Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
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Drug
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Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:3.4.23.15 (
renin
)
35,795
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The
renin
-angiotensin system was studied in experimental renal hypertension produced by ligation of the poles of the left kidney followed by contralateral nephrectomy. Plasma
renin
concentration of
renin
substrate was lower and that of
angiotensin I converting enzyme
was higher in hypertensive animals. The juxtaglomerular index decreased in the medial zone of the kidney, while heavily granulated areas appeared in the poles. Ligated kidneys of rats that remained normotensive showed juxtaglomerular indices intermediate between the control and the hypertensive rats. Differences in renal
renin
content between the groups correspond to those for the juxtaglomerular index, but were smaller. No differences between the experimental groups were observed in iso-
renin
content in the brain; however in all animals with ligated kidney poles, hypertensive or normotensive, there was a tendency for iso-
renin
in the adrenals, left ventricular myocardium, and especially aorta to be lower than in controls.
...
PMID:The renin-angiotensin system in rats made hypertensive by ligation of the kidney poles (38584). 16 76
An investigation of the relationship between nephrotensin and the
renin
angiotensin system was carred out. Nephrotensin was found in the plasma of rats with renal clip hypertension and with chemically induced kidney damage. There was no demonstrable correlation between presence of nephrotensin and plasma
renin
activity, and the pressor activity of nephrotensin was not altered by previous immunization of test animals with angiotensin II nor by pretreatment with
angiotensin I converting enzyme
inhibitor. These results indicate that nephrotensin is different from the components of the
renin
-angiotensin system.
...
PMID:Differentiation of nephrotensin from the renin angiotensin system. 16 47
Inhibition of the
angiotensin I converting enzyme
with SQ 20.881 results in a 2 to 35 fold increase in plasma
renin
concentration in normal rats and in spontaneously hypertensive rats. The effect is transient, lasting for 1 to 3 hours even in the presence of prolonged blockade. The relative increase is independent of the pretreatment plasma
renin
concentration. The blood pressure is unchanged in conscious rats in which the effect of SQ 20.881 on plasma
renin
is believed to be due to a blockade of the negative feedback of angiotensin II on
renin
release. In anaesthetized rats, SQ 20.88) has an additional hypotensive effect which augments the increase in plasma
renin
. Saralasin is without effect on blood pressure and plasma
renin
in conscious normal rats and in spontaneously hypertensive rats, while it causes a transient 3 to 27 fold increase in plasma
renin
concentration in anaesthetized rats. It is suggested that this increase is hardly due to an interception of the feedback, but to the concomitant fall in blood pressure, as a similar hypotension and increase in plasma
renin
is produced by dihydralazine. It is furthermore found that Saralasin blocks
renin
release induced by SQ 20.881. This demonstrates that Saralasin is bound to the receptors in the juxtaglomerular cells and has slight, agonistic properties there. Both in conscious rats and in anaesthetized adrenalectomized rats substituted with DOCA and salt, SQ 20.881 as well Saralasin causes transient increases in plasma
renin
concentration. If such rats are only substituted with salt and not with DOCA, the effects of both blockers are in the form of severe hypotension and a permanent elevation of plasma
renin
.
...
PMID:Time course of changes in plasma renin after blockade of the renin-system. Studies of conscious and anaesthetized, normal, adrenalectomized and spontaneously hypertensive rats. 17 Jul 88
Ingibition of the
angiotensin I converting enzyme
with SQ 20,881 results in a rapid marked increase in plasma
renin
concentration in mice. The maximum effect is short-lasting, but the values are still elevated 2 hours after the injection, the time course being similar to that previously found in rats. The relative increase is the same in normal and sialo-adenectomized mice. The plasma
renin
concentration of nephrectomized mice with their submaxillary glands intact is, however, totally uninfluenced by injection of the blocker. This finding indicates that
renin
release from the submaxillary glands is not controlled by the plasma angiotensin II concentration as is that of the
renin
release from the kidneys.
...
PMID:Different effects on renal and submaxillary renin release after blockade of the renin system in mice. 17 13
In 11 healthy, normotensive young women taking contraceptive medication (Enovid) for at least one year, plasma levels of angiotensin II were significantly higher than in healthy male and female controls. No significant difference was seen in the serum activity of angiotensin I-converting enzyme measured in vitro. Although serum
angiotensin I converting enzyme
activity is stimulated in several conditions in which other components of
renin
-angiotensin-aldosterone system are increased, this is not the case during administration of estrogens.
...
PMID:Angiotensin I-converting enzyme and angiotensin II levels in women receiving an oral contraceptive. 17 73
1. A specific method is described for the measurement of
angiotensin I converting enzyme
activity in plasma with 125 I-labelled angiotensin I used as substrate. 2. Converting enzyme activity in plasma from fifteen normal subjects, eleven patients with sarcoidosis, twelve patients with chronic obstructive pulmonary disease and three patients with shock lung was assayed by this technique. 3. Patients with sarcoidosis had increased plasma converting enzyme activity whether or not they were receiving steroid therapy. 4. Patients with chronic obstructive pulmonary disease and shock lung had decreased plasma converting enzyme activity, but extent of conversion did not correlate with the severity of the lung disease. 5. Converting enzyme activity in normal plasma could be completely inhibited by addition of exogenous angiotensin I in 0.5-2.5x107 times physiological concentration. Twice as much exogenous angiotensin I was needed to inhibit conversion completely in plasma from patients with sarcoidosis; one tenth as much in chronic obstructive pulmonary disease. These results indicate that plasma has a high capacity for angiotensin I conversion even in patients with pulmonary parenchymal disease. 6. Results suggest that plasma converting enzyme activity may be a reflection of pulmonary conversion and can be altered by pulmonary disease. 7. Measurement of plasma converting enzyme activity may be useful in studies designed to characterize the regulatory role of converting enzyme in the
renin
-angiotensin system and in cardiovascular homeostasis.
