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Cytochrome P-450 metabolites in renal circulation and excretion - interaction with nitric oxide [NO] system

100%

Kompanowska-Jezierska E. , Kuczeriszka M.

Journal of Physiology and Pharmacology. Supplement

2008

tom 59

nr 9

137-149

Intrarenal vasodilator systems: NO, prostaglandins and bradykinin. An integrative approach

84%

Sadowski J. , Badzynska B.

Journal of Physiology and Pharmacology. Supplement

2008

tom 59

nr 9

105-119

Arginine and tetrahydrobiopterin supplementation in rats with salt-induced blood pressure increase: minor hypotensive effect but improvement of renal haemodynamics

84%

Kuczeriszka M. , Walkowska A. , Olszynski K. H. , Rafalowska J. , Sadowski J. , Kompanowska-Jezierska E.

Journal of Physiology and Pharmacology

2019

tom 70

nr 2

Cytochrome P-450 monooxygenases in control of renal haemodynamics and arterial pressure in anaesthetized rats

67%

Kuczeriszka M. , Badzynska B. , Kompanowska-Jezierska E.

Journal of Physiology and Pharmacology. Supplement

2006

tom 57

nr 11

179-185

The renal regulatory role of cytochrome P450 dependent metabolites of arachidonic acid (AA), vasodilator epoxyeicosatrienoic acids (EETs) and vasoconstrictor 20-hydroxyeicosatetraenoic acid (20-HETE), was examined in anaesthetised rats. We measured renal artery flow (RBF), cortical (CBF) and medullary (MBF) perfusion (laser-Doppler) and medullary tissue nitric oxide (NO, selective electrode), after non-selective inhibition of CYP-450 pathway with 1-aminobenzotriazole (ABT, 10 mg/kg i.v.) or after selective inhibition of 20-HETE synthesis with HET0016 (Taisho Co, Yoshino-cho, Japan), infused into renal artery at 0.3 mg/kg/h or into renal medulla at rates increasing from 0.15 to 1.5 mg/kg/h. ABT caused significant (by 13.7%) decrease in RBF without changing MBF. Renal arterial HET0016 increased MBF (not RBF or CBF) from 152±12 to 174±12 perfusion units (+16%, P<0.001), while medullary tissue nitric oxide was significantly increased (P<0.001). After renal medullary HET0016, renal perfusion indices were significantly higher than after HET0016 solvent (ß-cyclodextrin). Total renal blood flow seems to be under vasodilator control of EETs whereas renal medullary perfusion under tonic suppression by 20-HETE. The data document, for the first in the whole kidney studies, the functional antagonism of 20-HETE and NO.

Specific features and roles of renal circulation: angiotensin II revisited

67%

Sadowski J. , Badzynska B.

Journal of Physiology and Pharmacology. Supplement

2006

tom 57

nr 11

169-178

The status of intrarenal circulation determines in part renal excretion, affects body fluid homeostasis and has a role in long term control of arterial blood pressure. The vascular resistance in the renal cortex and medulla is determined by interaction of a vast array of vasoactive hormones and paracrine factors; among these the role of constrictor angiotensin II and dilator prostaglandins and nitric oxide may appear to be dominating. The focus of this review and underlying studies is on the mechanisms whereby the microcirculation of the renal medulla is protected against the vasoconstrictor action of angiotensin II. In anaesthetized normal rats the three mentioned active agents or their inhibitors were applied and total renal blood flow and cortical, outer- and inner medullary laser-Doppler fluxes were determined; in some studies renal tissue nitric oxide was measured using selective electrodes. We conclude that angiotensin II, acting via AT1 receptors, constricts the renal cortical vasculature; in the medulla its action is effectively buffered by prostaglandin E2 but most probably not by nitric oxide.