The role of angiotensin II in regulating catecholamine secretion during hypoxia in rainbow troutOncorhynchus mykiss

2001 ◽  
Vol 204 (23) ◽  
pp. 4169-4176
Author(s):  
Katherine N. Lapner ◽  
Steve F. Perry
Keyword(s):  
Nicotinic Receptor ◽  
Nicotinic Receptors ◽  
Renin Angiotensin System ◽  
Catecholamine Release ◽  
Plasma Catecholamine ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Catecholamine Levels ◽  
Receptor Desensitisation

SUMMARYExperiments were performed in vivo on chronically cannulated adult rainbow trout (Oncorhynchus mykiss) to assess the involvement of serotonergic or muscarinic receptor stimulation or activation of the renin–angiotensin system in eliciting catecholamine release during acute hypoxia during periods of nicotinic receptor desensitisation.Despite nicotinic receptor desensitisation induced by intravenous infusion of nicotine (1.3×10–5 mol kg–1 h–1), plasma catecholamine levels were increased to levels (adrenaline plus noradrenaline 125–200 nmol l–1) similar to those in control fish during severe hypoxia (40–45 mmHg; 5.3–6.0 kPa). Blockade of serotonergic receptors using methysergide or of muscarinic receptors using atropine did not affect the ability of fish to elevate circulating catecholamine levels during hypoxia. However, selective blockade of the renin–angiotensin system, using lisinopril to inhibit angiotensin-converting enzyme, prevented the elevation of both angiotensin II and circulating catecholamine levels in acutely hypoxic fish experiencing nicotinic receptor desensitisation. In fish possessing functional nicotinic receptors, angiotensin-converting enzyme blockade attenuated but did not prevent the elevation of plasma catecholamine levels during hypoxia. The results of this study indicate that the renin–angiotensin system is activated during hypoxia and plays a role in eliciting catecholamine release that is secondary to activation of nicotinic receptors. However, under conditions of nicotinic receptor desensitisation, activation of the renin–angiotensin system during hypoxia is a prerequisite for catecholamine release.

Blood pressure regulation during hypotension in two teleost species: differential involvement of the renin-angiotensin and adrenergic systems

1999 ◽  
Vol 202 (12) ◽  
pp. 1677-1690 ◽  
Author(s):  
N.J. Bernier ◽  
J.E. Mckendry ◽  
S.F. Perry
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Catecholamine Release ◽  
Adrenergic Nerves ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Catecholamine Concentrations

The stimulatory effects of angiotensin II (Ang II) on catecholamine release and the contributions of the renin-angiotensin system, humoral catecholamines and adrenergic nerves to blood pressure regulation were investigated in rainbow trout (Oncorhynchus mykiss) and American eel (Anguilla rostrata). In trout, bolus injections of homologous [Asn1,Val5]-Ang II (100 or 500 pmol kg-1) increased catecholamine secretion rates and plasma catecholamine concentrations from in situ posterior cardinal vein preparations and chronically cannulated fish, respectively. In contrast, in situ or in vivo injections of similar doses of Ang II in eel did not affect catecholamine release. α -Adrenoceptor blockade (prazosin; 1 mg kg-1) reduced the pressor effect of exogenous Ang II (500 pmol kg-1) in both species. In eel, intravenous injection of the smooth muscle relaxant papaverine (10 mg kg-1) elicited a rapid decrease in dorsal aortic pressure (PDA; 58 %) followed by a gradual recovery back to the baseline value 85 min after the treatment. In trout, papaverine elicited a similar decrease in blood pressure (62 %); however, PDA recovered fully 20 min after treatment. Blockade of either α -adrenoceptors with prazosin or adrenergic nerves with bretylium (10 mg kg-1) prior to papaverine treatment did not alter PDA recovery in eel. In trout, α -adrenoceptor and adrenergic nerve blockade prior to the papaverine treatment prevented and attenuated PDA recovery, respectively. In both species, papaverine treatment elicited significant increases in plasma catecholamine and Ang II concentrations. However, the increases in plasma catecholamine concentrations were markedly greater in trout than in eel. Similarly, the papaverine-elicited increase in plasma Ang II levels occurred earlier and was greater in trout than in eel. Thus, while Ang II stimulates humoral catecholamine release in trout, there is no evidence for a similar interaction in eel. Moreover, during hypotensive stress, although the renin-angiotensin system is recruited in both species, an essential involvement of adrenergic nerves and humoral catecholamines in the restoration of blood pressure is only apparent in trout.

scholarly journals Pathological Role of Angiotensin II in Severe COVID-19

TH Open ◽  
2020 ◽  
Vol 04 (02) ◽  
pp. e138-e144 ◽  
Author(s):  
Wolfgang Miesbach
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Target Cells ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Novel Coronavirus

AbstractThe activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.

