[Asp1, Val5] Angiotensin-(1–8)octapeptide Does Not Stimulate Aldosterone Secretion in Sodium-Depleted Sheep

1981 ◽  
Vol 61 (1) ◽  
pp. 111-113 ◽  
Author(s):  
B. A. Scoggins ◽  
J. G. McDougall ◽  
Aldona Butkus ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Free Acid ◽  
Acid Form ◽  
Ang Ii ◽  
Aldosterone Secretion ◽  
Arterial Infusion ◽  
Sodium Deficiency ◽  
Amide Form ◽  
Potent Agonist ◽  
Free Acid Form

1. To test the hypothesis that [Asp1,Val5]-angiotensin-(1–8)octapeptide ([Asp1,Val5]ANG II) is a more potent agonist to aldosterone secretion in the sodium-depleted animal than is [Asn1,Val5]angiotensin-(1–8)octapeptide ([Asn1,Val5]ANG II), local adrenal arterial infusion of the two peptides has been carried out in sheep with cervical adrenal autotransplants. 2. Neither [Asp1,Val5]ANG II nor [Asn1,Vak5]-ANG II further stimulated the increased level of aldosterone secretion in conscious moderately sodium-depleted sheep. Greater sodium deficiency further increased aldosterone secretion. 3. The conclusion of Campbell, Schmitz & Itskovitz [Clinical Science (1979), 56, 325–333] that the free acid form of angiotensin II was a more potent agonist of aldosterone secretion than was the amide form under conditions of reduced sodium status is not supported by studies in sodium-depleted sheep.

scholarly journals IMMUNOLOGIC PRODUCTION OF ANTIANGIOTENSIN

1960 ◽  
Vol 111 (3) ◽  
pp. 429-439 ◽  
Author(s):  
Sharad D. Deodhar
Keyword(s):  
Angiotensin Ii ◽  
Protein Complex ◽  
Free Acid ◽  
Biological Action ◽  
Globulin Fraction ◽  
Acid Form ◽  
Angiotensin I ◽  
Precipitin Reaction ◽  
Amide Form ◽  
Free Acid Form

The parenteral administration of benzoylangiotensin II-azo-BGG to rabbits produced an antiserum with antiangiotensin activity. Antiangiotensin inhibited the biological action of p-aminobenzoylangiotensin II, valine5-angiotensin II (free acid form), isoleucine5-angiotensin II and valine5-angiotensin II (amide form), but it was totally inert towards angiotensin 1. Antiangiotensin activity was distinguished from that of serum angiotensinase by the following observations: (a) an angiotensinase-free γ-globulin fraction contained antiangiotensin, (b) angiotensinase inactivated angiotensin II (both the amide and free acid forms) and angiotensin I in contrast to the remarkable specificity for angiotensin II exhibited by antiangiotensin. Serological demonstration of antiangiotensin included: (a) a comparison of its precipitin reaction with the angiotensin BGG complex with the reaction with BGG alone, (b) the partial inhibition of the precipitin reaction with the angiotensin BGG complex by angiotensin II, (c) a precipitin reaction with a different angiotensin II protein complex (cat serum). Angiotensin II administered parenterally as the free polypeptide was not antigenic.

Angiotensin II Analogues and Aldosterone Secretion in Sodium-Deficient Sheep

1976 ◽  
Vol 51 (s3) ◽  
pp. 325s-327s
Author(s):  
J. R. Blair-West ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
H. D. Niall ◽  
B. A. Scoggins ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Agonist Activity ◽  
Converting Enzyme ◽  
Aldosterone Secretion ◽  
Arterial Infusion ◽  
Sodium Deficiency ◽  
Converting Enzyme Inhibitor ◽  
Angiotensin Ii Analogues ◽  
Permissive Role

1. The angiotensin analogues Sar1-Ala8-angiotensin II (AII), Sar1-Ile8-AII, Sar1-Leu8-AII, Sar1-Thr8-AII, [Des1-Asp]-Ile8-AII and [Des1-Asp]-Sar2-Ile8-AII and converting enzyme inhibitor (SQ 80221) infused by intra-adrenal arterial infusion had no effect on aldosterone secretion in sodium-deficient sheep at doses in excess of those shown to block exogenous angiotensin II or III infusion. 2. It is suggested that the intrinsic agonist activity of the analogues may fulfil the requirements for a permissive role for angiotensin in the aldosterone response to sodium deficiency.

