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Contribution of neuronal nitric oxide (NO) synthase to N-acetylcysteine-induced increase of NO synthase activity in the brain of normotensive and hypertensive rats

100%

Pechanova O., Kunes J., Dobesova Z., Vrankova S., Zicha J.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 4

21-25

The goal of our study was to determine a contribution of nNOS to the increase of brain NO synthase activity induced by chronic N-acetylcysteine (NAC) treatment. Young 4-week-old male Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were subjected to treatment with NAC (1.5 g/kg/day) for 8 weeks. At the end of experiment total NOS activity was determined in the brainstem and cerebellum with and without specific nNOS inhibitor S-methyl-L-thiocitrulline (SMTC, 10-6 mol/l) by measuring the formation of L-[3H] citrulline from L-[3H] arginine. Chronic NAC treatment had no effect on blood pressure (BP) of WKY, while it attenuated BP increase in young SHR. Total NOS activity was increased in the brainstem of SHR compared to WKY, but this strain difference was abolished by SMTC. Chronic NAC treatment of SHR increased total NOS activity by 32% in the brainstem and by 67% in the cerebellum. After the incubation of brainstem and cerebellum with SMTC there were no significant differences in NOS activity of NAC-treated rats compared to strain-matched controls. Taken together, nNOS seems to be responsible for the increase of total NOS activity in the brain of SHR. SMTC inhibited 86% and 70% of NAC-induced increase of total NOS activity in the brainstem and cerebellum, respectively. Thus, nNOS is responsible not only for strain differences but also for NAC-induced increase of total NOS activity in the brain.

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Effect of vasopressin and V1 receptors blockade on hypotensive action of ANP in normotensive [WKY] and spontaneously hypertensive rats

100%

Lapinski M., Stepniakowski K., Januszewicz A., Noszczyk B., Szczepanska-Sadowska E.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 1

The aim of the study was to find out whether vasopressin (AVP) modifies hypotensive and heart rate accelerating effects of atrial natriuretic peptide (ANP) in normotensive (WKY) and spontaneously hypertensive (SHR) conscious rats. The effect of i. v. administration of 1; 2 and 4 µg of ANP on blood pressure (MP) and heart rate (HR) was compared during i. v. infusion of 0.9% NaCl (NaCl), NaCl + AVP (1.2 ng kg⁻¹ min⁻¹) and NaCl + dEt₂ AVP (V₁ receptors antagonist, 0.5 µg kg⁻¹ min⁻¹). AVP increased MP in SHR and WKY and decreased HR in SHR. V₁ antagonist decreased MP and increased HR only in SHR. In SHR ANP decreased MP and increased HR during NaCl, AVP and V₁ antagonist infusion. In WKY these effects were observed only during AVP administration. In each experimental situation hypotension and tachycardia induced by ANP were greater in SHR than in WKY. In both strains ANP induced changes in MP and HR were enhanced during AVP in comparison to NaCl infusion. V₁ antagonist did not modify effects of ANP in WKY and SHR. The results indicate that ANP abolishes hypertensive response induced by blood AVP elevation and that the basal levels of endogenous vasopressin acting through V₁ receptors does not interfere with hypotensive action of ANP neither in WKY nor in SHR.

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Visual discrimination learning in spontaneously hypertensive [SHR] and Wistar normontensive rats: computerized analysis of choice strategies

100%

Niewiadomska G., Niewiadomski W.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

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nr 2

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Secretory dysfunction of vascular endothelium limits the effect of angiotensin converting enzyme inhibitor quinapril on aggregation of erythrocytes in experimental hypertension

100%

Korbut R. A., Madej J., Adamek-Guzik T., Korbut R.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 3

Using automatic erythrocyte aggregometer type MA-1 (Myrenne gmbh, Germany), we investigated the hypothesis that therapeutic effectiveness of quinapril - angiotensin converting enzyme inhibitor (ACEI) - in the treatment of hypertension would correlate with improvement of red blood cell (RBC) aggregability. Experiments were performed on commercially available inbred strain of spontaneously hypertensive male rats (SHR) aged 19-21 weeks. Age-matched normotensive Wistar-Kyoto (WKY) rats genetically related to SHR were used as a control. Aggregability of RBC in hypertensive rats was significantly higher than in control WKY animals. Quinapril (100 µg/kg) administered i.p. for 8 days improved RBC aggregability in normotensive rats but surprisingly not in SHR animals. Beneficial effect of quinapril on RBC aggregation observed in normotensive animals did not occur when this drug was injected in combination with aspirin (1 or 50 mg/kg) or with indomethacin (20 mg/kg) or with L-NAME (10 mg/kg). However, much the same damaging effects on RBC aggregability were observed when aspirin, indomethacin or L-NAME were each administered into normotensive animals without quinapril. In contrast with normotensive rats, aggregability of RBC in SHR was not affected either by quinapril or by indomethacin and by L-NAME, given separately or in combination. The only compound significantly worsening RBC aggregability in SHR was aspirin but this effect was not dose-dependent. Quinapril-induced improvement of RBC aggregability in normotensive rats (but not in SHR) was completely abolished by simultaneous administration of B2 receptor antagonist icatibant and successfully mimicked by 8 days of treatment with bradykinin. In vitro aggregability of RBC isolated from WKY was not affected by previous incubation (30 min at 37°C) with quinapril, indomethacin or L-NAME. Only aspirin (3 mM) significantly increased RBC aggregability as compared to placebo. It is concluded that under physiological conditions quinapril efficiently inhibits RBC aggregability and this effect is modulated by secretion of endothelial mediators, mainly prostacyclin and nitric oxide. In hypertension quinapril, in spite of lowering of arterial blood pressure, is unable to display its beneficial effects on RBC aggregability possibly due to the hypertension-induced/accompanied dysfunction of vascular endothelium. Aspirin revealed unique erythrocyte damaging properties, presumably independent of inhibition of cyclooxygenase but related to a direct membrane protein acetylation.

Ograniczanie wyników

3 Journal of Physiology and Pharmacology

1 Acta Neurobiologiae Experimentalis

1 Adamek-Guzik T.

1 Dobesova Z.

1 Januszewicz A.

1 Korbut R.

1 Korbut R. A.

1 Kunes J.

1 Lapinski M.

1 Madej J.

1 Niewiadomska G.

1 Niewiadomski W.

1 Noszczyk B.

1 Pechanova O.

1 Stepniakowski K.

1 Szczepanska-Sadowska E.

1 Vrankova S.

1 Zicha J.

1 2009

1 2003

1 1995

1 1992

Contribution of neuronal nitric oxide (NO) synthase to N-acetylcysteine-induced increase of NO synthase activity in the brain of normotensive and hypertensive rats

Effect of vasopressin and V1 receptors blockade on hypotensive action of ANP in normotensive [WKY] and spontaneously hypertensive rats

Visual discrimination learning in spontaneously hypertensive [SHR] and Wistar normontensive rats: computerized analysis of choice strategies

Secretory dysfunction of vascular endothelium limits the effect of angiotensin converting enzyme inhibitor quinapril on aggregation of erythrocytes in experimental hypertension