...
PMID:Altered angiotensin I conversion in pulmonary disease. 18 91
The
angiotensin I converting enzyme
has two important functions: it inactivates bradykinin and converts angiotensin I to angiotensin II. Inhibition of the enzyme blocks the
renin
-angiotensin system and decreases systemic blood pressure if the pressure is maintained or increased by
renin
. The enzyme occurs in a variety of tissues and cell forms. The vascular endothelial cells of the lung and of peripheral blood vessels, and the epithelial cells of the kidney tubules are major sources of the enzyme. In addition to inactivating hypotensive peptides and activating a hypertensive one in the systemic circulation, the enzyme may affect organ functions by hydrolyzing peptides that are formed and released locally.
...
PMID:Conversion of angiotensin I to angiotensin II. 19 Aug 81
Tonin, an enzyme present in rat submaxillary gland, converts angiotensin I to angiotensin II and is able to form angiotensin II directly from
renin
substrates. This enzyme was previously shown to be different from
renin
, tissue isorenins, and
angiotensin I converting enzyme
. The specific activity of tonin in rat submaxillary gland increases with the age of the animal and is much higher in male than in female rats; this sex difference is apparent from 60 to 70 days of age. There is a sharp drop of tonin activity in hypophysectomized animals, whereas adrenalectomy, thyroidectomy, and gonadectomy have have little effect. The marked increase in tonin activity was observed in animals bearing MtT-F4 transplantable tumors known to produce ACTH, prolactin, and growth hormone. Tonin specific activity in hypophysectomized male rats is restored to control levels by combined treatment with growth hormone and testosterone. Prolactin alone or in combination with testosterone, as well as transplanted pituitaries, has no effect in hypophysectomized animals. There is a significant specific binding of 125I-labeled growth hormone to isolated membranes of rat submaxillary gland.
...
PMID:Dependence of tonin activity in rat submaxillary gland on growth hormone and testosterone. 19 8
Changes in plasma
renin
activity (PRA) and mean arterial pressure (MAP) produced by renal arterial hypotension were studied in conscious, adrenalectomized dogs maintained on low-, normal-, or high-Na diet during constant steroid replacement therapy. In animals maintained on a low-Na diet, reduction of renal perfusion pressure to 50 mmHg for 45 min increased MAP 40 +/- 3 (SE) mmHg, while PRA rose rapidly by 36.5 +/- 6 ng ml-1 h-1. Similar renal hypotension in dogs maintained on a normal-Na diet increased MAP only 21 +/- 3 mmHg while PRA rose 5.5 +/- 0.9 ng ml-1 h-1; dogs on high-Na intake had a 6 +/- 1 mmHg pressure rise without a significant change in PRA. The rise in MAP correlated well with the log deltaPRA. Calculated open-loop gain was -1.2, -0.7, and -0.1 in dogs on low-, normal-, and high-Na diets, respectively. Nonpeptide
angiotensin I converting enzyme
inhibitor (CEI) reversed the elevated MAP observed during reduction of renal perfusion pressure in dogs on low- and normal-Na diets, but had little effect in dogs on high-Na intake. These observations suggest that the
renin
-angiotensin system becomes quantitatively more important in the regulation of blood pressure as Na intake is reduced.
...
PMID:Renin release and pressor response to renal arterial hypotension: effect of dietary sodium. 19 9
1. Prostaglandin E- and F-like material has been estimated in renal venous blood of the left kidney of anaesthetized rabbits following renal nerve section. Prostaglandins were estimated by bioassay following solvent extraction and column chromatography. 2. Electrical stimulation of the renal nerves of the left kidney to reduce renal blood flow by approximately 15% for 15 min resulted in a significant increase in the concentration of prostaglandin E-like material in the renal venous blood. The peak values were normally seen either in the last 5 min of the stimulation period or in the first 5 min after the end of the stimulation period. The concentration of prostaglandin F-like material was not significantly altered. 3. Similar reduction of renal blood flow of the left kidney by renal artery constriction also resulted in a significant increase in the concentration of prostaglandin E- but not F-like material in renal venous blood. The timing and magnitude of the response was comparable with that observed with renal nerve stimuation. 4. The effect of an
angiotensin I converting enzyme
inhibitor, SQ 20881, on the response to both renal nerve stimulation and renal artery constriction has been studied. The administration of the drug did not significantly reduce the release of prostaglandins from the denervated kidneys, however, the increase in prostaglandin E-like material, in response to both stimuli, was abolished. 5. The results suggest that the increase in prostaglandin E-like material released from the kidney in response to low frequency stimulation or to modest reductions in renal blood flow is dependent on the release of
renin
and that the effect is mediated by the formation of angiotensin II and not angiotensin I.
...
PMID:The effect of angiotensin I converting enzyme inhibitor (SQ 20881) on the release of prostaglandins by rabbit kidney, in vivo. 19 54
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