scholarly journals Cardiovascular “Patterns” of H2S and SSNO−-Mix Evaluated from 35 Rat Hemodynamic Parameters

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 293
Author(s):  
Lenka Tomasova ◽  
Marian Grman ◽  
Anton Misak ◽  
Lucia Kurakova ◽  
Elena Ondriasova ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Jugular Vein ◽  
Hemodynamic Parameters ◽  
Arterial Pulse ◽  
No Donor ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
The Right ◽  
Oxide Synthase ◽  
Blood Pressure Patterns

This work is based on the hypothesis that it is possible to characterize the cardiovascular system just from the detailed shape of the arterial pulse waveform (APW). Since H2S, NO donor S-nitrosoglutathione (GSNO) and their H2S/GSNO products (SSNO−-mix) have numerous biological actions, we aimed to compare their effects on APW and to find characteristic “patterns” of their actions. The right jugular vein of anesthetized rats was cannulated for i.v. administration of the compounds. The left carotid artery was cannulated to detect APW. From APW, 35 hemodynamic parameters (HPs) were evaluated. H2S transiently influenced all 35 HPs and from their cross-relationships to systolic blood pressure “patterns” and direct/indirect signaling pathways of the H2S effect were proposed. The observed “patterns” were mostly different from the published ones for GSNO. Effect of SSNO−-mix (≤32 nmol kg−1) on blood pressure in the presence or absence of a nitric oxide synthase inhibitor (L-NAME) was minor in comparison to GSNO, suggesting that the formation of SSNO−-mix in blood diminished the hemodynamic effect of NO. The observed time-dependent changes of 35 HPs, their cross-relationships and non-hysteresis/hysteresis profiles may serve as “patterns” for the conditions of a transient decrease/increase of blood pressure caused by H2S.

Nitric Oxide in Streptozotocin-Induced Diabetes Mellitus in Rats

1996 ◽  
Vol 90 (5) ◽  
pp. 379-384 ◽  
Author(s):  
Abed Maree ◽  
Gari Peer ◽  
Adrian Iaina ◽  
Miriam Blum ◽  
Yoram Wollman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Body Weight ◽  
Nitric Oxide Synthase ◽  
Creatinine Clearance ◽  
Diabetic Rats ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitrite Nitrate ◽  
Synthase Inhibitor ◽  
Oxide Synthase

1. The present study was performed to determine the relationship between diabetic glomerular hyperfiltration and nitic oxide as modulated by the chronic administration of l-arginine and/or N-ω-nitro-l-arginine, a known nitric oxide synthase inhibitor in streptozotocin-induced diabetic rats. 2. Normal rats and rats drinking hypertonic glucose (10%) were used as time-controlled groups. Six weeks after administration of streptozotocin the diabetic rats had significantly higher creatinine clearance (667 ± 53 μl min−1 100 g−1 body weight) than before and streptozotocin (456 ± 38 μl min−1 100 g−1 body weight, P<0.005) and very high plasma (37.8 ± 10.9 μmol/l) and urinary (3.492 ± 0.179 nmol min−1 100 g−1 body weight) nitrite + nitrate (stable metabolites of nitric oxide) values compared with before streptozotocin administration [19.3 ± 2.8 μmol/l (P<0.001) and 0.420 ± 0.051 nmol min−1 100 g−1 body weight (P<0.001) respectively]. The 6-week diabetic rats had higher systolic blood pressure (124.2 ± 2.9 mm Hg, P<0.05) than before streptozotocin (108 ± 8 mmHg), but had a value similar to that of the hypertonic-glucose-drinking rats. 3. The diabetic rats supplemented with l-arginine did not show an increase in creatinine clearance and had a lower urinary excretion of nitrite + nitrate (0.999 ± 0.27 nmol min−1 100 g−1 body weight, P<0.005) than the respective untreated streptozotocin-induced diabetic rats. Creatinine clearance increased in the normal and glucose-drinking rats that received l-arginine. The administration of l-arginine resulted in significant reduction in blood pressure in all groups studied. The chronic nitric oxide synthase inhibitor resulted in high blood pressure, and in a significant decrease in creatinine clearance and urinary nitrite + nitrate excretion in all groups studied. In both diabetic and glucose-drinking rats, the l-arginine therapy resulted in significantly lower plasma and urinary glucose levels than in their respective untreated control groups. 4. The nitric oxide synthase inhibitor increased the plasma and urinary glucose concentration in both diabetic and glucose-drinking rats. 5. Our results indicate that diabetic rats are characterized by high plasma concentrations and elevated urinary excretion of nitrite + nitrate, suggesting a state of high nitric oxide production. The vascular response to nitric oxide in diabetic rats may be different at the glomerular and peripheral vascular bed.

