Immunoreactive renin and angiotensin II in the afferent glomerular arterioles of rats with hypertension due to unilateral renal artery constriction

1982 ◽  
Vol 76 (1) ◽  
pp. 61-69 ◽  
Author(s):  
R. Taugner ◽  
M. Marin-Grez ◽  
R. Keilbach ◽  
E. Hackenthal ◽  
R. Nobiling
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Glomerular Arterioles ◽  
Renal Artery Constriction

scholarly journals RENAL HYPERTENSION IN RATS IMMUNIZED AGAINST ANGIOTENSIN I AND ANGIOTENSIN II

1974 ◽  
Vol 139 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Helen F. Oates ◽  
Gordon S. Stokes ◽  
Brian G. Storey ◽  
Robyn G. Glover ◽  
Beverley F. Snow
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Mechanism Of Action ◽  
Renal Hypertension ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Receptor Sites ◽  
Significant Difference ◽  
Blood Pressures ◽  
Renal Artery Constriction

Rats, actively immunized against angiotensin I (AI) and angiotensin II (AII), were subjected to unilateral renal artery constriction to determine whether the resulting hypertension, which may still ensue in the animal immunized against AII, could be prevented by such combined immunity. Sustained immunity to both AI and AII neither changed preoperative blood pressures of the rats from those of control mock-immunized rats nor altered the incidence or severity of renal dip hypertension. Vascular hyperresponsiveness to small quantities of free angiotensin could not be invoked to explain the hypertension, for there was no significant difference between mock-immunized hypertensive animals, and those remaining normotensive, regarding pressor sensitivity to intravenous AI, AII, renin, and norepinephrine. (AI + AII)-immunized hypertensive rats required AI doses averaging 260 times greater than nonimmune hypertensives to elicit equipressor responses, and were refractory to renin, but not to norepinephrine. Thus, while previous studies have not excluded direct participation of endogenous AI in renal clip hypertension in rats, evidence from our experiments makes it extremely difficult to sustain any pressor function therein for circulating AI or AII. Our results also preclude involvement of AII produced from circulating AI by conversion within arteriolar walls, close to receptor sites, since AI immunity would block this mechanism of action.

Changes of Plasma and Cerebrospinal Fluid Noradrenaline during Frusemide Administration and Acute Renal Artery Constriction in Dogs

1982 ◽  
Vol 63 (s8) ◽  
pp. 343s-345s ◽  
Author(s):  
Yoshiaki Masuyama ◽  
Yuji Ueno ◽  
Mikio Arita ◽  
Hidetoshi Suruda ◽  
Osamu Mohara
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Arterial Blood Pressure ◽  
Plasma Noradrenaline ◽  
Direct Role ◽  
Arterial Blood ◽  
Renal Artery Constriction

1. The effects of circulating angiotensin II on cerebrospinal fluid and plasma noradrenaline during frusemide administration and acute renal artery constriction were studied in dogs. 2. The administration of frusemide produced significant increases in cerebrospinal fluid and plasma noradrenaline. Intravertebral artery infusion of [Sar1, Ala8]angiotensin II (saralasin) significantly suppressed the frusemide-induced increases in cerebrospinal and plasma noradrenaline and resulted in a fall in arterial blood pressure. 3. Acute renal artery constriction produced the marked elevation of plasma noradrenaline and arterial blood pressure, although no significant increase was found in cerebrospinal fluid noradrenaline. Though intravertebral artery infusion of saralasin did not affect cerebrospinal fluid and plasma noradrenaline, intravenous infusion of saralasin reduced the increases in arterial blood pressure and plasma noradrenaline induced by acute renal artery constriction. 4. Plasma volume was significantly reduced by frusemide administration, but unchanged by acute renal artery constriction. 5. Therefore it is suggested that circulating angiotensin II may contribute to the regulation of blood pressure at least partially by acting on the central nervous system in the sodium- and volume-depleted states. However, the renin-angiotensin system appears to play a rather direct role in the mechanism of hypertension induced by renal artery constriction, not through the action of angiotensin II on the central sympathetic nervous system.

Paper chromatographic identification of angiotensins

1964 ◽  
Vol 207 (4) ◽  
pp. 759-763 ◽  
Author(s):  
Paul E. Wisenbaugh ◽  
Noah E. Wills ◽  
Robert W. Hill
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Paper Chromatography ◽  
Renal Hypertension ◽  
Nacl Solution ◽  
Angiotensin I ◽  
Experimental Renal Hypertension ◽  
Renal Artery Constriction

The separation of angiotensin I and angiotensin II by paper chromatography using an acid NaCl solution is described. When the pressor material recovered from the blood of dogs infused with renin was analyzed by this method, significant quantities of angiotensin I as well as angiotensin II were found in those infused at rates above 1 Goldblatt U/min. At infusion rates below 1 U/min, only angiotensin II was present. In each of six dogs with malignant experimental renal hypertension, significant increases in circulating pressor material were found 48 hr or more after renal artery constriction. Analysis of the material recovered from the blood of five of these dogs revealed only angiotensin II in four instances, and a mixture of angiotensin I and II in one instance.

