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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Angiotensin has previously been shown to inhibit distal renal tubular sodium reabsorption. As a consequence of this, or independently, it might influence the distal handling of other electrolytes. We have therefore examined the effects of angiotensin on the distal reabsorption or secretion of a spectrum of electrolytes. 2. Standard bilateral stop-flow studies were done on anaesthetized, adrenalectomized rabbits, in which the effects of intravenous infusions of either 0-02-0-05 mug min-1 kg-1 or 1 mug min-1 kg-1 of angiotensin were compared with control stop-flow results. 3. The lower dose of angiotensin inhibited distal sodium, chloride, water and magnesium reabsorption, inhibited distal hydrogen secretion and stimulated distal potassium secretion. The higher dose of angiotensin produced these changes and additionally inhibited distal calcium reabsorption. Most of the observed changes were dose-related. The low dose of angiotensin did not significantly raise blood pressure but the high dose was pressor. 4. Changes in the stop-flow patterns induced by the higher dose of angiotensin were compatible with, and may help to explain, the changes it produced in urinary excretion of sodium, chloride, potassium, magnesium and calcium in clearance studies before stop-flow. Suppression of hydrogen secretion caused by both doses of angiotensin in the stop-flow studies was also reflected by reductions in acid excretion produced by these infusion rates in additional experiments performed by clearance methods in acid-loaded, conscious rabbits. 5. The results support the view that angiotensin may have an important intrarenal role, at least in rabbits.
Clin Sci Mol Med 1976 Feb
PMID:Multiple changes in distal stop-flow electrolyte patterns and reduction of acid excretion induced in rabbits by angiotensin. 0 4

1. A colorimetric method was developed for the direct chemical assay of human carboxypeptidase A (carboxypolypeptidase; EC 3.4.12.2) with angiotensin converting enzyme-like activity in serum or plasma, with the substrate analogue glycyl-L-histidylglycine and the angiotensin converting enzyme substrate angiotensin I (A-I). This method was based on the spectrophototometric determination of histidylglycine and histidyl-leucine, products of the hydrolysis of glycyl-L-histidylglycine and A-I respectively. omicron-Phthalaldehyde reacted with the imidazole moiety of nu-terminal histidyl peptides to produce a yellow chromophore. 2. A large number of inhibitors were tested for their effects on carboxypolpeptidase activity. The hydrolysis of Gly-His-Gly and A-I was inhibited by histidyl-leucine and angiotensin II, both products of the hydrolysis of A-I. Bothrops jararaca venom extract, EDTA, rho-chloromercuribenzoate, 8-hydroxyquinoline and 2,3-dimercaptopropanol, previously reported as converting enzyme inhibitors, also inhibited carboxypolypeptidase activity. 3. Angiotensin converting enzyme activity in the serum of sixty-six adults ranged from 10 to 37 nmol of glycyl-L-histidylglygine hydrolysed in 10 min by 10 mu1 of serum at 37 degrees C and pH 7-25.
Clin Sci Mol Med 1976 May
PMID:The spectrophotometric determination of human serum carboxypolypeptidase with angiotensin converting enzyme-like activity. 17 49

1. 3H-labelled angiotensin II specfically binds to plasma membranes of rat uterine smooth muscle cells. Two classes of binding sites differing in their affinity for the hormone were demonstrated. The high-affinity binding sites (KD 29 degrees C approximately 2.0 X 10(-8) mol/l) probably correspond to the receptors involved in the biological response. 2. Bilateral nephrectomy significantly increases the concentration of 3H-labelled angiotensin-binding sites, a phenomenon which seems unrelated to the freeing of receptor sites secondary to the suppression of plasma angiotensin. This phenomenon may be responsible for the specific hypersensitivity in vitro to angiotensin of uteri excised in anephric rats as compared with normal rats. 3. Angiotensin II infusion in nephrectomized rats reduced the concentration of 3H-labelled angiotensin-binding sites. 4. It is suggested that the angiotensin receptor concentration is regulated by the concentration of circulating angiotensin.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Angiotensin-induced variations of receptors in rat uterine membranes. 21 Sep 90