Effect of adrenal arterial infusion of P-113 on aldosterone secretion in Na-deficient sheep

1979 ◽  
Vol 236 (4) ◽  
pp. F333-F341
Author(s):  
J. R. Blair-West ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
K. J. Hardy ◽  
B. A. Scoggins ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Renin Angiotensin System ◽  
Blood Levels ◽  
Aldosterone Secretion ◽  
Arterial Infusion ◽  
Sodium Deficiency ◽  
Arterial Blood ◽  
Conscious Sheep

To examine the role of the renin-angiotensin system in aldosterone regulation, P-113 ([Sar1,Ala8]angiotensin II) was infused into the arterial blood supply of the transplanted adrenal gland in conscious sheep. Effects on the aldosterone response to infused angiotensin II and III in sodium-replete sheep were compared with effects of P-113 on aldosterone secretion in sodium deficiency. P-113 infusion up to 1,000 microgram/h for 1-2 h did not consistently alter aldosterone secretion in sodium-deficient sheep. However, in sodium-replete sheep P-113 infusion for 20 min at 10 microgram/h or more abolished aldosterone responses to high blood levels of angiotensin II and III produced by systemic intravenous or adrenal intra-arterial infusion. P-113 infusions alone had minor agonist activity on aldosterone secretion in sodium-replete sheep. These results indicate that the increased secretion of aldosterone in Na-depleted sheep is not simply and commensurately determined by increase of angiotensin II and III concentration in the arterial blood perfusing the adrenal gland.

An ATP-sensitive conductance in cultured smooth muscle cells from pregnant rat myometrium

1989 ◽  
Vol 257 (2) ◽  
pp. C297-C305 ◽  
Author(s):  
E. Honore ◽  
C. Martin ◽  
C. Mironneau ◽  
J. Mironneau
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Voltage Clamp ◽  
Free Acid ◽  
Muscle Cells ◽  
Monovalent Cation ◽  
Acid Form ◽  
Pregnant Rat ◽  
Free Acid Form ◽  
Cultured Smooth Muscle Cells

The whole cell voltage-clamp technique was used to study the effects of extracellular ATP in cultured smooth muscle cells isolated from pregnant rat myometrium. An inward current was elicited by ATP (IATP) in cells held at -70 mV under voltage clamp. The amplitude of IATP was reduced by estrogen pretreatment and by the end of pregnancy. IATP not only did not undergo any desensitization but showed facilitation. The current-voltage relationship of IATP was linear and reversed close to 0 mV. Changing the sodium electrochemical gradient by decreasing extracellular or intracellular sodium resulted in a linear relationship between the reversal potential of IATP and Na equilibrium potential that, however, differed from the predicted curve for a purely sodium conductance. The conductance activated by ATP was monovalent cation selective with little discrimination between potassium, cesium, and sodium ions. IATP was depressed by divalent cations, and the rank order of potency was Co greater than Mg greater than Ca greater than Ba, suggesting that the free-acid form of ATP was the effective ligand. Adenosine, AMP, and ADP were ineffective in eliciting IATP, whereas ATP gamma S and alpha,beta-methylene ATP were capable of mimicking the effects of ATP, although they were less potent. These results are consistent with the free-acid form of ATP activating a monovalent cation-selective and estrogen-sensitive conductance in myometrium.

Effects of blockade of brain angiotensin II receptors in conscious, sodium-deprived dogs

1983 ◽  
Vol 245 (6) ◽  
pp. R881-R887 ◽  
Author(s):  
V. L. Brooks ◽  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Intravenous Infusion ◽  
Plasma Renin ◽  
Hypotensive Effect ◽  
Similar Degree ◽  
Central Action ◽  
Ang Ii ◽  
Sodium Deficiency ◽  
Low Sodium Diet

The present studies were designed to evaluate the physiological significance of the actions of angiotensin II (ANG II) on the brain. The effects of blockade of brain ANG II receptors by intracarotid or intravertebral infusions of saralasin were studied in conscious dogs with high circulating ANG II levels (142 +/- 16 pg/ml) due to a low-sodium diet. Three doses of saralasin were infused into each pair of arteries and intravenously: 0.1, 0.3, and 1.0 micrograms X kg-1 X min-1. Saralasin produced dose-related decreases in arterial pressure during infusion into the carotid or vertebral arteries, confirming that ANG II maintains arterial pressure during sodium deficiency. However, intravenous saralasin administration decreased pressure to a similar degree, suggesting that the hypotensive effect was due to recirculation of saralasin, rather than to blockade of a central action of circulating ANG II. Heart rate was not altered by infusion of saralasin by any route. Saralasin administration also caused a dose-dependent increase in plasma renin activity and plasma ANG II concentration. However, because the increases produced by intracarotid or intravertebral saralasin did not differ from the increase produced by intravenous infusion, these results do not provide evidence that renin release is modulated by a central action of ANG II during sodium deficiency. Plasma corticosteroid levels were reduced (2.4 +/- 0.5 to 1.4 +/- 0.2 micrograms/dl, P less than 0.05) by intravenous infusion of the highest dose of saralasin, but neither intracarotid nor intravertebral saralasin infusion altered plasma corticosteroid concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

ChemInform Abstract: Novel Solid-State 8H+-Heteropolyacid. Synthesis and Molecular Structure of a Free-Acid Form of a Dawson-Type Sandwich Complex, [Ti2{P2W15O54 (OH2)2}2]8-.

