Generation of Angiotensin II at Peripheral Vascular Level: Studies Using Angiotensin II Antisera

1973 ◽  
Vol 45 (5) ◽  
pp. 691-700 ◽  
Author(s):  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Angiotensin Ii ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
High Salt Diet ◽  
Angiotensin System ◽  
Salt Diet ◽  
High Doses ◽  
Renal Artery Constriction ◽  
Local Generation

1. When the renin-angiotensin system of rats had been suppressed by a high salt diet or by bilateral nephrectomy, large doses of angiotensin II antiserum were required to block the pressor action of exogenous angiotensin II. Infusion of renin profoundly lowered the blocking requirement of such animals. 2. It is postulated that renin bound to blood vessels generates angiotensin locally which is taken up by vascular receptors. Where such receptors are left unoccupied and free to bind exogenous angiotensin, high doses of blocking antisera are required. 3. Animals with hypertension produced by renal artery constriction with contralateral nephrectomy were shown to be in positive sodium balance. Nevertheless their blocking requirement was low. 4. It is suggested that the local generation of angiotensin may play a role in the production of renal hypertension and that this accounts for the development of hypertension even in animals immunized against angiotensin.

Blood pressure response to chronic episodic hypoxia: the renin-angiotensin system

2002 ◽  
Vol 92 (2) ◽  
pp. 627-633 ◽  
Author(s):  
Eugene C. Fletcher ◽  
Natalia Orolinova ◽  
Michael Bader
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
High Salt ◽  
High Salt Diet ◽  
Angiotensin System ◽  
Salt Diet ◽  
Renin Angiotensin ◽  
Low Salt ◽  
Episodic Hypoxia

By using an inspired oxygen fraction that produces oxyhemoglobin desaturation equivalent to that seen in human sleep apnea, we have demonstrated that 35 days of recurrent episodic hypoxia (every 30 s for 7 h/day) results in an 8–13 mmHg persistent increase in diurnal systemic mean arterial blood pressure (MAP) in rats. Blockade of angiotensin II receptors (AT1a) eliminates this response. Separate groups of male Sprague-Dawley rats were fed high-salt (8%), ad libitum-salt, or low-salt (0.1%) diets for 7 wk: 2 wk of wash-in for baseline blood pressure measurement and 5 wk of experimental conditions. Rats in each salt group were subjected to episodic hypoxia whereas controls remained unhandled under normoxic conditions. MAP remained at basal levels in all nonepisodic hypoxia controls as well as high-salt-diet episodic hypoxia-exposed rats. Ad lib and low-salt episodic hypoxia rats showed an increase in MAP from 106 and 104 mmHg at baseline to 112 and 113 mmHg, respectively ( P < 0.05). Whole kidney renin mRNA was suppressed in high-salt controls and episodic hypoxia rats, whereas kidney AT1a mRNA showed opposite changes. Suppression of the renin-angiotensin system with a high-salt diet blocks the increase in MAP in episodic hypoxia-challenged rats, in part by suppressing local tissue renin levels. Upregulation of the tissue angiotensin II system appears to be necessary for the chronic blood pressure changes that occur from episodic hypoxia.

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.

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.

Renovascular resistance and noradrenaline

1975 ◽  
Vol 229 (6) ◽  
pp. 1649-1653 ◽  
Author(s):  
L Bomzon ◽  
C Rosendorff
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Blocking Agent ◽  
Competitive Inhibitor ◽  
Renal Nerves ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alpha Adrenergic Receptors ◽  
High Doses ◽  
Adrenergic Blocking

Stimulation of the renal nerves can cause cortical vasoconstriction either by direct activation of vascular smooth muscle or by the generation of angiotensin II following renin release from the juxtaglomerular cells. High doses ( greater than 5 mug/min) of the renal neurotransmitter noradrenaline (NA) infused into the renal artery of the baboon causes cortical vasoconstriction. This NA-induced vasoconstriction is significantly reduced (P less than 0.001) by SQ20881, an inhibitor of converting enzyme, and by saralasin, a competitive inhibitor of angiotensin II. These results suggest that NA stimulates the renin-angiotensin mechanism. The further addition of the alpha-adrenergic blocking agent, phenoxybenzamine, to the NA-SQ20881 or NA-saralasin infusate completely abolishes NA-induced cortical vasoconstriction. These results suggest that NA-induced cortical vasoconstriction in the kidney is mediated by activation of both the renin-angiotensin system and alpha-adrenergic receptors.

