EVIDENCE OF A FUNCTIONAL RENIN-ANGIOTENSIN SYSTEM IN THE CHANNEL CATFISH (ICTALURUS PUNCTATUS)

2018 ◽  
Vol 70 (1) ◽  
Author(s):  
Justin C. Hunt ◽  
Kenneth A. Davis ◽  
Max G. Sanderford
Keyword(s):  
Blood Pressure ◽  
Ictalurus Punctatus ◽  
Channel Catfish ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Suitable Model ◽  
Dependent Manner ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Volume Balance

Abstract Salination of freshwater (FW) bodies has the potential to affect homeostatic regulation of osmotic and volume balance in FW organisms. The renin-angiotensin system (RAS) plays an important role in volume balance by maintaining blood pressure in marine and seawater acclimated euryhaline fish, but little is known about the RAS in FW adapted fish. The purpose of the present study was to first determine if the FW channel catfish (Ictalurus punctatus), demonstrates evidence of a functional RAS. Channel catfish (n = 6) were implanted with a catheter in the dorsal aorta to measure dorsal aortic pressure (PDA) and infuse drugs. Infusion of [Asn1,Val5,Asn9]-angiotensin I (ANGI) at 100, 400, and 1000 ng/kg significantly increased PDA in a dose dependent manner (P < 0.05). Pretreatment with 2 mg/kg of the angiotensin converting enzyme inhibitor, Captopril (CAP), essentially eliminated the pressor response to the highest dose of ANGI (P < 0.05). Finally, infusion of 400 ng/kg [Asn1,Val5]-angiotensin II (ANGII) significantly increased PDA from baseline (P < 0.05). The results suggest that channel catfish appear to have an operational RAS and may serve as a suitable model in which to study the role of ANGII in blood pressure regulation in FW adapted fish.

Role of renin-angiotensin system in glucocorticoid hypertension in rats

1982 ◽  
Vol 243 (1) ◽  
pp. E48-E51 ◽  
Author(s):  
H. Suzuki ◽  
M. Handa ◽  
K. Kondo ◽  
T. Saruta
Keyword(s):  
Blood Pressure ◽  
Intravenous Injection ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Dependent Manner ◽  
Concurrent Administration ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in the regulation of the blood pressure of dexamethasone-treated rats (Dex) was evaluated using saralasin, an angiotensin II antagonist, and SQ 14225 (SQ) (d-3-mercapto-2-methylpropranoyl-1-proline), an angiotensin-converting enzyme inhibitor. During a 7-day period blood pressure rose 65 +/- 10 mmHg (P less than 0.001) in Dex with no significant changes in plasma renin activity. Concurrent administration of dexamethasone and SQ attenuated the elevation of blood pressure (P less than 0.05). In the conscious, freely moving state, intravenous injection of SQ (10, 30, 100 micrograms/kg) reduced blood pressure of DEX in a dose-dependent manner (P less than 0.05). Also, intravenous injection of saralasin (10 micrograms.kg-1 . min-1) reduced blood pressure significantly (P less than 0.01). Bilateral nephrectomy abolished the effects of saralasin and SQ on blood pressure in Dex. These results indicate that the elevation of blood pressure in DEX depends partially on the renin-angiotensin system.

scholarly journals Rosiglitazone, a Ligand to PPARγ, Improves Blood Pressure and Vascular Function through Renin-Angiotensin System Regulation

PPAR Research ◽  
2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
María Sánchez-Aguilar ◽  
Luz Ibarra-Lara ◽  
Leonardo Del Valle-Mondragón ◽  
María Esther Rubio-Ruiz ◽  
Alicia G. Aguilar-Navarro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
In Silico ◽  
Vascular Function ◽  
Renin Angiotensin System ◽  
Dependent Manner ◽  
Insulin Sensitizer ◽  
Angiotensin System ◽  
Renin Angiotensin

