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)

In vivo administration of L-thyroxine (L-T4) in Anabas testudineus, while significantly stimulated the activities of cytochrome c oxidase and alpha-glycerophosphate dehydrogenase (alpha-GPDH), inhibited glucose-6-phosphate dehydrogenase (G-6-PDH), cytosolic and mitochondrial malate dehydrogenase (cyt. MDH; mit. MDH), and Mg2+ DNP-dependent adenosine triphosphatase (Mg2+ ATPase) activities. The activities of lactate dehydrogenase (LDH), succinate dehydrogenase (SDH), and catalase remained unaltered after L-T4 treatment. Administration of protein synthesis inhibitors such as actinomycin D, while significantly inhibited cytochrome oxidase, alpha-GPDH, catalase, SDH, and Mg2+ ATPase activities, did not change LDH, cyt. MDH, and mit. MDH activities. Chloramphenicol injection significantly stimulated cytochrome oxidase, alpha-GPDH, and G-6-PDH activities. Simultaneous injections of actinomycin D or chloramphenicol with 3,5,3'-triiodo-L-thyronine (L-T3) or L-T4 prevented the effects of thyroid hormones on enzyme activities, when compared to the respective controls.
Gen Comp Endocrinol 1989 Jan
PMID:Oxidative metabolism in a teleost, Anabas testudineus Bloch: effect of thyroid hormones on hepatic enzyme activities. 292 Sep 3

The evidence presented here suggests strongly that the kallikreins-kininogens-kinins-kininase II system has most significant role in regulation of systemic BP. This system is involved in mediation and modulation of renin-angiotensin-aldosterone, PGS and vasopressin in the regulation of sodium water balance, renal hemodynamic and BP. Therefore, reduction in the kinin-formation due to high production of kininase II, and lower formation of tissue kallikrein might result in an increased release of vasoconstrictor angiotensin II on one side, and on the other side much reduced production of PGE, vasodilator. These changes might lead to deranged vascular smooth muscle structures and cell membrane functions, retention of sodium and water, increased plasma volume, and renovascular constriction. These physiological defects might result in the development of essential hypertension (Fig. 4). Although, it is possible now to treat hypertensive conditions with tissue kallikrein and kininase II inhibitors. These discoveries have opened up new vistas to research on the pharmacological applications of kallikreins-kininogens-kinins-kininases in human diseases.
Gen Pharmacol 1988
PMID:Interrelationship between the kallikrein-kinin system and hypertension: a review. 328 Mar 99

Plasma ions and cortisol levels were measured sequentially during the adaptation of European eels (Anguilla anguilla) from fresh water (FW) to sea water (SW). The importance of the renin-angiotensin system in the regulation of this adaptation was assessed using captopril (SQ14225, an inhibitor of angiotensin I-converting enzyme). The effects of captopril on renal function in FW- and SW-adapted trout were also examined. During the first 5 hr in sea water, plasma levels of cortisol in eels increased threefold, plasma sodium rose steadily from 137 to 156 mmol/l and plasma potassium fell from 2.1 to 1.6 mmol/l. In contrast, captopril-treated eels when adapted to sea water had plasma cortisol levels twice those of controls. Captopril treatment did not affect the electrolyte responses to seawater adaptation. Captopril injected into eels which were fully adapted to and wholly maintained in sea water had no effect on plasma levels of cortisol, sodium, and potassium. Plasma cortisol was 30% lower in freshwater eels 2 hr after an injection of captopril but plasma sodium and potassium levels were unchanged. In both FW- and SW-adapted trout, captopril infusions doubled the glomerular filtration and urine production rates and the tubular transport maxima for glucose without changes in plasma composition.
Gen Comp Endocrinol 1985 Apr
PMID:Control of renal and adrenocortical function by the renin-angiotensin system in two euryhaline teleost fishes. 388 78

