Faecal Sodium/Potassium Ratio and Aldosteronism in Experimental Hypertension in the Rat

1972 ◽  
Vol 43 (4) ◽  
pp. 577-581 ◽  
Author(s):  
J. D. Swales ◽  
H. Thurston ◽  
F. P. Queiroz ◽  
J. D. Tange
Keyword(s):  
Renal Artery ◽  
Experimental Hypertension ◽  
Sham Operation ◽  
Normal Kidney ◽  
Sodium Depletion ◽  
Hypertensive Rats ◽  
Aldosterone Secretion ◽  
Sodium Potassium ◽  
Renal Artery Constriction

1. Renal artery constriction and sham operation produced a temporary fall in the faecal sodium/potassium (Na/K) ratio of rats. When contralateral nephrectomy had been performed, the ratio rose to normal with the development of hypertension. With an intact opposite kidney the ratio remained low, but was elevated by spironolactone. With or without contralateral nephrectomy, the ratio was normal in chronically hypertensive animals (>28 days). 2. Balance studies showed sodium depletion in hypertensive rats with a normal kidney in situ. It is suggested that this stimulates aldosterone secretion and the faecal electrolyte changes.

Chemical Renal Medullectomy; Effect upon Reversal of Two-Kidney, One-Clip Hypertension in the Rat

1981 ◽  
Vol 61 (s7) ◽  
pp. 335s-338s ◽  
Author(s):  
R. F. Bing ◽  
G. I. Russell ◽  
J. D. Swales ◽  
H. Thurston ◽  
A. Fletcher
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Urine Volume ◽  
Renal Medulla ◽  
Plasma Renin ◽  
Left Renal Artery ◽  
Hypertensive Rats ◽  
Plasma Renin Concentration ◽  
Complete Reversal ◽  
Renal Artery Constriction

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold. 2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter. 3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated. 4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.

Experimental hypertension in pregnant sheep

1960 ◽  
Vol 199 (4) ◽  
pp. 633-636 ◽  
Author(s):  
Louis W. Holm ◽  
Yale J. Katz ◽  
Harold R. Parker ◽  
Leon C. Chesley ◽  
Nicholas S. Assali
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Severe Hypertension ◽  
Renal Arteries ◽  
Renal Ischemia ◽  
Experimental Hypertension ◽  
Control Blood Pressure ◽  
Human Hypertension ◽  
Pregnant Sheep ◽  
Renal Artery Constriction

Sheep with spontaneously occurring or experimentally induced toxemia of pregnancy do not develop hypertension despite the presence of a marked renal ischemia. The present study was undertaken in order to investigate whether pregnant sheep, like pregnant dogs and rats, do not exhibit hypertension when subjected to renal artery constriction. Bilateral constriction of the renal arteries was performed on pregnant ewes by a modified Goldblatt-Wakerlin technique, after control blood pressure had been recorded for several days. Blood pressure and BUN were measured throughout pregnancy and following delivery. All the animals which had renal artery constriction developed severe hypertension with retinal changes similar to those of human hypertension. The pregnancy did not affect the course of the hypertension nor did the hypertension alter the course of pregnancy.

Vascular Sodium—Potassium Pump Activity in Various Models of Experimental Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 179s-181s ◽  
Author(s):  
M. B. Pamnani ◽  
D. L. Clough ◽  
S. J. Huot ◽  
F. J. Haddy
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Cell Membrane Permeability ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Primary Defect ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension ◽  
Pump Activity ◽  
Sodium Potassium Pump

1. Ouabain-sensitive 86Rb uptake was used to assess sodium-potassium pump activity in vascular smooth muscle of animals with various types of experimental hypertension. 2. The findings suggest that pump activity is suppressed in the non-genetic low renin, presumably volume-expanded forms of hypertension. 3. By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. In these genetic models the primary defect may be increased cell membrane permeability.

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.

Urinary Kallikrein and Plasma Renin during the Reversal of Renovascular Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 263s-266s
Author(s):  
O. P. Gulati ◽  
O. A. Carretero ◽  
T. Morino ◽  
N. B. Oza
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Renin Activity ◽  
Experimental Hypertension ◽  
Urinary Kallikrein ◽  
Sodium Potassium ◽  
Water Excretion

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.

Effects of dietary sodium restriction on peptide stimulation of aldosterone secretion by the isolated perfused rat adrenal gland in situ: a report of exceptional sensitivity to angiotensin II amide

1988 ◽  
Vol 119 (1) ◽  
pp. 83-88 ◽  
Author(s):  
J. P. Hinson ◽  
G. P. Vinson ◽  
B. J. Whitehouse
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Fold Increase ◽  
Threshold Concentration ◽  
Dietary Sodium ◽  
Bolus Administration ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Increased Sensitivity