Nitric oxide synthase inhibition reverses arteriolar hyporesponsiveness to catecholamines in septic rats

1993 ◽  
Vol 264 (2) ◽  
pp. H660-H663 ◽  
Author(s):  
S. M. Hollenberg ◽  
R. E. Cunnion ◽  
J. Zimmerberg
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cecal Ligation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Norepinephrine Concentration ◽  
Synthase Inhibitor ◽  
The Right ◽  
Oxide Synthase ◽  
Concentration Response Curve

Induction of nitric oxide synthase by cytokines has been hypothesized as a mechanism of the hyporesponsiveness to catecholamines that occurs in clinical septic shock. We measured responses of resistance arterioles in rat cremaster muscle to topically suffused norepinephrine in vivo with the use of image-shearing videomicroscopy. Rats made septic by cecal ligation and puncture were compared with controls that underwent sham ligation. The norepinephrine concentration-response curve was shifted to the right in septic rats [50% effective concentration (EC50) 9.1 +/- 5.4 vs. 0.10 +/- 0.02 microM, P < 0.05]. Contractions at doses of 10(-9), 10(-8), and 10(-7) M norepinephrine were 26, 41, and 38%, respectively, of sham controls. Superfusion of the muscle with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine at 100 microM restored the arteriolar responsiveness of the septic rats (EC50 0.14 +/- 0.07 vs. 6.8 +/- 3.1 microM, P < 0.05). This effect was reversed with superfusion of excess (1 mM) L-arginine. These experiments demonstrate impaired vasoconstriction in response to norepinephrine in resistance arterioles of septic rats in vivo. NG-monomethyl-L-arginine reversed this hyporesponsiveness, implying that nitric oxide synthase may mediate the decreased catecholamine responsiveness associated with sepsis.

scholarly journals Comparative effects of α-receptor stimulation and nitrergic inhibition on bronchovascular tone

2000 ◽  
Vol 88 (5) ◽  
pp. 1685-1689 ◽  
Author(s):  
Paula Carvalho ◽  
William H. Thompson ◽  
Nirmal B. Charan
Keyword(s):  
Blood Flow ◽  
Receptor Agonist ◽  
Systemic Arterial Pressure ◽  
Hemodynamic Parameters ◽  
Receptor Stimulation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Agonist Stimulation ◽  
Pulmonary Arterial ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Adrenergic agonists are known to influence bronchial blood flow and bronchovascular resistance. Recently, the nitrergic system has also been implicated in the control of bronchovascular tone. In this study, we compared the effects of the nitric oxide synthase inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) and the α1-receptor agonist phenylephrine on bronchovascular resistance in anesthetized sheep ( n = 9). Bronchial blood flow, cardiac output, and systemic and pulmonary arterial pressures were continuously monitored. Phenylephrine (1.2–3.4 μg ⋅ kg−1 ⋅ min−1) was infused intravenously to increase mean systemic arterial pressure above 95 Torr for 10 min and then was discontinued. When hemodynamic parameters returned to baseline, nebulized phenylephrine (10 mg) was given over 10 min. When parameters again normalized, l-NAME (30 mg/kg) was infused intravenously over 1 min. Intravenous phenylephrine increased systemic vascular resistance by 40% at 10 min with no concurrent increase in bronchovascular resistance, but inhaled phenylephrine increased bronchovascular resistance by 66% at 10 min. By comparison, intravenous l-NAME produced a rapid and sustained fivefold increase in bronchovascular resistance at 10 min. We conclude that, although α-agonist stimulation has some influence on bronchovascular resistance in sheep, the nitrergic system has predominant control of bronchovascular tone.

Upregulation of vascular inducible nitric oxide synthase mediates the hypotensive effect of ethanol in conscious female rats

