EFFET DE L’ACIDE ASCORBIQUE SUR L’HYPERTENSION EXPÉRIMENTAL

1951 ◽  
Vol 29 (4) ◽  
pp. 164-175
Author(s):  
O. Héroux ◽  
L.-Paul Dugal
Keyword(s):  
Ascorbic Acid ◽  
Initial Phase ◽  
Renal Hypertension ◽  
Chronic Phase ◽  
Hypotensive Effect ◽  
Experimental Hypertension ◽  
Normal Blood Pressure ◽  
Hypotensive Action ◽  
Exposure To Cold ◽  
Experimental Renal Hypertension

In previously reported observations, we have shown that (a) ascorbic acid, given in large doses, had a hypotensive effect on normal blood pressure, (b) the initial hypotension, due to sudden exposure to cold, was prevented by large doses of ascorbic acid, (c) the hypertension encountered upon long exposures to cold was lowered by ascorbic acid. The present paper confirms the last result and also shows that actually ascorbic acid has a hypotensive action on experimental hypertension obtained by the two following ways: (1) excess of sodium chloride in drinking water and (2) renal compression. The hypertension and adrenal hypertrophy caused by a long exposure to cold regress when the animals are brought back to normal temperature. In its initial phase, the experimental renal hypertension is lowered by ascorbic acid but not in its chronic phase.

THE HYPOTHALAMO-HYPOPHYSIAL NEUROSECRETORY SYSTEM IN EXPERIMENTAL HYPERTENSION IN THE RAT

1963 ◽  
Vol 26 (1) ◽  
pp. 107-111 ◽  
Author(s):  
S. TALANTI ◽  
A. EISALO
Keyword(s):  
Marked Reduction ◽  
Ganglion Cells ◽  
Renal Hypertension ◽  
Nuclear Volume ◽  
Neurosecretory System ◽  
Neurosecretory Material ◽  
Experimental Hypertension ◽  
Experimental Conditions ◽  
Hypothalamic Nuclei ◽  
Experimental Renal Hypertension

SUMMARY The effect of experimental renal hypertension on the hypothalamo-hypophysial neurosecretory system was studied histologically. The amount of neurosecretory material decreased, especially in the neurohypophysis. A marked reduction in the nuclear volume of the neurosecretory ganglion cells occurred, while that of the cells of the other hypothalamic nuclei investigated remained unchanged. The results suggest that the activity of the neurosecretory system is diminished in the experimental conditions used.

scholarly journals STUDIES ON EXPERIMENTAL HYPERTENSION

1943 ◽  
Vol 77 (4) ◽  
pp. 297-307 ◽  
Author(s):  
Harry Goldblatt ◽  
Joseph R. Kahn ◽  
Harvey A. Lewis
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renal Hypertension ◽  
Renal Arteries ◽  
Experimental Hypertension ◽  
Long Duration ◽  
Humoral Mechanism ◽  
Main Renal Artery ◽  
Experimental Renal Hypertension ◽  
The One

Persistent hypertension has been produced in the goat and sheep by constriction of the main renal arteries. The presence or absence of accompanying uremia depends upon the degree of constriction of the renal arteries. In both sheep and goat, constriction of one main renal artery also caused elevation of the blood pressure which tended to persist longer than in the dog. Excision of the one kidney with main renal artery constricted resulted in a prompt (24 hours) return of the blood pressure to normal. In the animals with hypertension of long duration but without renal excretory insufficiency, (the "benign" phase) no significant arterio- or arteriolosclerosis developed as a result of the hypertension alone. In the animals that had both hypertension and renal excretory insufficiency, (the "malignant" phase) the typical terminal arteriolar lesions developed in many organs. These lesions consisted of necrosis and fibrinoid degeneration of arterioles and necrotizing arteriolitis which should not be confused with arteriolosclerosis. The same humoral mechanism which is responsible for experimental renal hypertension in the dog and other animals also obtains in the pathogenesis of experimental renal hypertension in the sheep and goat.