ABSTRACT The effects of prior sodium depletion on the steroidogenic responses of the rat adrenal gland have been investigated using a method of perfusing the isolated adrenal gland of the rat in situ. Secretion rates of aldosterone in response to the known adrenocortical stimulants ACTH, angiotensin II amide and α-MSH were measured. In each case, the adrenals from sodium-deplete animals responded to a lower dose of the stimulant than the normal animals. This resulted in a 10-fold increase in sensitivity to ACTH, a 100-fold increase in sensitivity to angiotensin II amide, and a 1000-fold increased sensitivity to α-MSH, bringing the threshold concentration required for aldosterone secretion into the physiological range of α-MSH concentrations. The perfused adrenal gland is particularly sensitive to angiotensin II amide; a bolus administration of 1 amol gave a significant increase in aldosterone secretion in the sodium-deplete group. These data confirm previous reports of increased adrenal sensitivity to α-MSH and angiotensin II in sodium depletion, and also suggest the existence of intraglandular mechanisms for signal amplification which may be involved in mediating the adrenal response to very small concentrations of stimulant. J. Endocr. (1988) 119, 83–88

scholarly journals GENETIC INFLUENCE ON THE DEVELOPMENT OF RENAL HYPERTENSION IN PARABIOTIC RATS

1969 ◽  
Vol 129 (3) ◽  
pp. 507-522 ◽  
Author(s):  
J. Iwai ◽  
K. D. Knudsen ◽  
L. K. Dahl ◽  
M. Heine ◽  
G. Leitl
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Renal Tissue ◽  
Experimental Hypertension ◽  
Angiotensin System ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Genetically Determined ◽  
Renal Artery Constriction

The effects of several renal manipulations including uninephrectomy, unilateral renal artery constriction, and a combination of these two (Goldblatt procedure) were studied in two strains of rats with opposite constitutional predispositions to experimental hypertension. The protective value of intact renal tissue to protect against hypertension was shown to be genetically determined. The Goldblatt procedure carried out on only one member of a parabiotic pair induced hypertension in this operated rat but significant hypertension developed in the intact partner only when the operated animal belonged to the strain predisposed to hypertension. It was speculated that there were qualitative differences in the pressor signals of the two strains of rats. In the strain genetically predisposed to hypertension there are at least two pressor principles: (a) one which is common to both strains, not transmittable via the parabiosis junction and presumably related to the renin-angiotensin system; and (b) a second which is specific for the hypertension-prone strain and can be transmitted through the parabiosis junction. This transmittable agent is probably identical with the factor that produces salt hypertension and is associated with the salt-excreting mechanism.

Plasma Noradrenaline and Renovascular Hypertension in the Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 439s-442s
Author(s):  
J. L. Reid ◽  
H. J. Dargie ◽  
S. S. Franklin ◽  
Beverly Fraser
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Plasma Noradrenaline ◽  
Hypertensive Rats ◽  
Contralateral Kidney ◽  
Sympathetic Nervous ◽  
Peripheral Sympathetic Nervous System

1. Plasma noradrenaline was measured in groups of rats up to 4 weeks after application of a renal artery clip. 2. When renal artery clipping was accompanied by contralateral nephrectomy (one-kidney model) plasma noradrenaline was significantly higher in hypertensive rats than in sham-operated control rats at 7, 14 and 28 days. 3. Plasma noradrenaline was not altered at any time examined in the two-kidney model (unilateral clip and contralateral kidney left in situ). 4. Neurogenic mechanisms mediated by the peripheral sympathetic nervous system appear to participate in the development of one-kidney renovascular hypertension, but do not play a significant role in the two-kidney model.

Renal–adrenal interrelationships in experimental hypertension

1968 ◽  
Vol 46 (2) ◽  
pp. 179-188 ◽  
Author(s):  
D. Ostrovsky ◽  
F. R. Papsin ◽  
A. G. Gornall
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Renal Artery ◽  
High Blood Pressure ◽  
Salt Intake ◽  
Renal Tissue ◽  
Experimental Hypertension ◽  
Normal Blood Pressure ◽  
Renal Hypertrophy ◽  
High Salt Intake

For several weeks after partial constriction of one renal artery, the fate of this "clipped" kidney seems to exert a determining influence on blood pressure. Rats that remained hypertensive throughout the experiment almost invariably had clipped kidneys averaging 0.16 to 0.22% of body weight. Below 0.1%, this kidney was usually quite atrophic, and its presence was consistent with falling or normal blood pressure. The untouched kidney in such rats was, on the average, heavier in the hypertensive than in the normotensive animals. Since the latter also had less renal tissue on the clipped side, it appears that factors leading to high blood pressure stimulated hypertrophy beyond the level provoked by renoprival factors. In rats on a high salt intake, 5 μg/day of D-aldosterone for 3 months stimulated significant true renal hypertrophy in the absence of a rise in blood pressure. Such hypertrophy was more pronounced in similar rats that had been getting 250 μg DOCA/day for 3 months but were also normotensive. Rats that developed hypertension on this latter regimen had still heavier kidneys. Renal hypertrophy appears to be a prehypertensive phenomenon which persists and can become even more pronounced in hypertension. The highest levels of renal hypertrophy were usually associated with significant adrenal hypertrophy. Endocrine functions may be involved in renal hypertrophy. This concept is discussed in relation to a phospholipid "renin inhibitor" recently isolated from dog and hog kidneys.

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