2006 ◽  
Vol 100 (3) ◽  
pp. 1011-1018 ◽  
Author(s):  
Mahmoud M. El-Mas ◽  
Jian Zhang ◽  
Abdel A. Abdel-Rahman
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Hypotensive Effect ◽  
Female Rats ◽  
Hypotensive Action ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Previous reports from our laboratory have shown that ethanol elicits hypotension in female but not in male rats and that this effect of ethanol is estrogen dependent (El-Mass MM and Abdel-Rahman AA. Alcohol Clin Exp Res 23: 624–632, 1999; El-Mass MM and Abdel-Rahman AA. Clin Exp Hypertens 21: 1429–1445, 1999). In the present study, we tested the hypothesis that ethanol lowers blood pressure in female rats via upregulation of the inducible nitric oxide synthase (iNOS) in vascular tissues. The effects of pretreatment with NG-nitro-l-arginine (NOARG; nonselective nitric oxide synthase inhibitor) or aminoguanidine (selective iNOS inhibitor) on hemodynamic responses elicited by intragastric (ig) ethanol were determined in conscious female rats. Changes in vascular (aortic) iNOS protein expression evoked by ethanol in the presence and absence of aminoguanidine were also measured by immunohistochemistry. Compared with control (water treated) female rats, ethanol (1 g/kg ig) elicited hypotension that was associated with a significant increase in the aortic iNOS activity. The hypotensive effect of ethanol was virtually abolished in rats infused with the nitric oxide synthase inhibitor NOARG, suggesting a role for nitric oxide in ethanol hypotension. The inability of ethanol to lower blood pressure in NOARG-treated rats cannot be attributed to the presence of elevated blood pressure in these rats because ethanol produced hypotension when blood pressure was raised to comparable levels with phenylephrine infusion. Selective inhibition of iNOS by aminoguanidine (45 mg/kg ip), which had no effect on baseline blood pressure, abolished both the hypotensive action of subsequently administered ethanol and the associated increases in aortic iNOS content. These findings implicate vascular iNOS, at least partly, in the acute hypotensive action of ethanol in female rats.

Nitric oxide regulates HCO3- and Na+ transport by a cGMP-mediated mechanism in the kidney proximal tubule

1997 ◽  
Vol 272 (2) ◽  
pp. F242-F248 ◽  
Author(s):  
T. Wang
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Proximal Tubule ◽  
Renal Tubule ◽  
Rat Kidney ◽  
Na Transport ◽  
Nitric Oxide Synthase Inhibitor ◽  
Kidney Proximal Tubule ◽  
Synthase Inhibitor ◽  
Oxide Synthase

The effects of nitric oxide (NO) on blood pressure and renal hemodynamics are well established, but those of NO on renal tubule HCO3- and Na+ transport are not fully understood. In this study, we combined renal clearance and in situ microperfusion techniques to investigate the effects of NO on the renal excretion of Na (FE(Na%)) and the rates of renal tubule absorption of fluid (J(V)) and bicarbonate (J(HCO3)) in the rat kidney. Administration of the nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME, 6 mg/kg iv bolus) did not change mean blood pressure and glomerular filtration rate significantly. However, L-NAME significantly increased urine flow rate and FE(Na%), and these effects were maintained over a 60-min period. Addition of L-NAME markedly decreased both J(V) and J(HCO3) in the proximal tubule. In contrast, addition of 1 microM sodium nitroprusside (SNP) or S-nitroso-N-acetylpenicillamine (SNAP) significantly increased both J(V) and J(HCO3). Similar stimulation was also observed when 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 1 microM) was added to the luminal perfusate. The stimulatory effects of SNP and 8-BrcGMP on J(V) and J(HCO3) were not additive. The increments in J(V) and J(HCO3) due to SNP were abolished by the Na+/H+ exchange blocker ethylisopropylamiloride and the guanylate cyclase inhibitor methylene blue. These results indicate that NO stimulates proximal tubule Na+ and HCO3- transport through a cGMP-linked pathway in the kidney proximal tubule.

Glomerular and tubular interactions between renal adrenergic activity and nitric oxide

1995 ◽  
Vol 268 (6) ◽  
pp. F1004-F1008 ◽  
Author(s):  
F. B. Gabbai ◽  
S. C. Thomson ◽  
O. Peterson ◽  
L. Wead ◽  
K. Malvey ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Glomerular Filtration ◽  
Renal Nerves ◽  
Ang Ii ◽  
Nitric Oxide Synthase Inhibitor ◽  
Adrenergic Activity ◽  
Single Nephron ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Endothelium-dependent nitric oxide (EDNO) exerts control over the processes of glomerular filtration and tubular reabsorption. The importance of the renal nerves to the tonic influence of EDNO in the glomerular microcirculation and proximal tubule was tested by renal micropuncture in euvolemic adult male Munich-Wistar rats. The physical determinants of glomerular filtration and proximal reabsorption were assessed before and during administration of the nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA), in control animals and in animals 5–9 days after either ipsilateral surgical renal denervation (DNX) or after either sham surgery (SHX). L-NMMA caused single-nephron glomerular filtration rate to decline in control and SHX animals but not in DNX rats. L-NMMA caused a reduction in proximal reabsorption in control and SHX rats, which was prevented by prior DNX. DNX did not alter urinary guanosine 3',5'-cyclic monophosphate excretion, and, although DNX upregulates glomerular angiotensin II (ANG II) receptors, prior DNX did not alter intrarenal ANG II content as evaluated by radioimmunoassay. Some component of renal adrenergic activity is required for the full expression of the glomerular and tubular effects of blockade of nitric oxide synthase.

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