Pulmonary Vascular Reactivity of Spontaneously Hypertensive Rats Is Exacerbated in Response to the Central Administration of Exogenous Nitric Oxide

Schwenke, Daryl O.; Pearson, James T.; Tsuchimochi, Hirotsugu; Kangawa, Kenji; Shirai, Masamitsu

doi:10.1111/j.1440-1681.2007.04544.x

Cited by 6 publications

(5 citation statements)

References 36 publications

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“…In adult male SHR, molsidomine given for 1 wk at a similar dose as in our study increased blood pressure (14); however, in other studies effects of 1-6 wk of molsidomine on blood pressure were not significant (23,37). Shorter exposure times consistently induce pronounced blood pressure reduction (15,34,38). Interestingly, despite the increase in blood pressure in adult male SHR, molsidomine decreased both GFR and RPF and increased RVR (14), just as we observed in FHH in the present study.…”

Section: Discussionsupporting

confidence: 55%

A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats

Koeners¹,

Braam²,

Giezen³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Koeners MP, Braam B, van der Giezen DM, Goldschmeding R, Joles JA. A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats. Am J Physiol Regul Integr Comp Physiol 294: R1847-R1855, 2008. First published April 16, 2008 doi:10.1152/ajpregu.00073.2008.-Enhancing perinatal nitric oxide (NO) availability persistently reduces blood pressure in spontaneously hypertensive rats. We hypothesize that this approach can be generalized to other models of genetic hypertension, for instance those associated with renal injury. Perinatal exposure to the NO donor molsidomine was studied in fawn-hooded hypertensive (FHH) rats, a model of mild hypertension, impaired preglomerular resistance, and progressive renal injury. Perinatal molsidomine increased urinary NO metabolite excretion at 8 wk of age, i.e., 4 wk after treatment was stopped (P Ͻ 0.05). Systolic blood pressure was persistently reduced after molsidomine (42-wk females: 118 Ϯ 3 vs. 141 Ϯ 5 and 36-wk males: 139 Ϯ 4 vs. 158 Ϯ 4 mmHg; both P Ͻ 0.001). Perinatal treatment decreased glomerular filtration rate (P Ͻ 0.05) and renal blood flow (P Ͻ 0.01) and increased renal vascular resistance (P Ͻ 0.05), without affecting filtration fraction, suggesting persistently increased preglomerular resistance. At 4 wk of age natriuresis was transiently increased by molsidomine (P Ͻ 0.05). Molsidomine decreased glomerulosclerosis (P Ͻ 0.05). Renal blood flow correlated positively with glomerulosclerosis in control (P Ͻ 0.001) but not in perinatally treated FHH rats. NO dependency of renal vascular resistance was increased by perinatal molsidomine. Perinatal enhancement of NO availability can ameliorate development of hypertension and renal injury in FHH rats. Paradoxically, glomerular protection by perinatal exposure to the NO donor molsidomine may be due to persistently increased preglomerular resistance. The mechanisms by which increased perinatal NO availability can persistently reprogram kidney function and ameliorate hypertension deserve further study. proteinuria; renal hemodynamics; glomerulosclerosis A LARGE BODY OF experimental and epidemiological studies supports the concept that the intrauterine and early postnatal environment interacts with early development in that it can program metabolic and cardiovascular disease (5,18,27). Most of these studies focus on how aberrant perinatal factors increase the occurrence of pathologies in later life. When such factors are superimposed on a specific background of inherited disease, developmental programs will also be affected. Hence, programming can also have long-lasting effects against an abnormal genetic background. Accordingly, advantageous perinatal factors can prevent or correct abnormal development. Because hypertension is associated with decreased nitric oxide (NO) availability (52), it is plausible that factors that support NO availability in the perinatal phase can (re)program development beneficially. This might lead to norm...

