Aminoguanidine attenuates hypertension, whereas 7-nitroindazole exacerbates kidney damage in spontaneously hypertensive rats: The role of nitric oxide

2013 ◽  
Vol 699 (1-3) ◽  
pp. 233-240 ◽  
Author(s):  
Chien-Fu Huang ◽  
Chien-Ning Hsu ◽  
Shao-Ju Chien ◽  
Ying-Jui Lin ◽  
Li-Tung Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Kidney Damage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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.

Role of nitric oxide in lipopolysaccharide-induced mortality from spontaneously hypertensive rats

Life Sciences ◽  
1997 ◽  
Vol 60 (15) ◽  
pp. 1223-1230 ◽  
Author(s):  
Mao-Hsiung Yen ◽  
Yu-Chun Liu ◽  
Hong-Jye Hong ◽  
Joen-Rong Sheu ◽  
Chin-Chen Wu
Keyword(s):  
Nitric Oxide ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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