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Vascular kallikrein in deoxycorticosterone acetate-salt hypertensive rats
H Nolly1, O A Carretero, M C Lama
1Argentine Council of Research (CONICET), School of Medicine, UNC, Mendoza.
Insights
This study investigated vascular kallikrein in rats with deoxycorticosterone acetate-salt induced hypertension. Findings show altered kallikrein activity in blood and tissues, impacting blood pressure regulation.
Area of Science:
- Physiology
- Biochemistry
- Cardiovascular Research
Background:
- Hypertension is a significant global health concern.
- The kallikrein-kinin system plays a role in blood pressure regulation.
- Understanding vascular kallikrein's role in hypertension is crucial for therapeutic development.
Purpose of the Study:
- To determine the status of vascular kallikrein in rats with severe hypertension.
- To investigate the changes in active and total kallikrein activity in perfusate and arterial/venous tissues.
- To correlate kallikrein activity with elevated blood pressure.
Main Methods:
- Induction of severe hypertension in rats using deoxycorticosterone acetate (DOCA) and 1% NaCl solution for 6 weeks.
- Assay of active and total kininogenase (kallikrein) activity in perfusate, arterial, and venous tissues.
- Measurement of systolic blood pressure at 6 weeks.
Main Results:
- DOCA-salt rats exhibited significantly higher systolic blood pressure (214 mmHg) compared to controls.
- Perfusate active and total kallikrein initially increased, then significantly decreased by week 6.
- Arterial active kallikrein showed a transient increase followed by a significant decrease, while total kallikrein decreased significantly at week 6.
- Venous active and total kallikrein levels remained elevated throughout the experiment.
Conclusions:
- Severe hypertension induced by DOCA-salt treatment alters vascular kallikrein activity in a tissue-specific manner.
- Elevated venous kallikrein may represent an adaptive response or contribute to hypertension.
- Further research is needed to elucidate the precise role of vascular kallikrein in the pathogenesis of hypertension.
Abstract:
We determined the status of vascular kallikrein in rats with severe hypertension caused by treatment with deoxycorticosterone acetate (DOCA) and drinking of 1% NaCl for 6 weeks. We assayed active and total kininogenase (kallikrein) activity in the perfusate and in arterial and venous tissue. DOCA-salt rats had higher systolic blood pressure at 6 weeks (214 +/- 5 mm Hg) than rats drinking tap water (135 +/- 4 mm Hg) or saline (145 +/- 8 mm Hg). Kininogenase in the perfusate (nanograms bradykinin per minute per kilogram body weight) increased significantly at 2 weeks, from 5.8 +/- 2.1 to 8.9 +/- 1.4 for active kallikrein and from 28.7 +/- 0.4 to 48.7 +/- 2.9 for total kallikrein. Total kallikrein returned to control values at 4 weeks, whereas it was significantly reduced at 6 weeks (20.9 +/- 0.7). Active kallikrein was significantly depressed at 4 and 6 weeks (1.08 +/- 0.1 and 0.85 +/- 0.1, respectively [P < .05]). Active kallikrein in arterial tissue (picograms bradykinin per milligram per minute) showed a small but significant increase at 2 weeks, from 156 +/- 7 to 201 +/- 10 (P < .05), finally decreasing significantly by 6 weeks to 64 +/- 3; however, total kallikrein showed a significant decrease only at 6 weeks, from 844 +/- 17 to 427 +/- 27. Both active and total kallikrein in the veins were higher than control values at 2 weeks, changing from 437 +/- 7 to 541 +/- 19 and from 1619 +/- 17 to 2062 +/- 86, respectively. Venous kallikrein remained elevated until the end of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)