Effect of Antitonin on Blood Pressure in the One-Kidney Hypertensive Rat

1978 ◽  
Vol 54 (4) ◽  
pp. 457-461 ◽  
Author(s):  
R. Garcia ◽  
R. Boucher ◽  
J. Gutkowska ◽  
K. Kondo ◽  
S. Demassieux ◽  
...  

1. The tonin concentration of saliva and submaxillary glands was studied in one-clip hypertensive rats with or without the contralateral kidney. 2. Salivary tonin concentration was elevated in one-kidney hypertensive rats, but not in one-kidney normotensive or two-kidney, one-clip hypertensive rats. In contrast, an elevated submaxillary gland tonin concentration was found only in uninephrectomized animals, whether normotensive or hypertensive. 3. A single intravenous administration of rabbit tonin antiserum into one-kidney hypertensive rats restored blood pressure to normal in seven out of ten animals. There was little change in blood pressure in two-kidney, one-clip hypertensive, uninephrectomized or sham-operated rats. 4. These findings suggest a connection between the physiology of the kidney and of the submaxillary gland in the rat, and indicate that tonin may play a significant role in maintaining high blood pressure in one-kidney hypertensive animals.

1978 ◽  
Vol 55 (s4) ◽  
pp. 183s-186s ◽  
Author(s):  
R. Boucher ◽  
R. Garcia ◽  
J. Gutkowska ◽  
S. Demassieux ◽  
J. Genest

1. A single intravenous administration of rabbit tonin antiserum into one-kidney one-clip hypertensive rats restored blood pressure to normal in seven out of ten animals. There was little change in blood pressure in two-kidney one-clip hypertensive, uninephrectomized or sham-operated rats. 2. Infusion of tonin in control rats did not modify arterial blood pressure. However, in indomethacin salt-treated rats a marked increase in arterial blood pressure was observed under tonin infusion. 3. Plasma tonin activity was significantly increased in human essential and renovascular hypertension. 4. These findings strongly suggest that tonin is important in the maintenance of high blood pressure. However, other factors (possibly prostaglandins and sodium) have to be modified in order to activate the tonin—angiotensin II system.


1979 ◽  
Vol 57 (1) ◽  
pp. 53-62 ◽  
Author(s):  
R. G. Bengis ◽  
T. G. Coleman

1. The effect of chronic inhibition of angiotensin II formation was investigated in four groups of hypertensive rats. Benign hypertension was produced by placing a 0·25 mm-diameter silver clip on the renal artery; a 0·20 mm clip was used to create malignant hypertension. A two-kidney model had a clip plus intact contralateral kidney and a one-kidney model had a clip plus contralateral nephrectomy. Benign and malignant groups were prepared in both the one-kidney and two-kidney variations. Converting enzyme inhibitor (SQ 14.225) was given to these four groups for 1 week in drinking water and average intake ranged from 33 to 77 mg/day. 2. The two malignant groups had the highest plasma renin activities and they showed a precipitous fall in arterial pressure in the first 24 h of inhibition of angiotensin formation. All groups showed an additional slow decline in pressure during the remaining 6 days of inhibition. Changes in heart rate and sodium excretion were variable but, in general, heart rate decreased during inhibition. 3. Arterial pressure did not become normal with inhibition in either of the one-kidney models: decreases to 126 and 132 mmHg were observed in the benign and malignant groups respectively. Three of the malignant one-kidney animals became uraemic with inhibition and one died before inhibition was discontinued. 4. Arterial pressure was reduced to normal pressure (95 mmHg) after 1 week of inhibition in both the benign and malignant two-kidney models. 5. It appears that normal pressure was restored in the two-kidney model but not in the one-kidney model because of the presence of the intact contralateral kidney. The physiological basis for this difference is not known but changes in renal excretory function may be involved.


1983 ◽  
Vol 64 (5) ◽  
pp. 463-470
Author(s):  
Y. Takata ◽  
A. E. Doyle ◽  
M. Veroni ◽  
S. G. Duffy

1. Blood pressure, the hypotensive effect of captopril, plasma renin activity, renal renin content and kidney weight were measured in the two-kidney—one-clip model, the one-kidney—one-clip model and the two-kidney—one-clip model with the ureter of the contralateral kidney ligated in rats. The ureteric ligation was performed to abolish urinary excretion from the contralateral kidney in the two-kidney—one-clip model. 2. The development of hypertension after renal artery constriction was earlier and greater in the one-kidney—one-clip model and the two-kidney—one-clip model with ureter of the contralateral kidney ligated than in the two-kidney—one-clip model. A single oral dose of captopril produced a greater fall in blood pressure in both the two-kidney models than in the one-kidney—one-clip group. 3. Plasma renin activity and renal renin content of the clipped kidney were higher in the two-kidney model rats, whether or not the ureter had been ligated, than in the one-kidney—one-clip model animals, although more than half the rats from the two-kidney model had normal values. There was a significant correlation between plasma renin activity and the response to captopril in all groups, whereas in none of the three groups was the correlation between plasma renin activity and blood pressure significant. 4. The clipped kidney had a higher renin content than did the contralateral kidney, and the weight of the ischaemic kidney was decreased compared with the contralateral kidney whether it was untouched or had its ureter ligated. The weight of the clipped kidney was in the order one-kidney—one-clip model > two-kidney—one-clip model with ureter of the contralateral kidney ligated > two-kidney—one-clip model. 5. It was concluded that the renin-angiotensin system was stimulated to the similar degree in some animals for the two-kidney—one-clip models, whether or not the ureter of the contralateral kidney had been ligated, compared with the one-kidney—one-clip animals. This finding suggests that the contralateral kidney can stimulate renin secretion and synthesis in the clipped kidney independently of Na+ excretion.