Resveratrol ameliorates the cyclosporine-induced vascular and renal impairments: possible impact of the modulation of renin–angiotensin system

2019 ◽  
Vol 97 (12) ◽  
pp. 1115-1123 ◽  
Author(s):  
Seldag Bekpinar ◽  
Ece Karaca ◽  
Selin Yamakoğlu ◽  
F. İlkay Alp-Yıldırım ◽  
Vakur Olgac ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Immunosuppressive Drug ◽  
Oxidative Stress Marker ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
System Components ◽  
Renal Tubular

Cyclosporine, an immunosuppressive drug, exhibits a toxic effect on renal and vascular systems. The present study investigated whether resveratrol treatment alleviates renal and vascular injury induced by cyclosporine. Cyclosporine (25 mg/kg per day, s.c.) was given for 7 days to rats either alone or in combination with resveratrol (10 mg/kg per day, i.p.). Relaxation and contraction responses of aorta were examined. Serum levels of blood urea nitrogen, creatinine, angiotensin II, and angiotensin 1-7 were measured. Histopathological examinations as well as immunostaining for 4-hydroxynonenal and nitrotyrosine were performed in the kidney. RNA expressions of renin–angiotensin system components were also measured in renal and aortic tissues. Cyclosporine decreased the endothelium-dependent relaxation and increased vascular contraction in the aorta. It caused renal tubular degeneration and increased immunostaining for 4-hydroxynonenal, an oxidative stress marker. Cyclosporine also caused upregulations of the vasoconstrictive renin–angiotensin system components in renal (angiotensin-converting enzyme) and aortic (angiotensin II type 1 receptor) tissues. Resveratrol co-treatment prevented the cyclosporine-related deteriorations. Moreover, it induced the expressions of vasodilatory effective angiotensin-converting enzyme 2 and angiotensin II type 2 receptor in aorta and kidney, respectively. We conclude that resveratrol may be effective in preventing cyclosporine-induced renal tubular degeneration and vascular dysfunction at least in part by modulating the renin–angiotensin system.

Anti-Hypertensive Effect of Water Extract of Danshen on Renovascular Hypertension Through Inhibition of the Renin Angiotensin System

2002 ◽  
Vol 30 (01) ◽  
pp. 87-93 ◽  
Author(s):  
Dae Gill Kang ◽  
Yong Gab Yun ◽  
Jang Hyun Ryoo ◽  
Ho Sub Lee
Keyword(s):  
Plasma Concentration ◽  
Water Extract ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Dependent Manner ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ace Activity ◽  
Dose Dependent

A study was designed to elucidate the mechanism of anti-hypertensive effects of Danshen in the two-kidney, one clip (2K1C) Goldblatt renovascular hypertensive model, which is the renin-angiotensin system (RAS)-dependent hypertensive model. We investigated the effects of water extracts of Danshen on the angiotensin converting enzyme (ACE) activities, systolic blood pressure (SBP), and hormone levels in the plasma of 2K1C rats. ACE activity was inhibited by the addition of Danshen extract in a dose-dependent manner. SBP was decreased significantly after administration of Danshen extract in 2K1C, whereas plasma renin activity (PRA) was not changed. The plasma concentration of aldosterone (PAC) was decreased significantly in 2K1C group administered with Danshen extract, whereas the plasma concentration of ANP was increased by administration of Danshen extract for three weeks. These results suggest that Danshen has an anti-hypertensive effect through the inhibition of ACE, an essential regulatory enzyme of RAS.

scholarly journals Synergistic Expression of Angiotensin-Converting Enzyme (ACE) and ACE2 in Human Renal Tissue and Confounding Effects of Hypertension on the ACE to ACE2 Ratio

Endocrinology ◽  
2007 ◽  
Vol 148 (5) ◽  
pp. 2453-2457 ◽  
Author(s):  
Shigeyuki Wakahara ◽  
Tadashi Konoshita ◽  
Shinichi Mizuno ◽  
Makoto Motomura ◽  
Chikako Aoyama ◽  
...  
Keyword(s):  
Renal Function ◽  
Angiotensin Converting Enzyme ◽  
Pairwise Comparison ◽  
Renin Angiotensin System ◽  
Mrna Levels ◽  
Converting Enzyme ◽  
Gene Expressions ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Clinicopathological Variables

