scholarly journals Role of renin-angiotensin system in experimental hypertension in rats: Plasma renin and hypotensive effect of angiotensin II antagonist.

1977 ◽  
Vol 41 (6) ◽  
pp. 665-675 ◽  
Author(s):  
JIN YAMAMOTO
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Experimental Hypertension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Angiotensin Ii Antagonist

Effect of angiotensin II antagonist infusion on autoregulation of renal blood flow

1976 ◽  
Vol 231 (4) ◽  
pp. 1267-1271 ◽  
Author(s):  
Y Abe ◽  
T Kishimoto ◽  
K Yamamoto
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Pressure Reduction ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Autoregulation ◽  
Angiotensin Ii Antagonist

The role of the renin-angiotensin system in the autoregulation of renal blood flow was examined in the anesthetized dog. The angiotensin II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, was continuously infused into the renal artery at rates of 1 and 3 mug/min, and renin secretion rate and intrarenal distribution of blood flow as well as total renal blood flow were measured during acute reductions in renal perfusion pressure within and below the range of autoregulation. Renal autoregulation and redistribution of blood flow by pressure reduction were not disturbed by the angiotensin II antagonist. This result does not provide any evidence for a primary role of the renin-angiotensin system in renal autoregulation. Redistribution of blood flow by pressure reduction occurred independently of the renin-angiotensin system. It might depend on the differences in the resting tone among the zones.

Plasma renin and angiotensin in dehydrated and rehydrated rats

1986 ◽  
Vol 250 (5) ◽  
pp. R898-R901 ◽  
Author(s):  
R. Di Nicolantonio ◽  
F. A. Mendelsohn
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

The role of the renin-angiotensin system in the stimulation and termination of dehydration-induced drinking was examined in the rat. Rats dehydrated for 48 h had significantly elevated renin, angiotensin II, plasma Na+ concentration, osmolality, and hematocrit when compared with replete controls. Although plasma Na+ concentration, osmolality, and hematocrit of dehydrated rats had returned to control replete levels by 2-4 h after the return of water, the plasma renin and angiotensin II levels exhibited a further increase on rehydration and remained significantly above dehydration levels for 2-4 h after the return of water. The levels of renin and angiotensin II in rehydrated rats were maintained at levels in excess of the dipsogenic threshold for circulating angiotensin II during the 8-h period after rehydration, indicating that termination of the drinking is not dependent on a reduction of circulating angiotensin II. Finally, rehydrated rats did not drink significantly more than replete controls in the 1- to 8-h postrehydration period despite plasma angiotensin II levels in excess of that of the dipsogenic threshold for angiotensin II, indicating that mechanisms exist which override the dipsogenic action of circulating angiotensin II.

Renal vascular response to heat stress in baboons--role of renin-angiotensin

1977 ◽  
Vol 43 (4) ◽  
pp. 739-746 ◽  
Author(s):  
M. M. Eisman ◽  
L. B. Rowell
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Papio Cynocephalus ◽  
Renin Angiotensin ◽  
Renal Vasoconstriction ◽  
Ambient Temperatures ◽  
Angiotensin Ii Antagonist ◽  
Renal Vascular

To determine if hyperthermia in the baboon caused a reduction of renal blood flow (RBF) similar to that reported in man, we repeatedly exposed six unanesthetized male baboons (Papio cynocephalus) to ambient temperatures of 42.5–49.0 degrees C for 55–175 min. Internal temperatures rose 1.0–2.0 degrees C. On the average, RBF fell 23.7% per degrees C, renal vascular resistance (RVR) rose 34.0% per degrees C, and mean arterial pressure (MAP) fell by only 2.9 Torr. Plasma renin activity (PRA), measured in four baboons, rose 97.5% per degrees C. To investigate the role of the renin-angiotensin system in this renal response, we infused propranolol or saralasin (1-sar-8-ala-angiotensin II), an angiotensin II antagonist, systemically in 14 experiments on three baboons. Both propranolol and saralasin infusions prevented most of the reduction in RBF during hyperthermia. Propranolol prevented the increase in PRA. We conclude that renal vasoconstriction accompanies moderate hyperthermia in the awake baboon, and much of this response is mediated by a beta-adrenergic release of renin.