Rosiglitazone (RGZ), a peroxisome proliferator-activated receptor gamma (PPARγ) ligand, has been reported to act as insulin sensitizer and exert cardiovascular actions. In this work, we hypothesized that RGZ exerts a PPARγ–dependent regulation of blood pressure through modulation of angiotensin-converting enzyme (ACE)-type 2 (ACE2)/angiotensin-(1-7)/angiotensin II type-2 receptor (AT2R) axis in an experimental model of high blood pressure. We carried on experiments in normotensive (Sham) and aortic coarctation (AoCo)-induced hypertensive male Wistar rats. Both sham and AoCo rats were treated 7 days with vehicle (V), RGZ (5 mg/kg/day), or RGZ+BADGE (120 mg/kg/day) post-coarctation. We measured blood pressure and vascular reactivity on aortic rings, as well as the expression of renin-angiotensin system (RAS) proteins. We found that RGZ treatment in AoCo group decreases blood pressure values and improves vascular response to acetylcholine, both parameters dependent on PPARγ-stimulation. RGZ lowered serum angiotensin II (AngII) but increased Ang-(1-7) levels. It also decreased 8-hydroxy-2′-deoxyguanosine (8-OH-2dG), malondialdehyde (MDA), and improved the antioxidant capacity. Regarding protein expression of RAS, RGZ decreases ACE and angiotensin II type 1 receptor (AT1R) and improved ACE2, AT2R, and Mas receptor in AoCo rats. Additionally, an in silico analysis revealed that 5′UTR regions of RAS and PPARγ share motifs with a transcriptional regulatory role. We conclude that RGZ lowers blood pressure values by increasing the expression of RAS axis proteins ACE2 and AT2R, decreasing the levels of AngII and increasing levels of Ang-(1-7) in a PPARγ-dependent manner. The in silico analysis is a valuable tool to predict the interaction between PPARγ and RAS.

scholarly journals Mediation of humoral catecholamine secretion by the renin-angiotensin system in hypotensive rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 160 (3) ◽  
pp. 351-363 ◽  
Author(s):  
NJ Bernier ◽  
H Kaiya ◽  
Y Takei ◽  
SF Perry
Keyword(s):  
Blood Pressure ◽  
Rainbow Trout ◽  
Enzyme Inhibitor ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Renin Angiotensin System ◽  
Adrenergic System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The individual contributions of, and potential interactions between, the renin-angiotensin system (RAS) and the humoral adrenergic stress response to blood pressure regulation were examined in rainbow trout. Intravenous injection of the smooth muscle relaxant, papaverine (10 mg/kg), elicited a transient decrease in dorsal aortic blood pressure (PDA) and systemic vascular resistance (RS), and significant increases in plasma angiotensin II (Ang II) and catecholamine concentrations. Blockade of alpha-adrenoceptors before papaverine treatment prevented PDA and RS recovery, had no effect on the increase in plasma catecholamines, and resulted in greater plasma Ang II concentrations. Administration of the angiotensin-converting enzyme inhibitor, lisinopril (10(-4) mol/kg), before papaverine treatment attenuated the increases in the plasma concentrations of Ang II, adrenaline, and noradrenaline by 90, 79, and 40%, respectively and also prevented PDA and RS recovery. By itself, lisinopril treatment caused a gradual and sustained decrease in PDA and RS, and reductions in basal plasma Ang II and adrenaline concentrations. Bolus injection of a catecholamine cocktail (4 nmol/kg noradrenaline plus 40 nmol/kg adrenaline) in the lisinopril+papaverine-treated trout, to supplement their circulating catecholamine concentrations and mimic those observed in fish treated only with papaverine, resulted in a temporary recovery in PDA and RS. These results indicate that the RAS and the acute humoral adrenergic response are both recruited during an acute hypotensive stress, and have important roles in the compensatory response to hypotension in rainbow trout. However, whereas the contribution of the RAS to PDA recovery is largely indirect and relies on an Ang II-mediated secretion of catecholamines, the contribution from the adrenergic system is direct and relies at least in part on plasma catecholamines.

