Neurogenic Activity–Angiotensin II Interaction during the Development and Maintenance of Renal Hypertension in the Rat

1979 ◽  
Vol 57 (1) ◽  
pp. 25-29 ◽  
Author(s):  
G. Bellini ◽  
R. Fiorentini ◽  
M. Fernandes ◽  
G. Onesti ◽  
H. Hessan ◽  
...  

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase (5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delayed response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.

1978 ◽  
Vol 54 (6) ◽  
pp. 633-637 ◽  
Author(s):  
M. Fernandes ◽  
R. Fiorentini ◽  
G. Onesti ◽  
G. Bellini ◽  
A. B. Gould ◽  
...  

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.


1987 ◽  
Vol 73 (3) ◽  
pp. 271-275 ◽  
Author(s):  
E. C. H. Wallace ◽  
A. J. Balmforth ◽  
J. J. Morton

1. Chronic two-kidney, one-clip hypertensive rats were infused with captopril for 5 days and the daily variability of blood pressure compared with that for both hypertensive rats infused with glucose and normotensive animals. 2. Blood pressure was measured continuously using a computer data collecting system. 3. Normotensive animals showed a stable level of arterial pressure throughout each 24 h period with troughs occurring when they slept during the daytime. 4. Hypertensive animals given glucose had an enhanced diurnal rhythm of blood pressure compared with normotensive rats, with peaks occurring during periods of activity at night as well as troughs when they slept during the day. 5. Hypertensive rats given captopril retained this enhanced pressure variability, in spite of the fact that blood pressure was significantly lower and angiotensin II was suppressed. 6. These results suggest that angiotensin II is not involved in the increased blood pressure variability of renal hypertension and that some other irreversible mechanism is responsible.


1977 ◽  
Vol 52 (1) ◽  
pp. 107-109
Author(s):  
M. Fernandes ◽  
G. Onesti ◽  
R. Fiorentini ◽  
A. B. Gould ◽  
K. E. Kim ◽  
...  

1. Propranolol was administered to groups of mature rats before and during the development of renal hypertension induced by ligation of the aorta between the renal arteries. 2. At a dose 10 μmol (3 mg) of propranolol/kg, administered by intraperitoneal injection, the onset and severity of hypertension were not affected, although plasma renin concentration was significantly lower than in the untreated hypertensive rats in the first 5 days after the operation. 3. With 200 μmol (60 mg) of propranolol/kg, administered in the drinking water, peak blood pressure 5 days after aortic ligation was lower than in the untreated control rats, but plasma renin concentration was no lower than with the smaller dose. 4. The development of severe hypertension despite reduction in plasma renin concentration on the low dose of propranolol suggests the participation of renal vasopressor factors other than renin in this model. 5. A higher dose of propranolol reduced the rise in plasma concentration to an equal extent but the rise of blood pressure at 5 days was also reduced, which supports this concept.


Pharmacology ◽  
2011 ◽  
Vol 87 (5-6) ◽  
pp. 257-264 ◽  
Author(s):  
Zhih-Cherng Chen ◽  
Ja-Ping Shieh ◽  
Hsien-Hui Chung ◽  
Ching-Hsia Hung ◽  
Hung Jung Lin ◽  
...  

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.


2020 ◽  
Vol 19 (4) ◽  
pp. 789-796
Author(s):  
Moon Jain ◽  
Hina Iqbal ◽  
Pankaj Yadav ◽  
Himalaya Singh ◽  
Debabrata Chanda ◽  
...  

Purpose: To determine the effects of lysosomal inhibition of autophagy by chloroquine (CHQ) onhypertension-associated changes in the endothelial functions. Method: Angiotensin II (Ang II)-treated human endothelial cell line EA.hy926 and renovascularhypertensive rats were subjected to CHQ treatment (in vitro: 0.5, 1, and 2.5 μM; in vivo: 50 mg/kg/dayfor three weeks). Changes in the protein expressions of LC3b II (autophagosome formation marker) andp62 (autophagy flux marker) were assessed using immunoblotting. Cell migration assay, tubuleformation assay (in vitro), and organ bath studies (in vivo) were performed to evaluate the endothelialfunctions. Hemodynamic parameters were measured as well. Results: A higher expression of LC3b II and a reduced expression of p62 observed in the Ang II-treatedendothelial cells, as well as in the aorta of the hypertensive rats, indicated enhanced autophagy.Treatment with CHQ resulted in reduced autophagy flux (in vitro as well as in vivo) and suppressed AngII-induced endothelial cell migration and angiogenesis (in vitro). The treatment with CHQ was alsoobserved to prevent increase in blood pressure in hypertensive rats and preserved acetylcholineinducedrelaxation in phenylephrine-contracted aorta from the hypertensive rats. In addition, chloroquineattenuated Ang II-induced contractions in the aorta of normotensive as well as hypertensive rats. Conclusion: These observations indicated that CHQ lowers the blood pressure and preserves thevascular endothelial function during hypertension. Keywords: Angiotensin II, Autophagy, Chloroquine, Endothelial function, Hypertension, Vasculardysfunction


2005 ◽  
Vol 33 (06) ◽  
pp. 913-921 ◽  
Author(s):  
Hung-Che Shih ◽  
Tzu-Hsin Lee ◽  
Shu-Chen Chen ◽  
Chien-Ying Li ◽  
Takeshi Shibuya

This research investigated the anti-hypertension effect of the traditional Chinese medicine (TCM) Ju-Ling-Tang (JLT) on an animal model of hypertension induced by unilateral renal artery ligation. In the study of anti-hypertension effects, 60 minutes after oral administration with NG tube feeding of 240 mg/kg JLT, a significant decrease in blood pressure ( p < 0.05) was observed and sustained till 120 minutes. In the group given 50 mg/kg α-methyldopa orally, the effect was obvious 90 minutes after medication ( p < 0.01), and lasted until 240 minutes. In terms of organ pathology, a significant reduction in the extent of induced glomerular sclerosis was observed in rats given 240 mg/kg JLT compared with the control. From these results, we infer that JLT has a beneficial anti-hypertensive effect on renal hypertension.


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