The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

2020 ◽  
Vol 27 (6) ◽  
pp. 520-528 ◽  
Author(s):  
Izabela Guimarães Barbosa ◽  
Giulia Campos Ferreira ◽  
Diomildo Ferreira Andrade Júnior ◽  
Cássio Rocha Januário ◽  
André Rolim Belisário ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bipolar Disorder ◽  
Cardiovascular Diseases ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Receptors ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

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.

Hypotensive effect of [Sar1,Thr8]angiotensin II in spontaneously hypertensive sodium-depleted rats

1978 ◽  
Vol 234 (4) ◽  
pp. H447-H453
Author(s):  
H. Munoz-Ramirez ◽  
M. C. Khosla ◽  
F. M. Bumpus ◽  
P. A. Khairallah
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Normal Diet ◽  
Spontaneously Hypertensive ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Angiotensin Ii Antagonist

Under inactin anesthesia, intravenous infusion of [Sar1,Thr8]angiotensin II produced a hypotensive effect in young spontaneously hypertensive rats (SHR) treated with furosemide and in mature SH rats fed a low-sodium diet. The angiotensin antagonist also lowered blood pressure of young and mature SH rats receiving a normal diet. Deoxycorticosterone acetate (DOCA) plus saline reversed the hypotensive effect of [Saru,Thr8]angiotensin II in young SH rats, but did not do so in mature SH rats. Plasma renin activity (PRA) was not significantly changed by anesthesia. Furosemide or the low-sodium diet significantly increased PRA in young and mature SH rats. In contrast, DOCA plus saline significantly reduced PRA in both young and mature SH rats. However, there was no correlation between PRA and the action of the angiotensin II antagonist. These data suggest that the renin-angiotensin system is involved in genetic hypertension.

Is angiotensin essential in drinking induced by water deprivation and caval ligation?

1981 ◽  
Vol 240 (1) ◽  
pp. R75-R80 ◽  
Author(s):  
M. C. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Water Deprivation ◽  
Essential Role ◽  
Vena Cava ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The role of the renin-angiotensin system in drinking induced by water deprivation and caval ligation was assessed by infusion of saralasin into the lateral ventricles of rats. This technique was first validated by demonstrating its capability to specifically antagonize drinking to both systemic and central angiotensin II. However, neither the latency to drink nor the amount of water consumed following 24- or 30-h water deprivation was affected by saralasin. Furthermore, saralasin had no significant effect on the recovery of blood pressure or on the water intake following ligation of the abdominal vena cava. These observations suggest that the renin-angiotensin system alone does not play an essential role in the control of drinking following water deprivation or caval ligation in rats.

scholarly journals The ANG-(1–7)/ACE2/mas axis in the regulation of nephron function

2010 ◽  
Vol 298 (6) ◽  
pp. F1297-F1305 ◽  
Author(s):  
Carlos M. Ferrario ◽  
Jasmina Varagic
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Renin Angiotensin System ◽  
Therapeutic Interventions ◽  
Experimental Hypertension ◽  
Converting Enzyme ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
A Site

The study of experimental hypertension and the development of drugs with selective inhibitory effects on the enzymes and receptors constituting the components of the circulating and tissue renin-angiotensin systems have led to newer concepts of how this system participates in both physiology and pathology. Over the last decade, a renewed emphasis on understanding the role of angiotensin-(1–7) and angiotensin-converting enzyme 2 in the regulation of blood pressure and renal function has shed new light on the complexity of the mechanisms by which these components of the renin angiotensin system act in the heart and in the kidneys to exert a negative regulatory influence on angiotensin converting enzyme and angiotensin II. The vasodepressor axis composed of angiotensin-(1–7)/angiotensin-converting enzyme 2/mas receptor emerges as a site for therapeutic interventions within the renin-angiotensin system. This review summarizes the evolving knowledge of the counterregulatory arm of the renin-angiotensin system in the control of nephron function and renal disease.

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