Modulation of the intrahepatic renin–angiotensin system after stimulation of the gastric sodium monitor in the rat

1999 ◽  
Vol 98 (1) ◽  
pp. 57-64
Author(s):  
V. Z. C. YE ◽  
K. A. DUGGAN
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sprague Dawley Rats ◽  
Sodium Load ◽  
Ace Activity ◽  
Stimulation Of

Changes in the rate of formation of angiotensin II (ANG II) participate in mediating the natriuresis that occurs in direct response to a gastric sodium stimulus (upper-gut sodium monitor). As this natriuresis is also dependent on intrahepatic events, we investigated whether changes in hepatic and plasma angiotensinogen levels and hepatic angiotensin-converting enzyme (ACE) activity might explain the decrease in ANG II synthesis. Male Sprague–Dawley rats, equilibrated on a low-sodium diet, were anaesthetized and received a sodium load of 1.5 mmol/kg (using 3× normal saline) either intragastrically or intravenously. Blood and livers were sampled before and at various times after sodium administration. ACE activity in serum and tissues was determined by generation of histidyl-leucine. Angiotensinogen was determined by radioimmunoassay of angiotensin I generated by incubation in the presence of exogenous renin. Plasma angiotensinogen had decreased significantly by 15 min after sodium administration (P< 0.005), while hepatic angiotensinogen was also decreased significantly from 30 min after the sodium load (P< 0.01). Hepatic ACE activity decreased in response to sodium (P< 0.005) from 30 min. We conclude that stimulation of the gastric sodium monitor regulates angiotensinogen synthesis and secretion by the liver, as well as hepatic ACE activity.

Peripheral and central angiotensin II regulates expression of genes of the renin-angiotensin system

1992 ◽  
Vol 262 (5) ◽  
pp. E651-E657 ◽  
Author(s):  
K. Kohara ◽  
K. B. Brosnihan ◽  
C. M. Ferrario ◽  
A. Milsted
Keyword(s):  
Northern Blot Analysis ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Expression Of Genes ◽  
Sprague Dawley Rats ◽  
Renin Mrna ◽  
Lower Brain Stem

We investigated whether angiotensin (ANG) II has the potential to regulate expression of genes of the renin-angiotensin system (RAS) in peripheral and central tissues. ANG II (0.1 or 6.0 nmol/h) was infused by osmotic minipump into male Sprague-Dawley rats (225-250 g) for 5 days, either intravenously or intracerebroventricularly. We measured angiotensinogen mRNA in liver, adrenal glands, and brain (hypothalamus and lower brain stem), renin mRNA in the kidney, and angiotensin-converting enzyme (ACE) mRNA in the lung and testis by Northern blot analysis. We demonstrated that plasma ANG II increases the levels of liver angiotensinogen mRNA, decreases kidney renin mRNA, and decreases lung ACE mRNA. Intracerebroventricular administration of ANG II resulted in a different pattern of responses of the peripheral RAS components. Liver angiotensinogen mRNA was increased, and kidney renin mRNA was decreased by both doses of ANG II, whereas lung ACE mRNA remained unresponsive at either dose. Centrally mediated influences of ANG II are most likely indirect since plasma ANG II concentration was not changed. This study has revealed that ANG II has profound diverse effects that influence the regulation of its formation. Further, results indicate that genes of the RAS responded to exogenous ANG II in both tissue- and route-specific ways.

Endothelial function during stimulation of renin-angiotensin system by low-sodium diet in humans

2001 ◽  
Vol 280 (5) ◽  
pp. H2248-H2254 ◽  
Author(s):  
Torbjørn Omland ◽  
Wendy Johnson ◽  
Mary Beth Gordon ◽  
Mark A. Creager
Keyword(s):  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Concomitant Treatment ◽  
Double Blind ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Stimulation Of