Effect of digoxin on the in vitro secretion of renin and angiotensin II/III immunoreactivity by the human adrenal gland

1992 ◽  
Vol 127 (3) ◽  
pp. 210-214 ◽  
Author(s):  
Matteo Pistorello ◽  
Margherita Cimolato ◽  
Francesco Pedini ◽  
Donatella Piovan ◽  
Marco Boscaro ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Renin Angiotensin System ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Superfusion System ◽  
Sustained Reduction ◽  
High Doses

Cardiac glycosides in man inhibit renin secretion, probably through a direct effect at the renal level (i.e. inhibition of juxtaglomerular cell Na/K ATPase). Since there is evidence that the human adrenal possesses an intrinsic renin-angiotensin system, we investigated the effect of digoxin on the in vitro generation of renin and angiotensin II/III, as well as of aldosterone, by the human adrenal gland. Minced normal adrenal tissues were studied in a superfusion system, measuring in the 15-min superfusate fractions active renin by immunoradiometric assay and angiotensin II/III and aldosterone by radioimmunoassay, respectively. In a first set of four experiments using different concentrations of digoxin in sequence for 45 min periods, digoxin 10−5, but not 10−8 and 10−6 mol/l, significantly reduced renin and angiotensin II/III output from adrenals, while no change in aldosterone was observed. In a second set of three experiments, the addition of digoxin 10−5 mol/l for 120 min caused a sustained reduction of renin and angiotensin II/III, but not of aldosterone. In the final experiment, the decrease of renin and angiotensin II/III during superfusion with digoxin 10−5 mol/l was significantly greater than that observed during superfusion with digoxin in the presence of antidigoxin antibodies. Our data indicate that digoxin at high doses reduces renin and angiotensin II/III but not aldosterone secretion by the human adrenal gland. This suggests two different effects of digoxin, probably both mediated by inhibition of the Na/K ATPase activity, on the adrenal renin-angiotensin- and aldosterone-secreting cells.

scholarly journals Immunohistochemical expression of intrarenal renin angiotensin system components in response to tempol in rats fed a high salt diet

2017 ◽  
Vol 6 (1) ◽  
pp. 29 ◽  
Author(s):  
Gabriel Cao ◽  
Silvana Lorena Della Penna ◽  
Nicolás Martín Kouyoumdzian ◽  
Marcelo Roberto Choi ◽  
Susana Gorzalczany ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
High Salt ◽  
Immunohistochemical Expression ◽  
High Salt Diet ◽  
Angiotensin System ◽  
Salt Diet ◽  
Renin Angiotensin ◽  
System Components

scholarly journals Activation of the renin-angiotensin system by a low-salt diet does not augment intratubular angiotensinogen and angiotensin II in rats

2013 ◽  
Vol 304 (5) ◽  
pp. F505-F514 ◽  
Author(s):  
Weijian Shao ◽  
Dale M. Seth ◽  
Minolfa C. Prieto ◽  
Hiroyuki Kobori ◽  
L. Gabriel Navar
Keyword(s):  
Angiotensin Ii ◽  
Renal Injury ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Salt Diet ◽  
Low Salt ◽  
Renin Mrna ◽  
Excretion Rates ◽  
Stimulation Of

In angiotensin II (ANG II) infusion hypertension, there is an augmentation of intratubular angiotensinogen (AGT) and ANG II leading to increased urinary AGT and ANG II excretion rates associated with tissue injury. However, the changes in urinary AGT and ANG II excretion rates and markers of renal injury during physiologically induced stimulation of the renin-angiotensin system (RAS) by a low-salt diet remain unclear. Male Sprague-Dawley rats received a low-salt diet (0.03% NaCl; n = 6) and normal-salt diet (0.3% NaCl, n = 6) for 13 days. Low-salt diet rats had markedly higher plasma renin activity and plasma ANG II levels. Kidney cortex renin mRNA, kidney AGT mRNA, and AGT immunoreactivity were not different; however, medullary renin mRNA, kidney renin content, and kidney ANG II levels were significantly elevated by the low-salt diet. Kidney renin immunoreactivity was also markedly increased in juxtaglomerular apparati and in cortical and medullary collecting ducts. Urinary AGT excretion rates and urinary ANG II excretion rates were not augmented by the low-salt diet. The low-salt diet caused mild renal fibrosis in glomeruli and the tubulointerstitium, but no other signs of kidney injury were evident. These results indicate that, in contrast to the response in ANG II infusion hypertension, the elevated plasma and intrarenal ANG II levels caused by physiological stimulation of RAS are not reflected by increased urinary AGT or ANG II excretion rates or the development of renal injury.

Inhibition of angiotensin conversion and prevention of renal hypertension

1975 ◽  
Vol 228 (2) ◽  
pp. 448-453 ◽  
Author(s):  
Miller ED ◽  
AI Samuels ◽  
E Haber ◽  
AC Barger
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
The One ◽  
Renal Artery Constriction

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

Prenatal high-salt diet impaired vasodilatation with reprogrammed renin–angiotensin system in offspring rats

2018 ◽  
Vol 36 (12) ◽  
pp. 2369-2379 ◽  
Author(s):  
Yanping Liu ◽  
Linglu Qi ◽  
Jue Wu ◽  
Ting Xu ◽  
Chunli Yang ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
High Salt ◽  
High Salt Diet ◽  
Angiotensin System ◽  
Salt Diet ◽  
Renin Angiotensin
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