Dorsal aortic blood pressure (PSYS, systolic; PDIAS, diastolic; and PDA, mean) and heart rate (HR) were measured in resting freshwater bowfins (n = 6), Amia calva L., before and after i.v. injections of 50, 100, 200, 500, and 1000 ng.kg-1 of synthetic [Asn1, Val5]-angiotensin II (ANG II). Baseline PSYS, PDIAS, and PDA were 27.7 +/- 2.8, 22.4 +/- 1.8, and 24.5 +/- 2 mm Hg, respectively. Bowfins were only moderately responsive to ANG II in a stepwise manner and the increase in blood pressure became significant only at the two highest doses; lower doses tended only to increase arterial pressure. Pressor responses due to 200 and 500 ng.kg-1 decayed over a greater time period compared with other doses. alpha-Adrenergic blockade abolished 70% of the ANG II-mediated pressor responses. Eel, salmon, and goosefish angiotensin I (ANG I; 500 ng.kg-1) elicited similar vasopressor responses (magnitude and time course) which were eliminated by prior angiotensin converting enzyme inhibition (captopril; 2-10 mg.kg-1). Bullfrog ANG I evoked a pressor effect, only at a higher dose (5000 ng.kg-1). Consecutive norepinephrine (NE) injections (100, 200, 500, and 1000 ng.kg-1) increased PSYS, PDIAS, and PDA in a dose-dependent manner which was dependent on alpha-adrenoceptors since phentolamine (1-3 mg.kg-1) abolished 80% of the pressor action of NE. PSYS was elevated by 100 ng.kg-1 of NE but PDIAS and PDA were significantly increased only at 200 ng.kg-1 ANG II and NE had no measurable chronotropic effect and resting HR (27.2 +/- 0.8 beats.min-1) was unchanged. Captopril and phentolamine treatments produced rapid hypotension and bradycardia (25-30%) which lasted from 15 to 30 and 20 to 40 min, respectively. The rising and decreasing phases of the NE-mediated pressor responses had shorter durations than ANG II effects. Tachyphylaxis occurred with the high doses of ANG II and NE. The data show that in the ancient bowfin, which evidently lacks renal juxtaglomerular cells, the cardiovascular system can be regulated by the renin-angiotensin system and NE.
Gen Comp Endocrinol 1995 Jun
PMID:Angiotensin I- and II- and norepinephrine-mediated pressor responses in an ancient holostean fish, the bowfin (Amia calva). 762 88

Renin-like activity (RLA) and angiotensin I-converting enzyme-like activity (ACELA), two key enzymes of the renin-angiotensin cascade (RAS), were sought in the dogfish rectal gland. RLA was 1.1 +/- 0.2 ng Ang I/mg protein/hr after incubation with porcine angiotensinogen and 0.8 +/- 0.1 ng Ang I/mg protein/hr after incubation with homologous plasma. ACELA was 7.22 +/- 1.08 and 8.87 +/- 1.9 nmol hippurate generated/min/mg protein respectively, at 0 and 37 degrees. The presence of these enzymes may indicate the presence of an endogenous RAS-like system in the rectal gland. Angiotensin II (Ang II) and atrial natriuretic peptide (ANP) binding sites were demonstrated autoradiographically in the subcapsular region of the gland, suggesting a possible interaction of the two hormones in the blind outer ends of the rectal gland tubules. Immunoreactivities toward Ang II, ANP, bombesin, vasoactive intestinal polypeptide (VIP), glucagon, and somatostatin were differentially localized in the rectal gland within three concentric zones with potentially different functional activities. In the capsule, there was a strong positive ir-glucagon reaction and a slightly weaker reaction for ir-somatostatin and VIP. In the blind outer ends of the tubules (in the subcapsular zone), strong immunoreactivity was present toward all the tested peptides except glucagon and somatostatin. In the inner zone and in the central canal, only a weak immunoreactivity toward Ang II and glucagon was observed.
Gen Comp Endocrinol 1994 Feb
PMID:Renin-like activity, angiotensin I-converting enzyme-like activity, and osmoregulatory peptides in the dogfish rectal gland. 790 83

