS-13BN rats on normal diet;

P<0.05 vs. untreated aortas from SS rats on normal diet;

P<0.05 vs. corresponding untreated aortas. Number of rats is in parentheses.