We examined whether physiological stimulation of the endogenous renin-angiotensin system results in impaired endothelium-dependent vasodilatation in forearm resistance vessels of healthy subjects and whether this impairment can be prevented by angiotensin II type 1 receptor blockade. A low-sodium diet was administered to 27 volunteers who were randomized to concomitant treatment with losartan (100 mg once daily) or matched placebo in a double-blind fashion. Forearm blood flow was assessed by venous occlusion plethysmography at baseline and after 5 days. Endothelium-dependent and -independent vasodilation was assessed by intra-arterial infusion of methacholine and verapamil, respectively. The low-sodium diet resulted in significantly decreased urine sodium excretion (placebo: 146 ± 64 vs. 10 ± 9 meq/24 h, P < 0.001; losartan: 141 ± 56 vs. 14 ± 14 meq/24 h, P < 0.001) and increased plasma renin activity (placebo: 1.0 ± 0.5 vs. 5.0 ± 2.5 ng · ml−1 · h−1, P < 0.001; losartan: 3.8 ± 7.2 vs. 19.1 ± 11.2 ng · ml−1 · h−1, P = 0.006) in both the losartan and placebo groups. With the baseline study as the reference, the diet intervention was not associated with any significant change in endothelium-dependent vasodilation to methacholine in either the placebo ( P = 0.74) or losartan ( P = 0.40) group. We conclude that short-term physiological stimulation of the renin-angiotensin system does not cause clinically significant endothelial dysfunction. Losartan did not influence endothelium-dependent vasodilation in humans with a stimulated renin-angiotensin system.

Localization of components of the renin–angiotensin system in the suprachiasmatic nucleus of normotensive Sprague–Dawley rats

2004 ◽  
Vol 1008 (2) ◽  
pp. 212-223 ◽  
Author(s):  
Martin Alexander Thomas ◽  
Gerta Fleissner ◽  
Marion Stöhr ◽  
Stefan Hauptfleisch ◽  
Björn Lemmer
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Renin Angiotensin System ◽  
Sprague Dawley ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sprague Dawley Rats

Pressor resistance to vasopressin in sodium depletion, potassium depletion, and cirrhosis

1986 ◽  
Vol 251 (3) ◽  
pp. R525-R530 ◽  
Author(s):  
B. M. Murray ◽  
M. S. Paller
Keyword(s):  
Pressor Response ◽  
Potassium Depletion ◽  
Pressor Effect ◽  
Sodium Depletion ◽  
Sprague Dawley ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Sprague Dawley Rats ◽  
Low Potassium ◽  
Baroreceptor Reflexes

Resistance to the pressor effects of angiotensin II, but not norepinephrine, has been observed in sodium depletion, potassium depletion, and cirrhosis. We tested the response to arginine vasopressin (AVP) in each of these conditions. Male Sprague-Dawley rats were made sodium depleted with furosemide and a low-sodium diet for 3 days, potassium depleted by feeding a low-potassium diet for 14-21 days, or cirrhotic by inhalation of carbon tetrachloride for 8 wk. In conscious rats, the pressor response to graded doses of AVP was reduced in sodium depletion by 27-43% compared with control rats. Sodium-depleted rats were also found to have enhanced baroreceptor reflexes, since the decrease in heart rate for a given increase in mean arterial pressure was greater than in control rats. When the ganglionic blocker pentolinium tartrate was given to sodium-depleted rats the pressor response to AVP was restored to control levels. In potassium-depleted rats the pressor response to AVP was 21-52% lower than that in controls, whereas cirrhotic rats also had a blunted response to AVP (14-41% lower than control). However, there was no evidence in either of these two states of enhanced baroreceptor activity, and pretreatment with pentolinium tartrate did not restore the pressor response to normal. Therefore, although resistance to the pressor effect of AVP was found in all three conditions, the mechanism of this effect was different in sodium depletion compared with potassium depletion and cirrhosis. We conclude that resistance to the pressor action of AVP in sodium depletion was secondary to resetting of the baroreceptors.

Angiotensin mediates stimulation of ventilation after vasopressin V1 receptor blockade

1994 ◽  
Vol 76 (6) ◽  
pp. 2517-2526 ◽  
Author(s):  
J. K. Walker ◽  
D. B. Jennings
Keyword(s):  
Respiratory Control ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Circumventricular Organs ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Angiotensin System ◽  
Control Protocol ◽  
Respiratory Stimulation ◽  
Stimulation Of

