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      Urinary Kallikrein and Blood Pressure – Gender-Different Response to Potassium Supplementation in SHR

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          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.

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            Sodium and potassium handling by the aldosterone-sensitive distal nephron: the pivotal role of the distal and connecting tubule.

            Sodium reabsorption and potassium secretion in the distal convoluted tubule and in the connecting tubule can maintain the homeostasis of the body, especially when dietary sodium intake is high and potassium intake is low. Under these conditions, a large proportion of the aldosterone-regulated sodium and potassium transport would occur in these nephron segments before the tubular fluid reaches the collecting duct. The differences between these two segments and the collecting duct would be more quantitative than qualitative. The collecting duct would come into play when the upstream segments are overloaded by a primary genetic defect that affects sodium and/or potassium transport or by a diet that is exceedingly poor in sodium and rich in potassium. It is likely that the homeostatic role of the distal convoluted and connecting tubules, which are technically difficult to study, has been underestimated, whereas the role of the more easily accessible collecting duct may have been overemphasized.
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              Evidence for a stimulatory effect of high potassium diet on renal kallikrein.

              Considerable evidence indicates that the connecting tubule cells, a type of cell of the distal nephron which seems to participate on potassium secretion, may be the place where renal kallikrein is synthetized. As potassium secretion and kallikrein synthesis may occur in the same cells, we studied the effect of high potassium diet on renal kallikrein production. The kallikrein containing cells from rats fed a normal and high potassium diet were evaluated using a combination of morphometric analysis, conventional electron microscopy, and ultrastructural immunocytochemistry. High potassium diet produced hypertrophy and hyperplasia of the kallikrein containing cells. Hyperplasia was sustained by an increased number of immunoreactive cells/mm2 (151 +/- 14 vs. 86.4 +/- 12, P less than 0.01), an increased number of binucleated immunoreactive cells/mm2 (11.90 +/- 2.1 vs. 3.77 +/- 0.17, P less than 0.005), and by the presence of mitosis. Cell hypertrophy was sustained by an increased cross-sectional area of immunoreactive cells (mu 2) (320.4 +/- 21 vs. 104.5 +/- 6.1, P less than 0.001), by an increased area of basal plasma membrane infoldings, by an hypertrophy of the components of the Golgi complex, hypertrophy of the components of the rough endoplasmic reticulum, and by a larger number of secretory-like vesicles containing kallikrein. The rats fed with high potassium diet had higher values on urinary kallikrein excretion-amidase activity (3.70 +/- 0.51 vs. 2.01 +/-0.37 units/day, P less than 0.02), higher values on potassium excretion (18.8 +/- 1.7 vs. 1.31 +/- 0.1 mmol/day, P less than 0.001), and higher urinary volume (51.5 +/- 5.3 vs. 12.2 +/- 1.6 ml/day, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                April 2008
                03 March 2008
                : 108
                : 3
                : p37-p45
                Instituto de Investigaciones Médicas Alfredo Lanari, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina
                118939 Nephron Physiol 2008;108:p37
                © 2008 S. Karger AG, Basel

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                Figures: 6, Tables: 2, References: 25, Pages: 1
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