Decreased Binding Capacity of Central Angiotensin II Receptors Following Long-Term Administration of Angiotensin II

The effect of long-term administration of small amounts of tri-iodothyronine was examined on the nuclear tri-iodothyronine receptors in rat liver. The maximal binding capacity (Cmax.) and association constant (Ka) of the receptors were determined in thyroidectomized rats given vehicle alone (group A), 2μg of tri-iodothyronine/100g body wt. (group B) or 7μg of tri-iodothyronine/100g body wt. (group C) for 2 weeks. Scatchard analyses with correction for the amount of endogenous tri-iodothyronine revealed that Cmax. values per g of liver were increased to 1.5 and 2.7 times the control value in groups B and C respectively. Since concentrations of DNA per g of liver were significantly increased in the two groups of hormone-treated rats, Cmax. values per mg of DNA were nearly the same in group B, but still increased significantly in group C compared with group A. Ka values remained unchanged in all three groups of animals. Mitochondrial α-glycerophosphate dehydrogenase activity was 9.6 and 28.7 times as high in groups B and C, respectively, as in group A. Concentrations of endogenous tri-iodothyronine bound to non-histone protein were substantially increased in groups B and C, although concentrations of serum tri-iodothyronine remained rather low. The results obtained indicate that the long-term administration of tri-iodothyronine in small doses induces an increase in the nuclear receptors associated with increased DNA with and without accompanying a relative increase in the receptor concentration in thyroidectomized rats. Also the hormonal effect is closely related to the total number of the nuclear receptors and the concentrations of nuclear tri-iodothyronine bound to the receptors rather than the serum tri-iodothyronine concentrations.

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The angiotensin II receptor of rabbit liver: characterization in isolated hepatocytes and effect of GTP

Journal of Endocrinology ◽

10.1677/joe.0.1230131 ◽

1989 ◽

Vol 123 (1) ◽

pp. 131-136 ◽

Cited By ~ 6

Author(s):

A. Vandekerckhove ◽

S. Keppens ◽

H. De Wulf

Keyword(s):

Angiotensin Ii ◽

Rate Constant ◽

Plasma Membranes ◽

Binding Capacity ◽

Isolated Hepatocytes ◽

Dissociation Rate ◽

Angiotensin Ii Receptors ◽

Angiotensin Ii Receptor ◽

Binding Characteristics ◽

Binding Data

ABSTRACT A homologous population of specific angiotensin II receptors is present on the cell surface of isolated rabbit hepatocytes. The binding characteristics of [3H]angiotensin II to the cells were: association rate constant (K+1) 0·08 l/nmol per min and dissociation rate constant (K−1) 1·9/min, yielding a dissociation constant (Kd) of 24 nmol/l. A very similar Kd (32 nmol/l) has been derived from saturation binding data which indicate a maximal binding capacity of about 200 000 sites/cell. Analysis of the association binding data to purified liver plasma membranes indicated a Kd of 6 nmol/l in the absence and 30 nmol/l in the presence of GTP. Dissociation was clearly dependent upon the presence of the nucleotide, which shifted the K−1 from 0·12/min to 0·42/min. The studied binding sites are very likely to be involved in the glycogenolytic action of angiotensin II, since a highly significant correlation was established between the biological activity (activation of glycogen phosphorylase) and the binding affinity of a series of agonistic analogues. The reported characteristics of the rabbit hepatic angiotensin II receptors show much similarity with those of rat liver. Journal of Endocrinology (1989) 123, 131–136

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Regulation and Localization of HSP70 and HSP25 in the Kidney of Rats Undergoing Long-Term Administration of Angiotensin II

Hypertension ◽

10.1161/hy1201.096818 ◽

2002 ◽

Vol 39 (1) ◽

pp. 122-128 ◽

Cited By ~ 44

Author(s):

Nobukazu Ishizaka ◽

Toru Aizawa ◽

Minoru Ohno ◽

Shin-ichi Usui ◽

Ichiro Mori ◽

...

Keyword(s):

Angiotensin Ii ◽

Term Administration

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Changes in renal vessels following the long-term administration of an angiotensin II receptor blocker in Zucker fatty rats

Journal of the Renin-Angiotensin-Aldosterone System ◽

10.1177/1470320310387844 ◽

2011 ◽

Vol 12 (2) ◽

pp. 65-74 ◽

Cited By ~ 3

Author(s):

Kazushige Nakanishi ◽

Yohko Nagai ◽

Honglan Piao ◽

Tatsuo Akimoto ◽

Hirohito Kato ◽

...

Keyword(s):

Angiotensin Ii ◽

Receptor Blocker ◽

Angiotensin Ii Receptor Blocker ◽

Angiotensin Ii Receptor ◽

Renal Vessels ◽

Term Administration

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Long-term captopril treatment. Angiotensin II receptors and responses.

Hypertension ◽

10.1161/01.hyp.11.2_pt_2.i148 ◽

1988 ◽

Vol 11 (2_pt_2) ◽

Cited By ~ 26

Author(s):

K M Wilson ◽

W Magargal ◽

K H Berecek

Keyword(s):

Angiotensin Ii ◽

Angiotensin Ii Receptors ◽

Captopril Treatment

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Adrenal Angiotensin II Receptors and Vascular Reactivity to Angiotensin II in the Rat during Continuous Inhibition of Angiotensin Converting Enzyme

Clinical Science ◽

10.1042/cs059065s ◽

1980 ◽

Vol 59 (s6) ◽

pp. 65s-69s ◽

Cited By ~ 5

Author(s):

J. A. Millar ◽

D. J. Casey ◽

C. I. Johnston

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Arginine Vasopressin ◽

Vascular Reactivity ◽

Angiotensin Ii Receptors ◽

Converting Enzyme ◽

Angiotensin Ii Receptor ◽

Vascular Effects ◽

Converting Enzyme Inhibition

1. The effect of continuous infusion of captopril (80 μg/h) for up to 5 days on blood pressure, adrenal angiotensin II receptors and vascular reactivity to exogenous angiotensin II, arginine vasopressin and noradrenaline was studied in the rat. 2. In treated rats, blood pressure decreased transiently to a minimum after 2 days (−18 mmHg). Vascular reactivity to angiotensin II, but not to arginine vasopressin, was also increased significantly after 2 days, but vascular reactivity to noradrenaline decreased. After 5 days, vascular reactivity to angiotensin II had returned to normal and was similar to that of sham-treated controls. Adrenal angiotensin II receptor concentrations decreased significantly after 1 and 2 days, but at 5 days were again similar to controls. There was no change in receptor affinity. 3. Converting enzyme inhibition with captopril causes transient specific changes in adrenal angiotensin II receptors and vascular reactivity. The receptor and vascular effects may facilitate and oppose, respectively, the early changes in blood pressure with captopril, but a long-term contribution from either is unlikely.

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