Effects of Nitric Oxide Synthase Inhibitor on Tyrosine Hydroxylase mRNA in the Adrenal Medulla of Spontaneously Hypertensive and Wistar Kyoto Rats

Nitric Oxide ◽  
1999 ◽  
Vol 3 (4) ◽  
pp. 321-326 ◽  
Author(s):  
Toshio Kumai ◽  
Kentaro Asoh ◽  
Tomonori Tateishi ◽  
Masami Tanaka ◽  
Minoru Watanabe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tyrosine Hydroxylase ◽  
Nitric Oxide Synthase ◽  
Adrenal Medulla ◽  
Nitric Oxide Synthase Inhibitor ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Nitric Oxide Synthase Inhibitor in the Hypothalamus of the Spontaneously Hypertensive Rat (SHR)

1996 ◽  
Vol 90 (s34) ◽  
pp. 3P-3P
Author(s):  
J Alaghband-Zadeh ◽  
I Das ◽  
S Mehdizadeh ◽  
NS Khan ◽  
J De Belleroche ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rat ◽  
Nitric Oxide Synthase Inhibitor ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Nitric Oxide Modulation of Coronary Artery Myogenic Tone in Spontaneously Hypertensive and Wistar—Kyoto Rats

1998 ◽  
Vol 94 (3) ◽  
pp. 225-229 ◽  
Author(s):  
Susana R. Garcia ◽  
Stuart J. Bund
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Myogenic Tone ◽  
Internal Diameter ◽  
Nitric Oxide Synthase Inhibitor ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto ◽  
Synthase Inhibitor

1. The endothelium contributes substantially to the modulation of myogenic tone in coronary arteries from spontaneously hypertensive rats (SHR) and Wistar—Kyoto rats (WKY). This study has addressed the contributions of endothelium-derived nitric oxide and cyclo-oxygenase products to this modulation in small coronary arteries (approximately 200 μm internal diameter) from 20-week-old SHR and WKY under pressurized, no-flow conditions in an arteriograph. 2. Active pressure—diameter relationships were uninfluenced by the cyclo-oxygenase inhibitor indomethacin (10 μmol/l) in either rat strain. In the presence of indomethacin and the nitric oxide synthase inhibitor Nω-nitro-l-arginine (l-NNA, 0.1 mmol/l), coronary arteries from SHR and WKY generated significantly greater myogenic tone. This increase in tone was similar in both strains. 3. In endothelium-denuded arteries, indomethacin and l-NNA did not influence tone. 4. Therefore, these results demonstrate that endothelium-derived nitric oxide is basally released to attenuate SHR and WKY coronary artery myogenic tone, whereas endothelium-derived cyclo-oxygenase products have no net vasoactive influence. Additionally, these data suggest that basal nitric oxide-mediated relaxation is normal in SHR coronary arteries and is therefore unlikely to be a pathogenic mechanism in this animal model of hypertension.

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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