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Higher Level of Plasma Nitric Oxide in Spontaneously Hypertensive Rats

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Higher Level of Plasma Nitric Oxide in Spontaneously Hypertensive Rats AJH 1999;12:476–482 Higher Level of Plasma Nitric Oxide in Spontaneously Hypertensive Rats Chin-Chen Wu and Mao-Hsiung Yen Downloaded from https://academic.oup.com/ajh/article/12/5/476/181114 by guest on 30 September 2021 We had detected a slightly, but significantly, SHR treated with LPS for 3 h. In vitro, the ACh- higher level of plasma nitrite/nitrate in the induced relaxation was attenuated in the aortae sponstanously hypertensive rat (SHR) by using the obtained from SHR. However, this difference nitric oxide (NO) analyzer (Sievers 280 NOA), between SHR and WKY (without LPS treatment) which converts nitrate (including nitrate converted was abolished by treatment of rings with L-NAME from nitrite) to NO. Here, we examined whether (30 mmol/L), suggesting that an impairment of NO the release of NO from protein-bound dinitrosyl formation was observed in the SHR. After rats nonheme iron complexes (DNIC) contributes to the were treated with LPS for 3 h, the ACh-induced elevated plasma nitrate level in the SHR. The SHR relaxation was reduced in the WKY, but not in the and their genetic normotensive controls, Wistar- SHR. In addition, a 10-fold increase of L-NAME Kyoto rats (WKY), were anesthestized and was needed to abolish the difference in ACh- cannulized for monitoring blood pressure, induced relaxation between SHR and WKY, collecting a blood sample, and the administration indicating an expression of inducible NO synthase of endotoxin (lipopolysaccharide [LPS]). The in both strains treated with LPS. We suggest that nitrate levels (an indicator of NO formation) in the the elevated plasma NO level in SHR may be due plasma and the aorta were measured by an NO to the release of NO from DNIC in the vascular analyzer. In addition, the relaxation of bed to combat the hypertensive state. Am J acetylcholine (ACh) in the presence or absence of Hypertens 1999;12:476–482 © 1999 American v N -nitro-L-arginine methyl ester (L-NAME) was Journal of Hypertension, Ltd. also examined in thoracic aortae obtained from both strains. The slight, but significant, increase of v basal nitrate levels in the plasma and aorta were KEY WORDS: Nitric oxide, N -nitro-L-arginine methyl observed, and the former was further enhanced in ester, spontaneously hypertensive rats. he discovery by Furchgott and Zawadzki in ically equivalent to nitric oxide (NO)2,3 or a biochem- 1980 of endothelium-derived relaxing factor ical congener thereof.4 NO is produced by the conver- (EDRF)1 has now been proved to play a cen- sion of the terminal guanidine nitrogen atom(s) from tral role in the cardiovascular system. A few l-arginine into l-citrulline, or a complex molecule Tyears later, the EDRF had been identified to be chem- yielding NO.5,6 The importance of NO in the physio- Received April 2, 1998. Accepted November 11, 1998. Parts of this study had been presented in the 17th Scientific From the Department of Pharmacology, National Defense Medi- Meeting of the International Society of Hypertension. cal Center, Taipei, Republic of China, Taiwan. Address correspondence and reprint requests to Dr. Mao-Hsiung This work was supported by grants NSC 87-2314-B-016-058-M37 Yen, Department of Pharmacology, National Defense Medical Cen- (C. C. Wu) and NSC 87-2314-B-016-059-M37 (M. H. Yen) from the ter, P.O. Box 90048-504, Taipei, Republic of China, Taiwan. National Science Council, Republic of China, Taiwan. © 1999 by the American Journal of Hypertension, Ltd. 0895-7061/99/$20.00 Published by Elsevier Science, Inc. PII S0895-7061(99)00008-4 AJH–MAY 1999–VOL. 12, NO. 5 NITRIC OXIDE IN SHR 477 logic control of blood pressure is now well estab- protein-bound dinitrosyl nonheme iron complexes lished. In addition, NO also prevents the activation (DNIC) in blood vessels. Therefore, the aim of this and adhesion of platelets and neutrophils to the en- study was to delineate the effect of NO in hyperten- dothelium, dilates vascular smooth muscle, and inhib- sion and to evaluate whether the release of NO from its cell mitogenesis and proliferation.7,8 NO causes DNIC contributes to the higher plasma NO level in vascular smooth muscle relaxation by activation of SHR. In this study, we examined NO metabolite levels soluble guanylate cyclase and by increasing cyclic (ie, nitrite/nitrate) in the plasma and aorta by using guanosine 39,59-monophosphate (cGMP) levels,9,10 the NO analyzer. 