Response of Chronic Renovascular Hypertension to Surgical Correction or Prolonged Blockade of the Renin–Angiotensin System by Two Inhibitors in the Rat

1980 ◽  
Vol 58 (1) ◽  
pp. 15-20 ◽  
Author(s):  
H. Thurston ◽  
R. F. Bing ◽  
E. S. Marks ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Chronic Hypertension ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor

1. Removal of the renal artery constriction but not of the clipped kidney restored the blood pressure to normal levels in Goldblatt two-kidney rats with hypertension of more than 4 months' duration. 2. Despite the differences in blood pressure response, both surgical procedures lowered plasma renin concentration to normal or below normal values. 3. Administration of the oral converting enzyme inhibitor SQ 14 225 produced a marked fall in blood pressure in Goldblatt kidney rats with chronic hypertension. However, a prolonged infusion of the angiotensin II antagonist saralasin was quite ineffective. The difference in response to the two inhibitors may have been due to bradykinin potentiation by the converting enzyme inhibitor. 4. Although plasma renin is often elevated in Goldblatt two-kidney rats with hypertension of more than 4 months' duration, the renin-angiotensin system plays no role in the maintenance of blood pressure at this stage.

Sodium Restriction and Inhibition of the Renin—Angiotensin System in Renovascular Hypertension in the Rat

1977 ◽  
Vol 52 (4) ◽  
pp. 371-375
Author(s):  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Small Contribution ◽  
Bilateral Nephrectomy ◽  
Blood Pressure Lowering ◽  
Blood Pressure Lowering Effect ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Pressure Lowering

1. In the early phase of hypertension produced by renal artery constriction with the opposite kidney intact, infusion of the angiotensin antagonist Sar1-Ala8-angiotensin II or bilateral nephrectomy lowered blood pressure. However, the extent of the fall was variable and some animals remained hypertensive after each procedure. 2. To assess whether sodium retention was the additional factor which maintained blood pressure when the renin—angiotensin system was suppressed, rats were maintained on a low-salt diet before and during the development of hypertension. The blood pressure-lowering effect of bilateral nephrectomy or antagonist infusion was not enhanced. 3. Infusion of antagonist or converting-enzyme inhibitor 6 h after bilateral nephrectomy had only a minor blood pressure-lowering action, indicating that, at this late stage after nephrectomy, the renin—angiotensin system makes only a very small contribution to blood pressure maintenance.

Blood pressure effects of renin inhibition by human renin antiserum in normotensive marmosets

1984 ◽  
Vol 246 (3) ◽  
pp. F309-F316 ◽  
Author(s):  
J. B. Michel ◽  
J. Wood ◽  
K. Hofbauer ◽  
P. Corvol ◽  
J. Menard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Pressure Effects ◽  
Sodium Balance ◽  
New World Monkeys ◽  
Common Marmosets ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Human Renin

The effects on blood pressure of an antiserum against pure human kidney renin were studied in conscious and anesthetized (pentobarbital, 24 mg X kg-1 i.p.) small new world monkeys (common marmosets). The antiserum inhibited the enzymatic activity of renin by 50% in a dilution of 1:45,000 in marmoset and 1:50,000 in human plasma. The antiserum (0.2 ml i.v.) decreased blood pressure in conscious marmosets on normal sodium intake by 15 +/- 5 (SD) mmHg and after salt depletion by 31 +/- 13 mmHg. A converting enzyme inhibitor (teprotide, 2 mg X kg-1 i.v.) induced a comparable fall in blood pressure: -16 +/- 10 and -30 +/- 10 mmHg, respectively. Similar effects were observed on blood pressure of anesthetized marmosets. The correlation between pretreatment plasma renin concentration and the maximum fall in blood pressure was significant and identical for the experiments with antiserum and teprotide. These results demonstrate that antisera against human renin can be used for the specific blockade of the renin-angiotensin system in primates. In normotensive marmosets the renin-angiotensin system participates in the maintenance of blood pressure, to a degree depending on the state of sodium balance.