ChemInform ◽  
2008 ◽  
Vol 39 (7) ◽  
Author(s):  
Hideyuki Murakami ◽  
Kunihiko Hayashi ◽  
Ikuo Tsukada ◽  
Takeshi Hasegawa ◽  
Shoko Yoshida ◽  
...  
Keyword(s):  
Molecular Structure ◽  
Solid State ◽  
Free Acid ◽  
Acid Form ◽  
Sandwich Complex ◽  
Free Acid Form

Ratio confocal imaging of free cytoplasmic calcium gradients in polarising and polarisedFucuszygotes

Zygote ◽  
1993 ◽  
Vol 1 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Frederic Berger ◽  
Colin Brownlee
Keyword(s):  
Cell Division ◽  
Brown Alga ◽  
Free Acid ◽  
Confocal Imaging ◽  
Acid Form ◽  
Cytoplasmic Calcium ◽  
Molecular Weights ◽  
Free Acid Form ◽  
Marine Brown Alga ◽  
Calcium Green

SummaryIn the marine brown alga,Fucus, two poles are differentiated before cell division determining the future rhizoid or thallus. We have used a combination of the Ca2+-sensitive dye Calcium Green and the pH-sensitive dye SNARF monitored at pH-insensitive wavelengths to obtain confocal ratio images of free cytoplasmic calcium distribution at different stages in polarisingFucuszygotes. These dyes have the advantage that they can be used in most confocal microscopes and their longer excitation wavelengths greatly reduce autofluorescence problems. Dyes of varying molecular weights (free acid form, 10 000 mol.wt or 70 000 mol.wt dextran-conjugated) were pressure microinjected into early zygotes which were allowed to polarise in unidirectional light. Dextran-conjugated dyes remained non-compartmentalised and fluorescence could be monitored for up to 3 days following microinjection. Currently we have been able to detect Ca2+gradients at the tip of the rhizoid, confirming earlier results. Localised Ca2+elevations have also been observed at the rhizoid pole of the polarising zygote before the onset of rhizoid germination. Limitations of this technique and the significance of these Ca2+gradients are discussed.

Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation

1986 ◽  
Vol 250 (6) ◽  
pp. R960-R972 ◽  
Author(s):  
J. E. Hall
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Pressure Control ◽  
Ang Ii ◽  
Aldosterone Secretion ◽  
Body Fluid Volume ◽  
Proximal Tubular ◽  
Renal Medullary Blood Flow ◽  
Pressure Natriuresis

Angiotensin II (ANG II) is one of the body's most powerful regulators of Na excretion, operating through extrarenal mechanisms, such as stimulation of aldosterone secretion, as well as intrarenal mechanisms. Considerable evidence suggests that the intrarenal actions of ANG II are quantitatively more important than changes in aldosterone secretion in the normal day-to-day regulation of Na balance and arterial pressure. ANG II at physiological concentrations increases proximal tubular reabsorption, but further studies are needed to determine whether ANG II also has an important effect on more distal tubular segments. ANG II also markedly constricts efferent arterioles, tending to increase Na reabsorption by altering peritubular capillary physical forces and also helping to prevent excessive decreases in glomerular filtration rate. ANG II may also decrease Na excretion and increase urine concentrating ability by reducing renal medullary blood flow. Regulation of Na excretion by ANG II is closely linked with arterial pressure control and volume homeostasis through the renal pressure natriuresis mechanism. Under many physiological conditions, such as changes in Na intake, ANG II greatly multiplies the effectiveness of the pressure natriuresis mechanism to prevent fluctuations in body fluid volume and arterial pressure. In circumstances associated with circulatory depression, such as decreased cardiac function, reductions in blood pressure and increased ANG II formation cause Na retention until arterial pressure is restored to normal. However, in pathophysiological conditions in which ANG II is inappropriately elevated, increased arterial pressure (hypertension) is required for the kidney to "escape" the potent antinatriuretic actions of ANG II and to return Na excretion to normal via the pressure natriuresis mechanism.

Pressor action and dipsogenicity induced by angiotensin II and III in rats

1985 ◽  
Vol 249 (5) ◽  
pp. R514-R521 ◽  
Author(s):  
J. W. Wright ◽  
S. L. Morseth ◽  
R. H. Abhold ◽  
J. W. Harding
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Receptor Site ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Direct Stimulation ◽  
Arterial Infusion ◽  
Appropriate Treatment ◽  
Angiotensin Iii ◽  
Stimulation Of

The primary brain sites responsible for angiotensin-induced pressor action and dipsogenicity in the laboratory rat appear to be located in forebrain circumventricular organs (CVO). Because CVOs have a reduced blood-brain barrier, intracarotid infusion of angiotensin via a brachial arterial catheter results in direct stimulation of these sites. This investigation determined that brachial arterial infusion of angiotensin II (ANG II) into alert free-moving rats resulted in pressor and dipsogenic responses greater than those observed with equivalent doses of angiotensin III (ANG III). However, intracerebroventricular (ICV) injections of ANG II and ANG III yielded equivalent pressor and drinking responses. ICV pretreatment with the specific angiotensin receptor antagonist [Sar1, Ile8]-ANG II significantly reduced ANG II- and ANG III-induced pressor and drinking responses. This inhibition lasted approximately 20 min with recovery at 60-70 min. The results indicate that ICV-administered ANG III is a much more potent ligand than previously determined if the stickiness due to electrical charge of this compound is prevented by appropriate treatment of glassware. The receptor antagonist results encourage the possibility that ANG II and ANG III activate a common central receptor site.

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