Original Paper

Urinary Kallikrein and Blood Pressure - Gender-Different Response to Potassium Supplementation in SHR
Role of Aldosterone
Elisabeth M. Oddo, Verónica De Luca Sarobe, Rafael Krmar, Rodolfo S. Martín, Fernando R. Ibarra, Elvira E. Arrizurieta

Instituto de Investigaciones Médicas Alfredo Lanari, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina

Address of Corresponding Author

Nephron Physiol 2008;108:p37-p45 (DOI: 10.1159/000118939)

  Key Words

• Hypertension, sexual dimorphism
• Sexual dimorphism
• Potassium supplementation
• Urinary kallikrein activity, sexual dimorphism
• Mineralocorticoids
• Spontaneous hypertensive rat

  Abstract

Aims: To test whether blood pressure is affected by potassium supplementation which modifies urinary kallikrein (UK) in SHR of either sex, and to elucidate the mechanisms involved. Design: In SHR and WKY blood pressure, renal function and hormonal profile were studied after 1% oral potassium supplementation starting at 4 weeks of age and throughout until 12 weeks of age. Results were compared with those of untreated SHR and WKY of either sex. Results: Systolic blood pressure (mm Hg) started to rise in SHR and was significantly different at 6-8 weeks of age: 153.5 ± 7.9 versus 100 ± 5.6 in female and 157 ± 7.7 versus 98.4 ± 6.8 in male rats (p < 0.01). Systolic blood pressure increased progressively in female and male rats reaching 164.5 ± 4.8 and 204.5 ± 7.6, respectively, at 12 weeks of age. At this time systolic blood pressure was higher in male than in female SHR (p < 0.01) and UK activity (UKa; nkat/day/100 g body weight) was slightly lower in male SHR. After 1% oral potassium supplementation administered from 4 to 12 weeks of age, a decrease in systolic blood pressure was seen in male SHR: 204.5 ± 7.6 versus 173.5 ± 7.9 (p < 0.05); and 164.5 ± 4.8 versus 156.8 ± 5.5 in female rats (NS) at 12 weeks of age, concomitant with an increase in UKa, particularly in male rats (29.35 ± 1.92 versus 36.54 ± 2.61, p < 0.05). As expected, plasma aldosterone (pg/ml), increased markedly after potassium treatment from 129 ± 31.4 in untreated female and male SHR and WKY to 528 ± 180.7 in SHR and 473 ± 88.4 in WKY (p < 0.05 in both cases). After potassium supplementation, potassium excretion was significantly correlated with both aldosterone levels and UKa (p < 0.001 in both cases). No significantly concurrent changes in plasma renin activity were observed, but instead a significant decrease was seen in SHR (p < 0.01). The potassium blood pressure-lowering effect was blunted by aldosterone receptor antagonist treatment that also decreased UKa from 36.5 ± 2.61 to 19.5 ± 1.9, particularly in male SHR. No attempt was made in this experimental setting to block kallikrein or kinin receptors. Conclusions: UKa increases as a consequence of aldosterone stimulation by potassium load since an aldosterone receptor blockade abolishes UKa increment and blood pressure fall. These results further support the hypothesis that the kallikrein kinin system plays a role in blood pressure regulation and they also show a gender different response to potassium load in relation to UKa and blood pressure.

Copyright © 2008 S. Karger AG, Basel

  Author Contacts

Elvira E. Arrizurieta
IIM Alfredo Lanari
Combatientes de Malvinas 3150
Buenos Aires 1427 (Argentina)
Fax +54 11 4523 4094/4823 3426, E-Mail ilanari@pinos.com

  Article Information

Received: May 10, 2007
Accepted: December 19, 2007
Published online: March 3, 2008
Number of Print Pages : 9
Number of Figures : 6, Number of Tables : 2, Number of References : 25