Angiotensin-converting enzyme (ACE) 2, a newly emerging component of the renin-angiotensin system, is presumed to be a counterregulator against ACE in generating and degrading angiotensin II. It remains to be elucidated how mRNA levels of these two genes are quantitatively regulated in the kidney and also what kind of clinicopathological characteristics could influence the gene expressions in humans. Seventy-eight cases of biopsy-proven renal conditions were examined in detail. Total RNA from a small part of each renal cortical biopsy specimen was reverse transcribed, and the resultant cDNA was amplified for ACE, ACE2, and glyceraldehyde-3-phosphate dehydrogenase with a real-time PCR system. Then we investigated the relationship between clinicopathological variables and mRNA levels adjusted for glyceraldehyde-3-phosphate dehydrogenase. Statistically significant correlation was not observed between any clinicopathological variables and either of the gene expressions by pairwise comparison. However, a strong correlation was observed between the gene expressions of ACE and those of ACE2. Moreover, the ACE to ACE2 ratio was significantly higher in subjects with hypertension (HT) than that in subjects without HT. Whereas parameters of renal function, e.g. urinary protein excretion (UPE) and creatinine clearance (Ccr), are not significantly related to the ACE to ACE2 ratio as a whole, the HT status may reflect disease-induced deterioration of renal function. That is, UPE and Ccr of subjects with HT are significantly different from those without HT, in which a significant correlation is also observed between UPE and Ccr. Finally, stepwise regression analysis further revealed that only the HT status is an independent confounding determinant of the ACE to ACE2 ratio among the variables tested. Our data suggest that ACE2 might play an important role in maintaining a balanced status of local renin-angiotensin system synergistically with ACE by counterregulatory effects confounded by the presence of hypertension. Thus, ACE2 may exert pivotal effects on cardiovascular and renal conditions.

scholarly journals Effect of Dual Blockade of Renin-Angiotensin System on Proteinuria

2013 ◽  
Vol 1 (1) ◽  
pp. 18-20
Author(s):  
Eqerem Hasani ◽  
Alma Idrizi ◽  
Myftar Barbullushi
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Receptor Blocker ◽  
Enzyme Inhibitor ◽  
Combined Therapy ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Dual Blockade

Aim: Aim of the study was the evaluation of the effect of dual blockade of the renin-angiotensin system (RAS) on proteinuria. Material and Methods: Sixty patients, included in the study, were treated with angiotensin-converting enzyme inhibitor and angiotensin receptor blocker for a period of 3 months. Results: The dual blockade of RAS resulted with decrease of proteinuria, a slight increase of serum creatinine and was not associated with a lowering of blood pressure.Conclusion: Combined therapy with ACE-I and ARB results in a more complete blockade of the RAS than monotherapy. In proteinuric nephropathies it reduces significantly baseline proteinuria.

scholarly journals Association of seven renin angiotensin system gene polymorphisms with restenosis in patients following coronary stenting

2017 ◽  
Vol 18 (1) ◽  
pp. 147032031668877 ◽  
Author(s):  
Min Zhu ◽  
Minjun Yang ◽  
Jiangbo Lin ◽  
Huanhuan Zhu ◽  
Yifei Lu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Neointimal Hyperplasia ◽  
Renin Angiotensin System ◽  
Coronary Stenting ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Stent Restenosis ◽  
In Stent Restenosis

Background and objective: Percutaneous coronary intervention, despite being effective for coronary revascularization, causes in-stent restenosis due to neointimal hyperplasia in a large number of patients. The renin-angiotensin system is involved in neointimal hyperplasia. This study sought to evaluate seven gene polymorphisms of key renin-angiotensin system components, including angiotensinogen, angiotensin-converting enzyme and angiotensin II type 1a receptors, and their associations with in-stent restenosis in patients with coronary artery disease following coronary stenting. Methods and results: Three hundred and fifty-two patients undergoing coronary drug-eluting stent implantation were recruited. Seventy-five patients (21.3%) were diagnosed as restenosis by angiography. Genotyping for angiotensin-converting enzyme insertion/deletion demonstrated a significant association of angiotensin-converting enzyme DD genotype with the occurrence of restenosis. Direct DNA sequencing revealed no association of angiotensinogen (M235T, G217A, G152A, G-6A, and A-20C) or angiotensin II type I receptor A1166C polymorphisms with in-stent restenosis. However, angiotensin II type 1a A1166C polymorphism was significantly associated with increased susceptibility to restenosis in a subgroup of patients aged more than 60 years. Conclusion: Thus, our study suggests that genetic polymorphisms of angiotensin-converting enzyme insertion/deletion are associated with in-stent restenosis in coronary artery disease patients following coronary stenting.

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