Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intraperitoneal application of p-chloroamphetamine (PCA) is considered a suitable probe for investigation of central serotoninergic control on renin release in the rat, although it causes several behavioral and autonomic changes including negative water balance (increased urination and loss of body weight). The possibility that PCA-induced renin release is secondary to the alterations in water balance was investigated 1 hour after intraperitoneal PCA in male Wistar (Wi) (Experiment I). Long-Evans (LE) and diabetes insipidus (DI) (Experiment II), DI rats pretreated by the inhibitor of angiotensin I-converting enzyme captopril (Experiment III), and water-loaded or propranolol-pretreated Wi rats (Experiment IV). PCA treatment induced significant body weight loss, increase in hematocrit, stimulation of renin-aldosterone system (RAS) and elevation of plasma creatinine level. A toxic damage of the kidney and liver was documented histologically 72 h after 5 mg/kg PCA in Wi rats. The blockade of PCA-induced stimulation of RAS (by captopril or propranolol) markedly potentiated the attendant negative water balance, whereas positive water balance (oral water load) abolished PCA-induced renin secretion. In conclusion, intraperitoneal PCA is an unsuitable probe for investigation of central serotoninergic control on renin release in the rat since PCA-induced renin release is caused by the attendant negative water balance.
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PMID:Peripheral p-chloroamphetamine is an unsuitable probe for investigation of central serotoninergic control on renal renin secretion in the rat. 189 93

Angiotensin infusion increased glucose metabolism in 4 of 7 subdivisions of the rat subfornical organ, the effect being stronger in ventromedial compared to dorsolateral zones across the rostrocaudal axis. [Sar1-Leu8]Angiotensin II attenuated metabolic responses to intravenous angiotensin in all subfornical organ subregions. Brattleboro rats, having high circulating levels of angiotensin, displayed greater rates of glucose metabolism than Long-Evans rats in all subregions, differences that were eliminated by captopril, an inhibitor of angiotensin converting enzyme. The studies reveal focal subfornical organ zones where in vivo metabolic activity corresponds to cytoarchitectonic evidence for topographical processing within this angiotensin-sensitive structure.
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PMID:Focal metabolic effects of angiotensin and captopril on subregions of the rat subfornical organ. 219 50

The effect of stimulation of the cervical sympathetic ganglia on the upper limit of cerebral blood flow (CBF) autoregulation was studied in normotensive Wistar-Kyoto rats (WKY) and in spontaneously hypertensive rats (SHR) following intravenous administration of the angiotensin converting enzyme inhibitor captopril (10 mg/kg). CBF was measured using the intracarotid 133Xe injection method in halothane/nitrous oxide anaesthetized WKY and SHR. Arterial blood pressure was raised stepwise by the intravenous infusion of noradrenaline. Toward the end of the study, Evans blue was injected and the brains examined for gross blood-brain barrier breakdown. In SHR, sympathetic stimulation reextended the upper limit of CBF autoregulation, which was at a mean arterial blood pressure level of 120-139 mm Hg in the control group of eight SHR and above 170 mm Hg in the stimulated group of nine SHR. In the group of nine WKY subjected to sympathetic stimulation, the upper limit of CBF autoregulation was reached at a mean arterial blood pressure level of 110-129 mm Hg as opposed to 90-109 mm Hg in a previous unstimulated group of WKY. In the two groups subjected to sympathetic stimulation, there was no extravasation of Evans blue in any of the brains. In the control group of SHR, in which there had been marked increases in CBF, three out of eight brains had foci with extravasation of the dye. It is concluded that in normotensive and in hypertensive rats sympathetic stimulation attenuates the downward shift of the upper limit of CBF autoregulation, which is known to accompany intravenous administration of captopril.
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PMID:Angiotensin converting enzyme inhibition and the upper limit of cerebral blood flow autoregulation: effect of sympathetic stimulation. 265 65