Characterization of the postocclusive response of renal blood flow in the cat

1978 ◽  
Vol 235 (4) ◽  
pp. F286-F290 ◽  
Author(s):  
W. S. Spielman ◽  
H. Osswald
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Artery Occlusion ◽  
Renal Nerves ◽  
Vasoconstrictor Response ◽  
Renal Artery Occlusion ◽  
Chronic Denervation

In contrast to the postocclusive hyperemia of brain, heart, and skeletal muscle, the hemodynamic response of the kidney following renal artery occlusion is highly variable in that both hyperemia and ischemia have been reported. The present study evaluates the factors influencing the renal response to complete renal artery occlusion (5-60 s) in the anesthetized cat. Marked postocclusive vasoconstriction could only be domonstrated in meclofenamate-treated (10 mg/kg) cats. The delta% renal blood flow (RBF) (30-s occlusion) was 16 +/- 4 in controls and 54 +/- 4 after meclofenamate (n= 10; P less than 0.001). Chronic denervation of the kidney, alpha-adrenergic receptor blockade, or infusion of [Sar1, Ile8]angiotensin II(2 microgram/min per kg) did not affect the postocclusive reduction of RBF, indicating that the vasoconstriction was independent of renal nerves, catecholamines, and circulating angiotesin II. Adenosine injected into the renal artery of five cats caused a dose-dependent transient fall of RBF. A dose of 100 nmol adenosine reduced RBF by 44 +/- 6% whereas after meclofenamate only 1 nmol produced the same degree of vasoconstriction. In summary, this study demonstrates a marked potentiation of the postocclusive vasoconstrictor response and the vasoconstrictive action of adenosine by meclofenamate in the anesthetized animal. No evidence was obtained to support a role for the sympathetic nervous system or circulating angiotensin II in mediating the postocclusive vasoconstriction.

Salt and water balance and renin activity in renal hypertension of rats

1975 ◽  
Vol 228 (6) ◽  
pp. 1847-1855 ◽  
Author(s):  
J Mohring ◽  
B Mohring ◽  
H-J Naumann ◽  
A Philippi ◽  
E Homsy ◽  
...  
Keyword(s):  
Water Balance ◽  
Renal Artery ◽  
Renal Hypertension ◽  
The Body ◽  
Renin Activity ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Contralateral Kidney ◽  
Salt And Water Balance ◽  
Renal Artery Constriction

In male Sprague-Dawley rats, renal artery constriction in the presence of an inact contralateral kidney induced sodium retention (for 2-3 wk), moderate potassium loss,elevation of blood volume (BV), and an increase in water turnover. It is suggestedthat renal artery constriction activates the renin-angiotensin-aldosterone system, resulting in disordered regulation of salt and water balance and in blood pressure (BP) elevation. Subsequently, sodium balance was reestablished in one group of hypertensive rats. The previously retained sodium was kept in the body, and BV and reninactivity remained elevated. In a second group of animals, a malignant course of hypertension developed: BP surpassed a critical level of about 180 mmHg; sodium, potassium, and water were lost; BV declined; renin activity was further stimulated; and in the contralateral kidney malignant nephrosclerosis occurred. It is assumed that pressure diuresis and natriuresis induce a vicious circle: the increasing renin activity may maintain or further increase BP level, therby inducing further salt and water loss, etc.; high BP levels and high renin activities induce vascular damage and deterioration of renal function.

Reflex cholinergic vasodilatation during renal artery constriction in the unanesthetized dog

1969 ◽  
Vol 217 (1) ◽  
pp. 239-246 ◽  
Author(s):  
JM Stinson ◽  
AB Barnes ◽  
RM Zakheim ◽  
JE Chimoskey ◽  
FR Spinelli ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renal Artery Constriction ◽  
Cholinergic Vasodilatation

Inactivation of Bradykinin and Angiotensin I Conversion in Conscious Rats with Two-Kidney, One-Clip Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 199s-201s ◽  
Author(s):  
Inge E. K. Trindade ◽  
Eduardo M. Krieger
Keyword(s):  
Enzyme Activity ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Renal Artery ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Parallel Increase

1. The extents of pulmonary degradation of bradykinin (BK) and angiotensin I (ANG I) to angiotensin II (ANG II) conversion were measured simultaneously to determine whether converting enzyme activity, in vivo, is altered in two-kidney, one-clip hypertensive rats (15, 60 and 180 days after renal artery clipping). 2. Inactivation of BK (estimated by comparing equipressor doses injected intravenously and intra-aortically) was markedly increased in these hypertensive rats: 98.5% (15 days), 98.4% (60 days) and 99.5% (180 days) vs 95.6% in control rats. All groups of hypertensive rats exhibited hyper-reactivity to intra-aortic BK, requiring doses 14–38 times smaller than the control rats to produce the same depressor response. 3. The percentage of ANG I conversion (calculated from equipressor doses of ANG I and ANG II injected intravenously) was elevated after 15 days (46.0% vs 28.1% in control rats), unchanged after 60 days (27.7%) and slightly elevated after 180 days (36.0%). Hyporeactivity to ANG II was observed 15 and 180 days after renal artery clipping (doses six times were needed to produce a standard increase in mean arterial pressure). No alterations were found in the rats at 60 days after artery clipping. 4. The increased degradation of BK cannot be explained solely by elevation of converting enzyme activity since no parallel increase in ANG I conversion was observed, indicating that other bradykininases in the lung may be involved.

scholarly journals Regional angiotensin II production in essential hypertension and renal artery stenosis.

Hypertension ◽  
1993 ◽  
Vol 21 (2) ◽  
pp. 173-184 ◽  
Author(s):  
P J Admiraal ◽  
A H Danser ◽  
M S Jong ◽  
H Pieterman ◽  
F H Derkx ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Artery Stenosis
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