Vasopressin and Malignant Deoxycorticosterone Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 45s-48s ◽  
Author(s):  
J. Möhring ◽  
B. Möhring ◽  
M. Petri ◽  
D. Haack
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Renal Hypertension ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Volume Depletion ◽  
Angiotensin System ◽  
Plasma Arginine ◽  
Normotensive Control

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin—angiotensin system plays in the pathogenesis of malignant renal hypertension.

The Pressor Role of Angiotensin in Salt Deprivation and Renal Hypertension in Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 45s-48s
Author(s):  
T. G. Coleman ◽  
A. C. Guyton
Keyword(s):  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Enzyme Inhibitor ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renal Artery Constriction ◽  
Normotensive Control

1. Angiotensin may influence arterial pressure either by direct vasoconstriction or by more slowly developing effects on thirst and renal function. The importance of direct vasoconstriction was estimated in rats during salt deprivation and renal hypertension by observing the fall in blood pressure that immediately followed injection of converting-enzyme inhibitor. 2. Chronically salt-deprived rats had normal arterial pressure, cardiac output and total peripheral resistance before inhibition. However, inhibiting the formation of angiotensin II caused marked decreases in arterial pressure (−47 mmHg) and total peripheral resistance (−30%). 3. Animals made hypertensive by renal artery constriction showed large decreases in arterial pressure when angiotensin formation was inhibited only during the first few days after constriction. In the chronic, benign phase of hypertension, animals with both clamp plus contralateral nephrectomy and with unilateral clamp only, showed decreases in pressure after inhibition (−12 to 16 mmHg) that were only slightly greater than decreases observed in normotensive control animals. 4. These results indicate that total peripheral resistance and the activity of the renin-angiotensin system can change separately. In salt deprivation, even though an increased fraction of resistance was due to angiotensin, total peripheral resistance was normal. In chronic renal hypertension, total resistance was undoubtedly elevated, but only partially because of the vasoconstrictor effect of angiotensin.

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.

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 Changes in Angiotensin Receptor Distribution and in Aortic Morphology Are Associated with Blood Pressure Control in Aged Metabolic Syndrome Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Verónica Guarner-Lans ◽  
Elizabeth Soria-Castro ◽  
Rocío Torrico-Lavayen ◽  
Araceli Patrón-Soberano ◽  
Karla G. Carvajal-Aguilera ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Renin Angiotensin System ◽  
Pressure Control ◽  
Premature Aging ◽  
Compensatory Mechanism ◽  
Histological Changes ◽  
Angiotensin System ◽  
Elevated Expression

The role of the renin-angiotensin system (RAS) in blood pressure regulation in MS during aging is unknown. It participates in metabolic syndrome (MS) and aging regulating vascular tone and remodeling. RAS might participate in a compensatory mechanism decreasing blood pressure and allowing MS rats to reach 18 months of age and it might form part of therapeutical procedures to ameliorate MS. We studied histological changes and distribution of RAS receptors in aortas of MS aged rats. Electron microscopy images showed premature aging in MS since the increased fibrosis, enlarged endothelium, and invasion of this layer by muscle cells that was present in control 18-month-old aortas were also found in 6-month-old aortas from MS rats. AT1, AT2, and Mas receptors mediate the effects of Ang II and Ang 1-7, respectively. Fluorescence from AT2 decreased with age in control and MS aortas, while fluorescence of AT1 increased in aortas from MS rats at 6 months and diminished during aging. Mas expression increased in MS rats and remained unchanged in control rats. In conclusion, there is premature aging in the aortas from MS rats and the elevated expression of Mas receptor might contribute to decrease blood pressure during aging in MS.

Effect of Administration of Sar1-Ala8-Angiotensin II during the Development and Maintenance of Renal Hypertension in the Rat

1978 ◽  
Vol 54 (6) ◽  
pp. 633-637 ◽  
Author(s):  
M. Fernandes ◽  
R. Fiorentini ◽  
G. Onesti ◽  
G. Bellini ◽  
A. B. Gould ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Early Phase ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Renal Arteries ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Origin