1962 ◽  
Vol 202 (4) ◽  
pp. 795-799 ◽  
Author(s):  
H. Brunner ◽  
P. A. Desaulles ◽  
D. Regoli ◽  
F. Gross

To determine relationship between kidney renin content and excretory function, rats with renal hypertension induced by unilateral clamping of the renal artery were given an oral load of 3 ml of 0.9% saline/100 g body wt. Excretion of the saline load was accelerated in rats with renal hypertension as well as in animals with hypertension due to overdosage with cortexone and salt, provided that the loading experiment was made 3–4 weeks after hypertension was established, but not when animals had been hypertensive for 11–14 weeks. Renin concentration was markedly reduced in the unclamped kidney and also in the kidney of the rats overdosed with cortexone and salt. Excreting capacity of the clamped kidney was compared with that of the unclamped kidney, after removal or after functional elimination of the contralateral kidney, by ligation of the ureter, 3, 24, and 48 hr after the operation. In all experiments excretion of saline load by the unclamped kidney was more rapid than by the clamped kidney, but the highest values were reached in the presence of a functional clamped kidney. Only in rats with elevated blood pressure was the load more rapidly excreted than in normal rats, but hypertension alone cannot be the only factor responsible, the excretion not being accelerated in unilaterally nephrectomized hypertensive rats. Although these hint at a connection between the renin concentration and renal function the nature of this relationship remains uncertain.


1999 ◽  
Vol 276 (3) ◽  
pp. H944-H952 ◽  
Author(s):  
Stephanie W. Watts ◽  
Gregory D. Fink

We previously demonstrated a change in the receptors mediating 5-hydroxytryptamine (5-HT)-induced contraction in arteries of deoxycorticosterone acetate (DOCA)-salt-hypertensive rats. Specifically, contraction to 5-HT is mediated primarily by 5-HT2A receptors in arteries from normotensive sham rats and by both 5-HT2A and 5-HT2B receptors in arteries from hypertensive rats. We hypothesized that the 5-HT2B receptor may play a role in maintaining the high blood pressure of DOCA-salt-hypertensive rats, and herein we provide data connecting in vitro and in vivo findings. The endothelium-denuded isolated superior mesenteric artery of DOCA-salt rats displayed a marked increase in maximum contraction to the newly available 5-HT2B-receptor agonist BW-723C86 compared with that of arteries from sham rats, confirming that the 5-HT2B receptor plays a greater role in 5-HT-induced contraction in arteries from DOCA-salt rats. In chronically instrumented rats, the 5-HT2B-receptor antagonist LY-272015 (0.3, 1.0, and 3.0 mg/kg iv at 30-min intervals) was given cumulatively 1 time/wk during 4 wk of continued DOCA-salt treatment. LY-272015 did not reduce blood pressure of the sham-treated rats at any time or dose. However, LY-272015 (1.0 and 3.0 mg/kg) significantly reduced mean blood pressure in a subgroup of week 3 (−20 mmHg) and week 4 DOCA-salt (−40 mmHg) rats that had extremely high blood pressure (mean arterial blood pressure ∼200 mmHg). Blockade of 5-HT2Breceptors by in vivo administration of LY-272015 (3.0 mg/kg) was verified by observing reduced 5-HT-induced contraction in rat stomach fundus, the tissue from which the 5-HT2B receptor was originally cloned. These data support the novel hypothesis that 5-HT2B-receptor expression is induced during the development of DOCA-salt hypertension and contributes to the maintenance of severe blood pressure elevations.


1964 ◽  
Vol 206 (6) ◽  
pp. 1361-1364 ◽  
Author(s):  
G. Schaechtelin ◽  
D. Regoli ◽  
F. Gross

In isovolemic cross-circulation experiments, a nephrectomized donor rat, into which various doses of hog renin were injected, was connected to a nephrectomized indicator rat. The blood pressure increase thus produced in the indicator rat was compared with the blood pressure response obtained during cross circulation using either intact normotensive or renal hypertensive rats as donor animals. An exponential dose-response relationship was found between hog renin injected into a nephrectomized donor and the blood pressure increase of the indicator rat. Using the cross-circulation technique, the disappearance rate of endogenous reninlike material in the blood of donor animals and of exogenous renin injected into nephrectomized donor animals was examined. If an intact normotensive animal or a unilaterally nephrectomized hypertensive animal is totally nephrectomized, reninlike material disappears from the blood within 1 hr. In renal hypertensive rats with an untouched contralateral kidney which have a higher concentration of reninlike material in the blood, it takes about twice the normal time until reninlike material disappears from the blood after nephrectomy. The increased and prolonged blood pressure response of the nephrectomized animal to renin is not connected with a prolonged persistence of renin in the blood.


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