1. We examined the effect of spirapril, a potent angiotensin converting enzyme (ACE) inhibitor, on the number of capsaicin-induced coughs in rats and compared with that of enalapril. 2. Chronic treatment with enalapril, at doses of 1 and 3 mg/kg, p.o., significantly and dose-dependently enhanced the number of capsaicin-induced coughs. 3. Chronic treatment with higher dose of spirapril (3 mg/kg, p.o.) also significantly enhanced the number of capsaicin-induced coughs. However, lower dose (1 mg/kg, p.o.) of spirapril had no significant effect on the number of capsaicin-induced coughs. 4. These results suggest that cough induced activity, one of the most serious side effects associated with chronic treatment with ACE inhibitors, of spirapril is relatively lower than that of enalapril.
Gen Pharmacol 1993 Nov
PMID:Cough induced activity of spirapril in rats. 811 17

We evaluated the effect of endothelin-1 (ET) on the angiotensin converting enzyme (ACE) activity in rat aortic smooth muscle cells (VSMCs). ACE activity was determined by radioimmunoassay of the amount of angiotensin II generated after the addition of angiotensin I (500 pg/ml) to cultured VSMCs. The antibody used had less than 0.1% cross-reactivity with angiotensin I. ACE activity increased 1.9-fold 5 hr after the addition of 10(-6) M ET under serum-free conditions. This stimulatory effect of ET on ACE activity in VSMCs was completely inhibited by 10(-7) M captopril. Results suggested that the ACE present in SMCs is stimulated by ET.
Gen Pharmacol 1996 Apr
PMID:Effect of endothelin on angiotensin converting enzyme activity in cultured vascular smooth muscle cells. 872 27

Angiotensin II exerts its action via at least two distinct receptor subtypes designated AT1 and AT2. AT1 receptors seem to be responsible for most of the known angiotensin II effects while the role of AT2 receptors is not yet clear. Adipocytes of adult rats express exclusively the AT1 subtype. Angiotensin II stimulates prostacyclin release in adult rat adipocytes and in mouse preadipocytes. In the latter prostacyclin release is completely blocked by an AT2 receptor antagonist. Adipocyte angiotensin II receptors seem to be regulated by age and fat mass. Blockade of these receptors by an AT1 antagonist seems to prevent adipose tissue hypertrophy. Moreover, adipose tissue contains all the main components of the renin-angiotensin system such as angiotensinogen, angiotensin converting enzyme, angiotensin II and angiotensin II receptors. Angiotensinogen expression in adipocytes is stimulated by a high fat diet concurrent with enlargement of fat mass, associated with insulin resistance. Angiotensin converting enzyme inhibitors improve insulin sensitivity. Taken together, there is evidence of interaction between insulin and angiotensin II in regulation of adipose tissue metabolism and cellularity. Clarification of these interactions could lead to significant progress in pharmacological treatment of obesity and its comorbidity.
Gen Physiol Biophys 1995 Oct
PMID:The role of angiotensin II and its receptors in regulation of adipose tissue metabolism and cellularity. 878 38

1. Alterations in the function of the endothelium and arterial smooth muscle may be important in the establishment of hypertension. Thus, the possible favorable influences of blood pressure-lowering agents on vascular responsiveness may be important in the chronic antihypertensive actions of these compounds. 2. A number of reports have suggested that ACE inhibitors can improve arterial function in hypertension, whereas the knowledge about the vascular effects of other antihypertensive drugs, like beta-blockers, calcium channel blockers, and diuretics remains rather limited. 3. In this article, the effects of antihypertensive therapy on arterial function in human and experimental hypertension are reviewed.
Gen Pharmacol 1996 Mar
PMID:Antihypertensive therapy and arterial function in experimental hypertension. 891 35

Echocardiography is now considered to be the key investigation when heart failure is suspected, and should improve clinical management. An open-access echocardiography service was piloted to 24 general practitioners and the service was audited after 250 cases. The impact on clinical management was assessed by reviewing general practice notes 2 months after the echocardiogram. Significant impairment of left ventricular function was found in 49 patients (20%). Out of these subjects, 38 had been started on an ACE inhibitor. Twenty patients were considered to have a significant valve lesion by echocritiera, of whom 14 had been referred for a cardiological opinion. The provision of an open-access echocardiography service was popular with general practitioners and the information resulted in appropriate management decisions being made.
Br J Gen Pract 1996 Aug
PMID:Open-access echocardiography to general practitioners for suspected heart failure. 894 28


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