The contribution of vasopressin and angiotensin II to the maintenance of blood pressure after short-term autonomic blockade was investigated in conscious Long-Evans and Brattleboro (vasopressin-deficient; hereditary diabetes insipidus) rats. After short-term autonomic blockade by atropine (1 mg/kg), propranolol (5 mg/kg), and pentolinium (5 mg/kg and 10 mg/kg/hr), the fall in blood pressure was significantly greater in Brattleboro rats than in Long-Evans rats (48 +/- 3 vs 32 +/- 2 mm Hg; p less than 0.01). Administration of the vasopressin vascular receptor antagonist D(CH2)5Tyr-(Me)AVP (2 micrograms/kg) caused further blood pressure decreases only in Long-Evans rats, so that the final blood pressure in both groups was identical. Administration of enalaprilat (10 mg/kg), an angiotensin converting enzyme inhibitor, further reduced blood pressure in both strains. When enalaprilat was given first after autonomic blockade, it reduced blood pressure in Brattleboro rats but not in Long-Evans rats. Administration of the vasopressin antagonist after enalaprilat further reduced blood pressure only in Long-Evans rats. The fall in blood pressure following vasopressin blockade was greater than that occurring after angiotensin converting enzyme inhibition (14 +/- 1 vs 6 +/- 1 mm Hg; p less than 0.05) in autonomic blockade Long-Evans rats. Plasma levels of vasopressin in Long-Evans rats increased markedly after short-term autonomic blockade, whereas plasma renin and angiotensin II levels were unchanged. Plasma angiotensin II levels were increased by the vasopressin antagonist and decreased by enalaprilat. We conclude that, due to sympathetic nervous system blockade and consequent blunting of renal renin release, vasopressin has a greater capacity than the renin-angiotensin system for maintaining blood pressure after short-term autonomic blockade.
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PMID:The contribution of vasopressin and angiotensin to the maintenance of blood pressure after autonomic blockade. 298 71

The activity of the angiotensin-converting enzyme (ACE) (kininase II, EC 3.4.15.1) was examined in 5 discrete hypothalamic nuclei of rats lacking vasopressin (homozygous Brattleboro rats, DI, di/di) and their corresponding controls (heterozygous Brattleboro rats, HZ, di/+, and Long Evans, LE, +/+ rats), with and without hormonal replacement with arginine-vasopressin (AVP). DI rats showed a vasopressin-reversible increased ACE activity when compared with LE controls, HZ rats showing intermediate activity. These changes occurred only in the supraoptic and periventricular hypothalamic nuclei, and were absent in other hypothalamic areas studied, including the paraventricular nucleus. These results provide biochemical evidence in support of previous anatomical and physiological data, for an interaction between the brain vasopressin and angiotensin systems in discrete hypothalamic nuclei, and suggest that vasopressin could regulate the formation of brain angiotensin II by modulating the activity of the converting enzyme.
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PMID:Vasopressin-reversible increase in angiotensin-converting enzyme in specific hypothalamic nuclei of Brattleboro rats. 628 72

We studied the activity of angiotensin I converting enzyme (ACE, kininase II, E.C. 3.4.15.1) in discrete areas of the brainstem and limbic system, and in circumventricular organs, pineal gland and choroid plexus of homozygous Brattleboro rats (DI) which are characterized by vasopressin deficiency and diabetes insipidus, with or without vasopressin replacement. We also determined ACE activity in heterozygous Brattleboro (HZ) and Long-Evans (LE) control rats. We found changes in ACE activity in several brain areas and the pineal gland of Brattleboro rats. ACE activity was increased in DI rats with respect to HZ and LE controls in the A1 area of the brainstem, locus coeruleus, and triangular nucleus of the septum. ACE activity in the A2 area of the brainstem, the nucleus tractus spinalis nervi trigeminii and the pineal gland was enhanced in both HZ and DI rats with respect to that of LE controls, but was not different between HZ and DI rats. ACE activity did not change in the other extrahypothalamic areas studied. The elevated ACE activity in extrahypothalamic areas of DI rats was not reversed by vasopressin replacement. These results suggest that a relationship between central vasopressin and angiotensin or bradykinin systems may exist in selective extrahypothalamic areas of the rat brain, and that peripherally administered vasopressin cannot influence this relationship.
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PMID:Selective increase of angiotensin-converting enzyme activity in discrete extrahypothalamic areas of Brattleboro rats. 631 41

An angiotensin I-converting enzyme inhibitor (captopril) was given by gastric lavage at a dose of 30 mg/kg body weight per day to Long-Evans rats for a 13-day period during which they received a sodium-deficient diet. This regime was preceded by a 3-day period during which measurements were made on the animals on a sodium-replete dietary intake. Control sodium-deprived rats showed increased plasma renin activities, increased peripheral aldosterone concentrations and reduced urinary sodium excretion; they maintained positive sodium balance and the zona glomerulosa of the adrenal cortex hypertrophied. Captopril-treated sodium-deprived rats failed to reduce urinary sodium excretion sufficiently and entered a period of marked and sustained negative sodium balance. Peripheral aldosterone concentrations after 12 days of sodium deprivation in the presence of captopril treatment were similar to those of sodium-replete rats. The adrenocortical zona glomerulosa of the captopril-treated rats did not increase in size and regressive changes were noted.
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PMID:Influence of captopril on fluid and electrolyte balances and adrenocortical responses during sodium deprivation in the rat. 634 99

