Quinapril Prevents Hypertension and Enhanced Vascular Reactivity in Nitroarginine-treated Rats

Charpie, John R.; Charpie, Peggy M.; Goud, Chetan; Pitt, Bertram; Webb, R. Clinton

doi:10.3109/08037059709061810

Cited by 3 publications

(4 citation statements)

References 41 publications

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“…Quinapril also protected rat small resistance arteries during chronic NOS inhibition (Charpie et al, 1997). In addition, ACEi inhibit cell proliferation and hypertrophy, as well as accumulation of extracellular matrix (Ito et al, 1997).…”

Section: Discussionmentioning

confidence: 97%

“…Changes occurring during pregnancy and in various pathophysiological states, such as acute renal failure or salt-sensitive hypertension, critically depend on the renal NO systems (Nathan and Xie, 1994;Person, 2002). Long-term inhibition of NOS by substituted arginine analogues has previously been shown to induce systemic hypertension in several animal species (Charpie et al, 1997). The chronic inhibition of NOS promotes severe and progressive renal structural injury in Wistar normotensive rats, consisting of glomerular ischemia, glomerulosclerosis, and interstitial expansion (Baylis et al, 1992;Ribeiro et al, 1992;Arcos et al, 2000;Pereira and Mandarim-de-Lacerda, 2001).…”

Section: Introductionmentioning

confidence: 98%

“…Angiotensin converting enzyme inhibitors (ACEi) improve pressure natriuresis and it is very effective in the treatment of various hypertension forms associated with normal or enhanced activity of the RAAS (Granger and Schnackenberg, 2000) and might retard the progression of renal failure and prevents glomerular hypertrophy and glomerular and tubulointerstitial fibrosis due to hypertension (Anderson et al, 1986;Charpie et al, 1997;Zoja et al, 1997;Gilbert et al, 1998;Susic, 2000) and completely prevented vascular structural and functional alterations due to NOS inhibition suggesting that NOSinhibition-induced hypertension in rats is associated with enhanced vascular reactivity due both to direct inhibition of endothelial NOS and to stimulation of the RAAS (Charpie et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Kidney adaptation in nitric oxide-deficient Wistar and spontaneously hypertensive rats

2004

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Kidney adaptation in nitric oxide-deficient Wistar and spontaneously hypertensive rats

2004

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“…L -Arg is the precursor of EDRF (Endothelium derived relaxing factors)/NO. Shortage of EDRF/NO is essential to the occurrence of cardiovascular diseases including CHD ( Charpie et al, 1997 ). On the other hand, L -Arg decreased ANP gene expression of mice with myocardial hypertrophy caused by isoprenaline ( Shen et al, 2004 ).…”

Section: Discussionmentioning

confidence: 99%

Prediction of Molecular Mechanisms for LianXia NingXin Formula: A Network Pharmacology Study

Yang

Teng

et al. 2018

Front. Physiol.

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Objectives: Network pharmacological methods were used to investigate the underlying molecular mechanisms of LianXia NingXin (LXNX) formula, a Chinese prescription, to treat coronary heart disease (CHD) and disease phenotypes (CHD related diseases and symptoms).Methods: The different seed gene lists associated with the herbs of LXNX formula, the CHD co-morbid diseases and symptoms which were relieved by the LXNX formula (co-morbid diseases and symptoms) were curated manually from biomedical databases and published biomedical literatures. Module enrichment analysis was used to identify CHD-related disease modules in the protein–protein interaction (PPI) network which were also associated to the targets of LXNX formula (LXNX formula’s CHD modules). The molecular characteristics of LXNX formula’s CHD modules were investigated via functional enrichment analysis in terms of gene ontology and pathways. We performed shortest path analysis to explore the interactions between the drug targets of LXNX formula and CHD related disease phenotypes (e.g., co-morbid diseases and symptoms).Results: We identified two significant CHD related disease modules (i.e., M146 and M203), which were targeted by the herbs of LXNX formula. Pathway and GO term functional analysis results indicated that G-protein coupled receptor signaling pathways (GPCR) of M146 and cellular protein metabolic process of M203 are important functional pathways for the respective module. This is further confirmed by the shortest path analysis between the drug targets of LXNX formula and the aforementioned disease modules. In addition, corticotropin releasing hormone (CRH) and natriuretic peptide precursor A (NPPA) are the only two LXNX formula target proteins with the low shortest path length (on average shorter than 3) to their respective CHD module and co-morbid disease and symptom gene groups.Conclusion: G-protein coupled receptor signaling pathway and cellular protein metabolic process are the key LXNX formula’s pathways to treat CHD disease phenotypes, in which CRH and NPPA are the two key drug targets of LXNX formula. Further evidences from Chinese herb pharmacological databases indicate that Pinellia ternata (Banxia) has relatively strong adjustive functions on the two key targets.

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Mechanisms of Hypertension Induced by Nitric Oxide (NO) Deficiency: Focus on Venous Function

Thakali

Lau

Fink

et al. 2006

Journal of Cardiovascular Pharmacology

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Loss of endothelial cell-derived nitric oxide (NO) in hypertension is a hallmark of arterial dysfunction. Experimental hypertension created by the removal of NO, however, involves mechanisms in addition to decreased arterial vasodilator activity. These include augmented endothelin-1 (ET-1) release, increased sympathetic nervous system activity, and elevated tissue oxidative stress. We hypothesized that increased venous smooth muscle (venomotor) tone plays a role in Nomega-nitro-L-arginine (LNNA) hypertension through these mechanisms. Rats were treated with the NO synthase inhibitor LNNA (0.5 g/L in drinking water) for 2 weeks. Mean arterial pressure of conscious rats was 119 +/- 2 mm Hg in control and 194 +/- 5 mm Hg in LNNA rats (P<0.05). Carotid arteries and vena cava were removed for measurement of isometric contraction. Maximal contraction to norepinephrine was modestly reduced in arteries from LNNA compared with control rats whereas the maximum contraction to ET-1 was significantly reduced (54% control). Maximum contraction of vena cava to norepinephrine (37% control) also was reduced but no change in response to ET-1 was observed. Mean circulatory filling pressure, an in vivo measure of venomotor tone, was not elevated in LNNA hypertension at 1 or 2 weeks after LNNA. The superoxide scavenger tempol (30, 100, and 300 micromol kg(-1), IV) did not change arterial pressure in control rats but caused a dose-dependent decrease in LNNA rats (-18 +/- 8, -26 +/- 15, and -54 +/- 11 mm Hg). Similarly, ganglionic blockade with hexamethonium caused a significantly greater fall in LNNA hypertensive rats (76 +/- 9 mm Hg) compared with control rats (35 +/- 10 mm Hg). Carotid arteries, vena cava, and sympathetic ganglia from LNNA rats had higher basal levels of superoxide compared with those from control rats. These data suggest that while NO deficiency increases oxidative stress and sympathetic activity in both arterial and venous vessels, the impact on veins does not make a major contribution to this form of hypertension.

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Quinapril Prevents Hypertension and Enhanced Vascular Reactivity in Nitroarginine-treated Rats

Cited by 3 publications

References 41 publications

Kidney adaptation in nitric oxide-deficient Wistar and spontaneously hypertensive rats

Kidney adaptation in nitric oxide-deficient Wistar and spontaneously hypertensive rats

Prediction of Molecular Mechanisms for LianXia NingXin Formula: A Network Pharmacology Study

Mechanisms of Hypertension Induced by Nitric Oxide (NO) Deficiency: Focus on Venous Function

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