Aging Increases Neuronal Nitric Oxide Release and Superoxide Anion Generation in Mesenteric Arteries from Spontaneously Hypertensive Rats

2003 ◽  
Vol 40 (6) ◽  
pp. 509-519 ◽  
Author(s):  
Mercedes Ferrer ◽  
Margarita Sánchez ◽  
Nuria Minoves ◽  
Mercedes Salaices ◽  
Gloria Balfagón
Keyword(s):  
Nitric Oxide ◽  
Superoxide Anion ◽  
Spontaneously Hypertensive Rats ◽  
Mesenteric Arteries ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nitric Oxide Release ◽  
Superoxide Anion Generation

scholarly journals Lisinopril Alters Contribution of Nitric Oxide and KCa Channels to Vasodilatation in Small Mesenteric Arteries of Spontaneously Hypertensive Rats

2015 ◽  
pp. 39-49 ◽  
Author(s):  
S. ALBARWANI ◽  
S. AL-SIYABI ◽  
I. AL-HUSSEINI ◽  
A. AL-ISMAIL ◽  
I. AL-LAWATI ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Mesenteric Arteries ◽  
Bkca Channel ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Kca Channels ◽  
Reserve System

To investigate lisinopril effect on the contribution of nitric oxide (NO) and KCa channels to acetylcholine (ACh)-induced relaxation in isolated mesenteric arteries of spontaneously hypertensive rats (SHRs). Third branch mesenteric arteries isolated from lisinopril treated SHR rats (20 mg/kg/day for ten weeks, SHR-T) or untreated (SHR-UT) or normotensive WKY rats were mounted on tension myograph and ACh concentration-response curves were obtained. Westernblotting of eNOS and KCa channels was performed. ACh-induced relaxations were similar in all groups while L-NMMA and indomethacin caused significant rightward shift only in SHR-T group. Apamin and TRAM-34 (SKCa and IKCa channels blockers, respectively) significantly attenuated ACh-induced maximal relaxation by similar magnitude in vessels from all three groups. In the presence of L-NMMA, indomethacin, apamin and TRAM-34 further attenuated ACh-induced relaxation only in SHR-T. Furthermore, lisinopril treatment increased expression of eNOS, SKCa and BKCa proteins. Lisinopril treatment increased expression of eNOS, SKCa, BKCa channel proteins and increased the contribution of NO to ACh-mediated relaxation. This increased role of NO was apparent only when EDHF component was blocked by inhibiting SKCa and IKCa channels. Such may suggest that in mesenteric arteries, non-EDHF component functions act as a reserve system to provide compensatory vasodilatation if (and when) hyperpolarization that is mediated by SKCa and IKCa channels is reduced.

Regional Renal Nitric Oxide Release in Stroke-Prone Spontaneously Hypertensive Rats

Hypertension ◽  
1997 ◽  
Vol 30 (6) ◽  
pp. 1479-1486 ◽  
Author(s):  
Andrea Zuckerman ◽  
Praveen N. Chander ◽  
Guillermo A. Zeballos ◽  
Charles T. Stier
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nitric Oxide Release

Superoxide Dismutase Mimetic Increases Neuronal Nitric Oxide Synthase Influence on Afferent Arteriolar Diameter in Spontaneously Hypertensive Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 712-713
Author(s):  
Atsuhiro Ichihara ◽  
Matsuhiko Hayashi ◽  
Nobuhisa Hirota ◽  
Takao Saruta
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Superoxide Anion ◽  
Spontaneously Hypertensive Rats ◽  
Neuronal Nitric Oxide Synthase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase ◽  
Arteriolar Diameter

P108 This study was designed to determine the influence of increased superoxide anion production in neuronal nitric oxide synthase (nNOS)-dependent regulation of afferent arteriolar diameter in spontaneously hypertensive rats (SHR). Afferent arteriolar diameters of male Wister-Kyoto rats (WKY) and SHR (300-350 g) were assessed in vitro using the blood-perfused juxtamedullary nephron technique and averaged 21.6 ± 1.6 (n = 6) and 18.8 ± 1.2 μm (n = 7); respectively. Superfusion with the superoxide dismutase mimetic, tempol (1, 10, and 100 μmol/L), did not influence afferent arteriolar diameters of WKY, but significantly increased afferent arteriolar diameters of SHR by 20.6 ± 5.5%, 25.2 ± 5.4% and 23.3 ± 4.9%; respectively. In WKY (n = 6), superfusion with the nNOS inhibitor, S -methyl-L-thiocitrulline (L-SMTC; 10 μmol/L), and the NOS inhibitor, N w -nitro-L-arginine (L-NNA; 100 μmol/L), significantly decreased afferent arteriolar diameters (19.6 ± 1.6 μm) by 11.9 ± 3.1% and 21.0 ± 3.9%; respectively. In SHR (n = 7), L-SMTC treatment did not influence afferent arteriolar diameters (21.0 ± 1.5 μm), but L-NNA treatment exerted a significant afferent arteriolar constriction (14.8 ± 3.2%) which was similar to that observed in WKY. Experiments were also performed in the presence of 100 μmol/L tempol. In WKY (n = 6), tempol treatment did not modulate basal afferent arteriolar diameters (21.5 ± 1.2 μm) or afferent arteriolar constrictor responses to L-SMTC (10.6 ± 2.1%) and L-NNA (19.3 ± 3.3%). In SHR (n = 8), tempol treatment significantly increased afferent arteriolar diameters by 22.5 ± 4.3% and enhanced afferent arteriolar constrictor responses to L-SMTC (18.4 ± 2.7%) and L-NNA (31.9 ± 2.6%). However, superfusion with the nitric oxide donor, S -nitroso-N-acetylpenicillamine (10 μmol/L), which exerted a similar afferent arteriolar vasodilation (19.7 ± 3.8%, n = 4), did not influence afferent arteriolar responses to L-SMTC (-2.1 ± 3.1%) or L-NNA (15.1 ± 3.3%). These results suggest that increased superoxide anion inhibits nNOS-dependent regulation of afferent arteriolar diameters in SHR.

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