The purpose of this study was to determine the effects of bradykinin (BK), substance P (SP) and histamine on plasma exudation in the skin of conscious dogs with and without pacing-induced heart failure. We also determined the role tissue angiotensin I-converting enzyme (ACE) and neutral endopeptidase (NEP) play in modulating these responses. We found that intradermal injection of BK, SP and histamine induced a significant, concentration-dependent Evans blue exudation in normal dogs (p < 0.05). Bradykinin-induced responses were significantly potentiated by captopril (p < 0.05). In contrast, phosphoramidon potentiated BK-induced responses only at low concentrations of BK. Both captopril and phosphoramidon had no significant effects on SP- and histamine-induced Evans blue exudation. BK- and SP-induced responses were significantly attenuated, whereas histamine-induced Evans blue exudation was significantly potentiated in dogs with heart failure. We conclude that heart failure is associated with attenuation of BK- and SP-, but not histamine-induced plasma exudation in the peripheral microcirculation and that these responses are not modulated by tissue ACE and NEP.
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PMID:Plasma exudation in conscious dogs with experimental heart failure. 753 20

We used Evans blue dye to assess the effects of bradykinin on vascular extravasation in nasal mucosa of pathogen-free F344 rats. There was a dose-dependent increase in Evans blue extravasation when bradykinin was delivered by topical instillation in the nose (doses, 25-100 nmol). Only the highest intravenous doses (2 and 5 mumol/kg) of bradykinin caused increased extravasation. When bradykinin was delivered by either route, its effect on extravasation was exaggerated by pharmacological inhibition of the enzymes neutral endopeptidase (NEP) and kininase II [angiotensin-converting enzyme (ACE)]. When bradykinin was instilled locally, the effect of NEP inhibition was predominant; when bradykinin was injected intravenously, the effect of ACE inhibition was predominant. The mechanism of extravasation also varied with the mode of bradykinin delivery: when bradykinin was instilled locally in the nose, the selective neurokinin 1 (NK1) receptor antagonist CP-96,345 markedly inhibited the response, whereas it had no effect on Evans blue extravasation when bradykinin was injected intravenously. We conclude that bradykinin causes dose-related increases in Evans blue dye extravasation in the nose and that these effects are exaggerated when NEP and ACE are inhibited. Topically instilled bradykinin causes vascular extravasation to a large extent via NK1 receptor stimulation, thus suggesting a major role for tachykinins released from sensory nerve endings.
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PMID:Role of peptidases and NK1 receptors in vascular extravasation induced by bradykinin in rat nasal mucosa. 839 2

The increase in vascular permeability associated with neurogenic inflammation in the nasal mucosa is mediated by neuropeptides such as substance P released from sensory nerves. Substance P is degraded by the peptidases neutral endopeptidase-24.11 (NEP-24.11) and angiotensin converting enzyme (ACE). In the present study, we used capsaicin to produce neurogenic inflammation in the nasal mucosa of rats, and we examined the effect of inhibition of NEP-24.11 by phosphoramidon, inhibition of ACE by captopril or inhibition of both enzymes by giving both inhibitors. Using as tracers intravenous Evans blue dye to quantify the extravasation and Monastral blue pigment to localize the sites of leakage, we examined the magnitude and distribution of capsaicin-induced plasma extravasation in the nasoturbinates, maxilloturbinates, ethmoidal turbinates and septum. Capsaicin caused a dose-dependent increase in Evans blue extravasation in the naso- and maxilloturbinates but had only a slight effect in the septum. The leaky blood vessels responsible for this plasma extravasation, as manifested by Monastral blue labeling, were most numerous in the naso- and maxilloturbinates, particularly near the front and free borders. After phosphoramidon, the leakage of Monastral blue was more widespread and extended in a more caudal direction. The response to capsaicin was augmented by phosphoramidon alone but not by captopril alone. However, in the presence of phosphoramidon, captopril further augmented the capsaicin-induced extravasation. We conclude that neurogenic inflammation in the rat nasal mucosa is greatest in the naso- and maxilloturbinates and can be modulated by NEP-24.11 and, to a lesser extent, by ACE.
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PMID:Neurogenic plasma extravasation in the rat nasal mucosa is potentiated by peptidase inhibitors. 842 49


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