scholarly journals Effects of Phytochemicals on Blood Pressure and Neuroprotection Mediated Via Brain Renin-Angiotensin System

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2761 ◽  
Author(s):  
Hae Rin Kim ◽  
Woo Kyoung Kim ◽  
Ae Wha Ha
Keyword(s):  
Blood Pressure ◽  
Cholinergic System ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Positive Control ◽  
Control Group ◽  
Dietary Intakes ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

Background: The renin-angiotensin system (RAS) in the brain plays a crucial role in maintaining blood pressure as well as neuroprotection. This study compared the effects of curcumin, quercetin, and saponin on blood pressure, the brain RAS, and cholinergic system using perindopril, an angiotensin converting enzyme inhibitor (ACEI), as a positive control. Methods: Five-week-old male mice were stabilized and randomly assigned into a control group (n = 8), three phytochemical-treated groups (curcumin (n = 8), quercetin (n = 8), and saponin (n = 8)), and a positive control group (n = 8). The groups treated with the phytochemical were orally administered daily at a dose of 50 mg/kg body weight of phytochemicals. During the experiments, the weight and dietary intakes were measured regularly. After experiments, the brain tissue was homogenized and centrifuged for an additional assay. The concentrations of ACE, angiotensin II (AngII), and aldosterone levels were measured, and the mRNA expressions of renin and ACE were measured. As biomarkers of neuroprotection, the concentrations of acetylcholine(Ach) as well as the concentration and activity of acetylcholine esterase (AChE) were measured. Results: After 4 weeks of treatment, the perindopril group showed the lowest blood pressure. Among the groups treated with the phytochemicals, treatment with curcumin and saponin significantly reduced blood pressure, although such effect was not as high as that of perindopril. Among phytochemicals, curcumin treatment significantly inhibited the concentration and activity of ACE, concentration of AngII, and mRNA expression of ACE. All phytochemical treatments significantly increased the concentration of ACh. The levels of AChE activity in groups exposed to curcumin or saponin (not quercetin) were significantly inhibited, Conclusion: Curcumin administration in rats reduced blood pressure by blocking the brain RAS components and protected the cholinergic system in brain by inhibiting the activity of AChE.

Vasodepressor Property of the Converting Enzyme Inhibitor Captopril (SQ 14 225): The Role of Factors other than Renin-Angiotensin Blockade in the Rat

1980 ◽  
Vol 58 (1) ◽  
pp. 1-6 ◽  
Author(s):  
E. S. Marks ◽  
R. F. Bing ◽  
H. Thurston ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Converting Enzyme Inhibitor ◽  
Blood Pressure Fall ◽  
Angiotensin Blockade ◽  
Pressure Fall

1. The peptide converting enzyme inhibitor captopril was given (1·25 mg/kg intravenously) to normal and nephrectomized rats and rats with renovascular and deoxycorticosterone hypertension. 2. Captopril lowered blood pressure to a small extent in normal and nephrectomized rats. Bradykinin infusion in nephrectomized animals, however, potentiated the vasodepressor action of captopril. 3. Captopril produced a major blood pressure fall in the early stages of Goldblatt two-kidney one-clip hypertension: even when hypertension had been present for more than 4 months, a substantial vasodepressor action was seen. Rats with deoxycorticosterone-induced hypertension also showed a significant blood pressure fall. 4. Captopril was given to salt-loaded and salt-depleted rats in which the renin-angiotensin system had been blocked by infusion of the competitive angiotensin II antagonist saralasin. Captopril still lowered blood pressure in the salt-depleted group. 5. Captopril lowers blood pressure in situations where the renin-angiotensin system is not responsible for blood pressure maintenance. Further, the fall in blood pressure produced in Goldblatt two-kidney one-clip hypertension is greater than would be predicted on the basis of renin-angiotensin blockade. It is likely therefore that captopril lowers blood pressure by an action additional to angiotensin blockade. Bradykinin potentiation is one possible mechanism by which this may take place.

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