1 causing a decrease in intracellular Ca2 . Therefore, MATERIALS AND METHODS alterations in NO synthesis may be an important fac- tor in the pathogenesis of hypertension. In Vivo Experiments Sixteen-week–old male SHR It has been shown that the generation of NO from and WKY rats, whose stock originated from the Downloaded from https://academic.oup.com/ajh/article/12/5/476/181114 by guest on 30 September 2021 l-arginine by NO synthase (NOS) is an important Charles River Breeding Laboratories in Japan, were autocrine and paracrine signaling pathway in the reg- purchased from the Deparment of Laboratory Animal 7 ulation of various cell functions. In the vascular wall, Science of the National Defense Medical Center. Sys- 21 endothelial cells express a constitutive Ca -calmod- tolic blood pressure was measured in conscious rats 11 ulin–dependent NOS (NOS III). A second type of by the tail-cuff method using a MOD 59 tail sphyg- 21 NOS (Ca -calmodulin–independent [NOS II]) can be mograph (Blood Pressure Meter/Amplifier, Itic Inc., expressed in smooth muscle cells and fibroblasts by Woodland Hills, CA) every week. The systolic blood b cytokines such as interleukin-1 or tumor necrosis pressure of SHR and WKY rats was 189 6 11 mm Hg a factor- , or by mechanical, viral, or bacterial inju- (n 5 36) and 144 6 7mmHg(n5 20), respectively. 7,12 ries. The NOS II induced by cytokines and endo- Animals were anesthetized by intraperitoneal injec- toxin (lipopolysaccharide [LPS]) produces larger tion of a combination of urethane (0.6 g/kg) and chlo- amounts of NO than NOS III does. ral hydrate (0.4 g/kg). The trachea was cannulated to There are numerous reports showing that endothe- facilitate respiration and rectal temperature was main- lium-dependent relaxations of isolated vascular rings tained at 37°C with a homeothermic blanket (Harvard from spontaneously hypertensive rats (SHR) are im- Apparatus Ltd., South Natick, MA). The right femoral paired when compared with those from Wistar-Kyoto artery was cannulated and connected to a pressure 13–15 (WKY) rats. These results suggest that dysfunc- transducer (P23ID, Statham, Oxnard, CA) for the mea- tion of the endothelium causes an abnormal relax- surement of phasic and mean arterial blood pressure 16,17 ation, or a simultaneous release of endothelium- (MAP) and heart rate, which were displayed on a dependent contracting factor(s) decreases the relaxing Grass model 7D polygraph recorder (Grass Instru- 17,18 activity of NO. Any decrease in NO generation ments, Quincy, MA). The left femoral vein was can- may have a substantial effect on blood pressure and nulated for the administration of Escherichia coli LPS (5 tissue blood flow. mg/kg). Please note that the injection of LPS in rats The NO Analyzer (Sievers 280 NOA, Sievers Inc., was further done to examine the effect of basal expres- Boulder, CO) has been developed for the direct assess- sion of iNOS in SHR on hemodynamic changes. Upon 19–21 ment of NO level in exhaled air and of NO me- completion of the surgical procedure, cardiovascular 22–24 tabolites in the liquid system (eg, plasma), and has parameters were allowed to stabilize for 20 min. After 25–28 been used extensively in recent years. This ma- recording baseline hemodynamic parameters, animals chine is more sensitive than the Griess assay and more received either saline (ie, sham-operated) or LPS and 29 stable than the electrode system, indicating that the were monitored for 3 h. NO Analyzer is reliable for the detection of NO and its metabolites. Determination of Levels of Plasma Nitrate Before Recently, a study has shown that an overproduction and at 1, 2, and 3 h after injection of LPS, 0.25 mL of of NO is involved in the interaction between macro- blood was collected from a catheter placed in the phages or vascular smooth muscle cells and lympho- femoral artery. Any blood withdrawn was immedi- cytes in SHR, suggesting a general activation of the ately replaced by intravenous (iv) injection of an equal NO synthesis system in SHR.30 In contrast to earlier amount of saline. The blood sample was centrifuged studies, Nava and colleagues have recently reported (7200 g for 3 min) to prepare plasma and plasma was that increased activity of NOS III is observed in car- kept in a 270°C freezer. At a later stage, plasma diac endothelium in SHR.31 In addition, our previous samples were thawed and deproteinized by incubat- studies also showed a basal expression of NOS II in ing them with 95% ethanol (4°C) for 30 min. These the aorta from SHR.32,33 A recent study demonstrated samples were subsequently centrifuged for 5 min at that NO can be generated independently of NOS.34 It 14,000 g. The nitrate concentration in plasma depicted proposed that NO reacts with nonheme iron to form in this study is actually the total nitrite and nitrate 478 WU AND YEN AJH–MAY 1999–VOL. 12, NO. 5 concentration in plasma. In this method nitrate is re- ation of ACh was also examined in the presence of the v duced to NO via nitrite.
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