We tested the hypothesis that respiration would be stimulated after vasopressin (AVP) V1 receptor blockade because of disinhibition and activation of the renin-angiotensin system. Intravenous infusion of angiotensin II (ANG II) stimulates respiration, presumably centrally, via circumventricular organs. In the present study, the AVP V1 receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine]-Arg8-AVP (PMP; 10 micrograms/kg i.v.) was administered to six awake resting dogs. Measurements were made 30 min prior, and 60 min subsequent, to injection of PMP (protocol 1). In three other protocols, the ANG II blocker saralasin (0.5 microgram.kg-1.min-1 i.v.) was infused starting 20 min before PMP (protocol 2) and 30 min after PMP (protocol 4) and saline was infused (0.2 ml/min) over 90 min as a control (protocol 3). After PMP in protocol 1, alveolar ventilation increased and arterial PCO2 decreased (approximately 3 Torr). ANG II receptor blockade prevented (protocol 2) and reversed (protocol 4) respiratory stimulation by PMP. Despite ventilatory stimulation, plasma renin activity and ANG II were not increased after PMP relative to control (protocol 3). We conclude that AVP acts at V1 receptors to inhibit formation of brain ANG II. Brain ANG II must modulate respiratory control via a circumventricular organ, because systemically administered saralasin, which does not cross the blood-brain barrier, blocked stimulation of respiration.

Myocardial renin is neither necessary nor sufficient to initiate or maintain ventricular hypertrophy

2000 ◽  
Vol 278 (3) ◽  
pp. R578-R586 ◽  
Author(s):  
Stephen A. Katz ◽  
John A. Opsahl ◽  
Shane E. Wernsing ◽  
Lynn M. Forbis ◽  
Juline Smith ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Salt Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Low Salt ◽  
Necessary And Sufficient

We tested the hypothesis that the myocardial renin-angiotensin system (RAS) is both necessary and sufficient to initiate and maintain all classes of ventricular hypertrophy. Myocardial and plasma renin and angiotensinogen were measured in rats during initiation and maintenance of ventricular hypertrophy associated with DOCA implants and 1% NaCl drinking water, with and without the AT1 ANG II receptor blocker losartan. Additional groups of rats were given a low-sodium diet (0.04%) for 3 wk. Ventricular hypertrophy was initiated within 7 days and maintained for 35 days in DOCA-treated rats despite significantly low myocardial and plasma renin, normal or low myocardial and plasma angiotensinogen, or the presence of losartan. Furthermore, there was no ventricular hypertrophy in low-salt diet-fed animals despite increased myocardial and plasma renin levels and normal angiotensinogen levels. Therefore, the myocardial RAS is not necessary to initiate or maintain cardiac hypertrophy in DOCA-treated rats and is not sufficient to initiate cardiac hypertrophy in low-salt diet-fed rats. Additionally, myocardial renin and angiotensinogen were significantly correlated with corresponding plasma levels.

Effects of ANG II, ETA, and TxA2 receptor antagonists on cyclosporin A renal vasoconstriction

1994 ◽  
Vol 267 (3) ◽  
pp. F443-F449 ◽  
Author(s):  
J. D. Conger ◽  
G. E. Kim ◽  
J. B. Robinette
Keyword(s):  
Cyclosporin A ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Receptor Antagonists ◽  
Renal Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Nonspecific Effects ◽  
Oxide Synthase ◽  
Renal Vascular

The renin-angiotensin system, endothelin (ET), and vasoconstrictor prostaglandins have been reported in separate studies to mediate the renal vasoconstrictor effect of cyclosporin A (CsA). However, direct comparison of the relative importance of these potential mediators has not been performed. In this study, the attenuating effects of comparable agonist-inhibiting doses of receptor antagonists for angiotensin II (ANG II), DuP-753 at 2.5 mg/kg, for ETA, BQ-123 at 0.5 mg/kg, and for thromboxane A2 (TxA2), SQ-29,548 at 1.6 mg.kg-1.h-1, or saline vehicle on acute CsA (20 mg/kg) renal vasoconstriction were compared in anesthetized Sprague-Dawley rats. All three receptor antagonists significantly limited the CsA-induced increase in renal vascular resistance; however, BQ-123 and SQ-29,548 were more effective than DuP-753. Because all three receptor antagonists demonstrated at least some attenuation of CsA-induced renal vasoconstriction, the potential role of acute CsA-related nitric oxide synthase (NOS) inhibition and nonspecific heterologous effects of specific receptor antagonists on other agonists were determined to exclude the possibilities that there was a general increased agonist sensitivity and that detection of a single or primary constrictor mediator was obscured by "crossover" receptor antagonist effects. CsA significantly reduced renal blood flow (39%) in the presence of the NOS inhibitor, N omega-nitro-L-arginine methyl ester, and there was negligible indication that receptor antagonists had nonspecific effects. It is concluded that CsA-induced renal vasoconstriction is complex and involves activation of multiple constrictor agonists independently or sequentially.

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