scholarly journals STUDIES ON EXPERIMENTAL HYPERTENSION

1937 ◽  
Vol 65 (2) ◽  
pp. 233-241 ◽  
Author(s):  
Harry Goldblatt ◽  
Jerome Gross ◽  
Ramon F. Hanzal
Keyword(s):  
Renal Hypertension ◽  
Sympathetic Ganglia ◽  
Renal Ischemia ◽  
Renal Nerves ◽  
Experimental Hypertension ◽  
Human Beings ◽  
Human Hypertension ◽  
Beneficial Effects ◽  
Splanchnic Nerves ◽  
Experimental Renal Hypertension

Excision of the thoracic portion of the splanchnic nerves and the lower four dorsal sympathetic ganglia on both sides failed to prevent the development of persistent hypertension which, in dogs, follows the production of renal ischemia by partial clamping of the renal arteries (1). In dogs with this type of experimental renal hypertension existent for varying lengths of time (up to about 4 years), excision of the splanchnic nerves and the lower four dorsal sympathetic ganglia failed to effect any degree of permanent lowering of the blood pressure. For the dog, at least, these results tend to minimize the importance of the splanchnic vasomotor mechanism in the pathogenesis of renal hypertension. This is in agreement with the conclusions of Prinzmetal and Wilson (6) and of Pickering (7) about the part played by the vasomotor system in human hypertension. It is also in agreement with the work of Page (8), and of Collins (9), who showed that in dogs excision of the extrinsic renal nerves alone does not prevent experimental hypertension due to renal ischemia. Although the results of this investigation fail to give experimental support for the operation that is being practised on human beings with hypertension, yet they do not necessarily controvert the reports of beneficial effects in some cases of human hypertension. Further study of the effects on man is necessary before the results of this operation can be adequately evaluated.

scholarly journals PRODUCTION OF ANTIRENIN TO HOMOLOGOUS RENIN AND ITS EFFECT ON EXPERIMENTAL RENAL HYPERTENSION

1964 ◽  
Vol 119 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Sharad D. Deodhar ◽  
Erwin Haas ◽  
Harry Goldblatt
Keyword(s):  
Blood Pressure ◽  
Large Scale ◽  
Renal Hypertension ◽  
Chronic Phase ◽  
Partial Purification ◽  
Subcutaneous Injections ◽  
Progressive Development ◽  
Arterial Blood ◽  
Experimental Renal Hypertension ◽  
The Mean

1. Procedures are described for the extraction and partial purification of dog renin, on a large scale, as well as for the acetylation of rat, rabbit, and dog renin. 2. Untreated homologous renin was not antigenic in rat, rabbit, or dog, but the acetylation of homologous renin made it antigenic. 3. Immunization of rats, rabbits, and dogs, with acetylated rat, rabbit, and dog renin, respectively, resulted in each case in the development of anti-renin to the homologous, untreated, as well as to the acetylated renin. 4. The progressive development of antirenin as a result of repeated, subcutaneous injections of acetylated dog renin, in a dog with experimental renal hypertension for more than 6 years, was accompanied by a correspondingly progressive fall of the mean arterial blood pressure to the prehypertensive level. This points up the important part played by the renin-angiotensin mechanism in the maintenance of the hypertension, even in the chronic phase of experimental renal hypertension.

scholarly journals Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

1970 ◽  
Vol 27 (5) ◽  
pp. 799-810 ◽  
Author(s):  
CARLOS M. FERRARIO ◽  
IRVINE H. PAGE ◽  
JAMES W. McCUBBIN
Keyword(s):  
Cardiac Output ◽  
Renal Hypertension ◽  
Contributory Factor ◽  
Experimental Renal Hypertension

scholarly journals Effect of Experimental Renal Hypertension on Experimental Thiouracil-Cholesterol Atherosclerosis in Dogs

1957 ◽  
Vol 5 (4) ◽  
pp. 426-434 ◽  
Author(s):  
G. E. WAKERLIN ◽  
W. G. MOSS ◽  
J. P. KIELY ◽  
Mrs. Gloria Fein ◽  
Mr. Frank Kejikawa
Keyword(s):  
Renal Hypertension ◽  
Experimental Renal Hypertension

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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