1. Angiotensin II receptors from rat adrenal gland and myometrium were studied during variation of sodium intake. 2. In both target-tissues low Na+ diet increased the number of receptors whereas a high Na+ diet did not modify the adrenocortical receptors but increased the number of uterine receptors. 3. Deoxycorticosterone and one kidney Goldblatt hypertension were associated with a decrease in the number of adrenal receptors. 4. Alterations of angiotensin II receptors alone cannot explain satisfactorily the variations of sensitivity of target-cells to angiotensin II during sodium balance changes.
Clin Sci Mol Med Suppl 1978 Dec
PMID:Alterations of adrenal and uterine angiotensin II receptors during variation of sodium intake and/or experimental hypertension. 21 72

1. Angiotensin II blockade before and after marked sodium depletion in patients with hypertension [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar1-Ala8-angiotensin II (saralasin). 2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respectively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity. 3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension subgroups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate decreased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion. 4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently independent of the aetiology of the hypertension. The decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.
Clin Sci Mol Med 1978 Jan
PMID:Angiotensin II blockade before and after marked sodium depletion in patients with hypertension. 62 Apr 96

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.
Clin Sci Mol Med 1978 Jun
PMID:Effect of administration of Sar1-Ala8-angiotensin II during the development and maintenance of renal hypertension in the rat. 65 33

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.
Clin Sci Mol Med 1977 Sep
PMID:Potentiation of pressor effects of noradrenaline and potassium ions in the rat mesenteric arteries by physiological concentrations of angiotensin II: effects of prostaglandin E2 and cortisol. 91 46

1. A method for extraction, partial purification and radioimmunoassay of angiotensin II in tissues and application of the method to the kidneys of sodium-deficient rats are described. 2. Angiotensin in acid-ethanol extracts of kidney were adsorbed on to a cation-exchange resin, eluted and further purified with an immobilized angiotensin II antiserum, before radioimmunoassay. 3. Thin-layer chromatography was used, in some experiments, to separate fmol amounts of angiotensin II from its immunoreactive peptide fragments before radioimmunoassay. 4. Angiotensin II-immunoreactive material isolated from rat kidney resembled angiotensin II in many of its physicochemical properties and chromatographic mobility. 5. The concentration of immunoreactive material in kidney greatly exceeded that which could be accounted for by trapped blood and suggests that the peptide may have a local role in the organ.
Clin Sci Mol Med 1976 Aug
PMID:A method for measurement of angiotensin II in tissues and its application to rat kidney. 95 57

1. Central and peripheral haemodynamic effects of intravenous infusion of angiotensin II have been investigated in ten normotensive subjects. Angiotensin II was given at the rate of 0-12-5-0 microng/min. 2. The pressor response to angiotensin II was accompanied by a significant increase in the total peripheral resistance, central venous pressure and by a marked reduction of the intravascular forearm volume and venous distensibility. Forearm circulation time was shortened. 3. Cardiac index, heart rate, forearm vascular resistance and the forearm blood flow did not change significantly in the whole group but in the individual subjects some of the variables changed markedly in either direction. 4. Direct action of angiotensin II on the vessels and its central and peripheral sympathomimetic aciton as well as the role of the baroreflex as responsible causes for haemodynamic changes after angiotensin II are discussed.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The effect of intravenous angiotensin II on the peripheral circulation with particular reference to its bearing on general haemodynamics. 107 12

1. The arteriolar lesions of rats with deoxycorticosterone (DOCA)-salt hypertension have been studied by colloidal carbon injection and light- and electron-microscopy. 2. Colloidal carbon particles enter the media of arterioles to form focal deposits when hypertension develops. 3. The focal lesions are similar to those seen after angiotensin infusion or renal artery constriction. They are characterized by endothelial damage and plasma deposition in the media. 4. Heavy deposition of carbon in the glomeruli of DOCA-treated animals was found to be caused by increased mesangial uptake and not by hypertensive vascular damage. 5. Angiotensin II concentrations fell during the development of hypertension and vascular lesions. The renin-angiotensin system was not implicated in the development of vascular damage in this form of hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:The arteriolar lesions of steroid hypertension in rats. 107 33


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