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Section: Discussionsupporting

confidence: 55%

A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats

Koeners¹,

Braam²,

Giezen³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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show abstract

“…Three different gas mixtures were employed in this study, (i) air, (ii) hyperoxic gas: 50% O 2 balanced with N 2 (OX), and (iii) hypoxic gas: 10% O 2 balanced with N 2 (HOX) [37].…”

Section: Compositions Of Gasesmentioning

confidence: 99%

Impact of liver damage on blood-borne variables and pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

Sepehrinezhad

Dehghanian

Rafati

et al. 2020

BMC Cardiovasc Disord

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Background: Liver disorders may be associated with normal pulmonary hemodynamic, hepatopulmonary syndrome (HPS), or portopulmonary hypertension (POPH). In this study, we aimed to investigate the effect of the severity of liver dysfunctions on blood-borne variables, and pulmonary hemodynamic during repeated ventilation with hyperoxic and hypoxic gases. Methods: Female Sprague Dawley rats were assigned into four groups of Sham (n = 7), portal vein ligation (PPVL, n = 7), common bile duct ligation (CBDL, n = 7), and combination of them (CBDL+ PPVL, n = 7). Twenty-eight days later, right ventricular systolic pressure (RVSP) and systemic blood pressure were recorded in anesthetized animals subjected to repeated maneuvers of hyperoxia (O 2 50%) and hypoxia (O 2 10%). Besides, we assessed blood parameters and liver histology. Results: Liver histology score, liver enzymes, WBC and plasma malondialdehyde in the CBDL+PPVL group were higher than those in the CBDL group. Also, the plasma platelet level in the CBDL+PPVL group was lower than those in the other groups. On the other hand, the serum estradiol in the CBDL group was higher than that in the CBDL+PPVL group. All the above parameters in the PPVL group were similar to those in the Sham group. During ventilation with hyperoxia gas, RVSP in the CBDL+PPVL group was higher than the ones in the other groups, and in the CBDL group, it was more than those in the PPVL and Sham groups. Hypoxic pulmonary vasoconstriction (HPV) was not detected in both CBDL+PPVL and CBDL groups, whereas, it retained in the PPVL group. Conclusion: Severe liver damage increases RVSP in the CBDL+PPVL group linked to the high level of ROS, low levels of serum estradiol and platelets or a combination of them. Furthermore, the high RVSP at the noted group could present a reliable animal model for POPH in female rats.

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“…Three different gas mixtures were employed in this study, (i) air, (ii) hyperoxic gas: 50% O 2 balanced with N 2 (OX), and (iii) hypoxic gas: 10% O 2 balanced with N 2 (HOX) [34].…”

Section: Compositions Of Gasesmentioning

confidence: 99%

Impact of liver damage and blood-borne variables on pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

Sepehrinezhad

Dehghanian

Rafati

et al. 2019

Preprint

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Background : Liver disorders may lead to a wide spectrum of pulmonary complications from hepatopulmonary syndrome to portopulmonary hypertension. In this study, we aimed to investigate the effect of severity of liver dysfunctions on blood-borne variables, and pulmonary hemodynamic during repeated ventilation of animals with hypoxic and hyperoxic gases. Methods: Female Sprague Dawley rats were divided into four groups of Sham, common bile duct ligation (CBDL), portal vein ligation (PPVL), and combination of them (CBDL+ PPVL). Twenty-eight days later, right ventricular systolic pressure (RVSP) and systemic blood pressure were recorded in anesthetized animals. Besides, we assessed blood parameters in parallel with liver histology. Results: Data of liver histology and enzymes indicated a larger liver damage in the CBDL+PPVL group as compared with the other groups. Moreover, low platelet level was only observed in the CBDL+PPVL group. Besides, the enhancement of serum estradiol in the CBDL+PPVL group was less pronounced than that in the CBDL group. The baseline RVSP in the CBDL groups were significantly higher than those in the Sham and PPVL groups, and in the CBDL+PPVL group was higher than the ones in the other groups. Hypoxic pulmonary vasoconstriction (HPV) were eliminated in both CBDL groups, whereas, it was recovered in the PPVL group. Conclusion: In this study, we presented, for the first time, ligations of both CBDL and PPVL as a possible animal model for POPH. High RVSP in this model may be linked to ROS production, serum estradiol level, low platelet level or a combination of them.

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Pulmonary Vascular Reactivity of Spontaneously Hypertensive Rats Is Exacerbated in Response to the Central Administration of Exogenous Nitric Oxide

Cited by 6 publications

References 36 publications

A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats

A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats

Impact of liver damage on blood-borne variables and pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

Impact of liver damage and blood-borne variables on pulmonary hemodynamic responses to hypoxia and hyperoxia in anesthetized rats

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