1. Sar1-Ala8-Angiotensin II (an angiotensin antagonist) was infused in rats during the development and maintenance of renal hypertension produced by aortic ligation between renal arteries. 2. In the early phase (5 and 12 days after ligation), infusion of the antagonist markedly decreased blood pressure although it did not reach normal pressures. Later (day 40) only a modest decrease in blood pressure was noted. 3. Removal of the small left kidney always decreased the blood pressure to normal pressures. 4. It is concluded that the renin—angiotensin system is the major pressor component in the initiation of this hypertension. Later, other factors of renal origin assume a pressor function.

scholarly journals The discovery of hypertension: evolving views on the role of the kidneys, and current hot topics

2015 ◽  
Vol 308 (3) ◽  
pp. F167-F178 ◽  
Author(s):  
Richard J. Johnson ◽  
Miguel A. Lanaspa ◽  
L. Gabriela Sánchez-Lozada ◽  
Bernardo Rodriguez-Iturbe
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sodium Excretion ◽  
Extracellular Volume ◽  
Renin Angiotensin System ◽  
Autoimmune Response ◽  
Angiotensin System ◽  
History Of ◽  
Important Disease

Primary hypertension is increasingly common and is associated with significant morbidity. Here, we review the history of its discovery and rise during the last century with an emphasis on studies trying to identify its cause. Early studies identified a defect in sodium excretion by the kidney as being central to the pathogenesis. Recent studies have focused on a variety of genetic, congenital (fetal programming), and acquired mechanisms for causing the defect in natriuresis. Certain risk factors are apparent, including genetic polymorphisms that regulate sodium excretion, a congenital reduction in nephron number, obesity and hyperleptinemia, an elevated sympathetic nervous system, diet (salt and fructose), and metabolic (hyperuricemia) mechanisms. The kidney shows evidence for renal arteriolar vasoconstriction, an intrarenal inflammatory response, local oxidative stress, and intrarenal activation of the renin-angiotensin system. Recent studies suggest that intrarenal T cells have an important role in causing hypertension to be persistent, likely due to the induction of a local autoimmune response to neoantigens such as heat shock protein 70 and protein aggregates formed by isoketals resulting from lipid peroxidation. Salt retention due to impairment in pressure-diuresis leads to the release of cardiotonic steroids and central nervous system effects that cause systemic vasoconstriction and a rise in blood pressure. Some recent studies suggest that salt may increase blood pressure not simply by effects on extracellular volume but rather as a consequence of hyperosmolarity. These new insights could lead to new approaches for the prevention and treatment of this important disease.

AT1 antagonism and renin inhibition in mice: pivotal role of targeting angiotensin II in chronic kidney disease

2012 ◽  
Vol 303 (7) ◽  
pp. F1037-F1048 ◽  
Author(s):  
Christoph Fraune ◽  
Sascha Lange ◽  
Christian Krebs ◽  
Alexandra Hölzel ◽  
Jana Baucke ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Injury ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Pivotal Role ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renin Inhibition

The role of the renin-angiotensin system in chronic kidney disease involves multiple peptides and receptors. Exerting antipodal pathophysiological mechanisms, renin inhibition and AT1 antagonism ameliorate renal damage. However, it is unclear which mechanism exerts better nephroprotection. We compared the renin inhibitor aliskiren with the AT1 antagonist losartan in mice with chronic kidney disease due to renal ablation. Doses were adjusted to equipotent inhibition of the renin-angiotensin system, determined via a dose-response quantifying plasma and renal renin expression. Six-week treatment with either 500 mg/l drinking water losartan or 50 mg·kg−1·day−1 aliskiren significantly decreased albuminuria, glomerular damage, and transcription rates of renal injury markers to a similar extent. An array analysis comparing renal gene expression of losartan- and aliskiren-treated mice evaluating >34,000 transcripts demonstrated regulation for 14 genes only, with small differences. No superior nephroprotection was found by combining losartan and aliskiren. Compared with plasma concentrations, aliskiren accumulated ∼7- to 29-fold in the heart, liver, lung, and spleen and ∼156-fold in the kidney. After withdrawal, plasma concentrations dropped to zero within 24 h, whereas renal tissue concentrations declined slowly over days. Withdrawal of aliskiren in mice with chronic kidney disease revealed a significantly delayed re-increase in albuminuria compared with withdrawal of losartan. This study demonstrates equieffective nephroprotection of renin inhibition and AT1 antagonism in mice with chronic kidney disease without additional benefit of combination therapy. These observations underscore the pivotal role of targeting ANG II to reduce renal injury.

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