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

---

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

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.
...
PMID:Angiotensin converting enzyme inhibition and the upper limit of cerebral blood flow autoregulation: effect of sympathetic stimulation. 265 65

In order to investigate whether angiotensin II (Ang II) may contribute to cardiovascular regulation through facilitation of the adrenergic function, we examined the haemodynamic and humoral effects of the application of lower-body negative pressure (LBNP) in sodium-replete patients with essential hypertension before and after acute and chronic angiotensin converting enzyme (ACE) inhibition. We measured the changes in blood pressure, heart rate, central venous pressure, forearm blood flow, plasma noradrenaline, renin activity and Ang II induced by LBNP of two different magnitudes: a milder one deactivating predominantly the cardiopulmonary receptors (mild LBNP), and a greater one deactivating both the cardiopulmonary and the arterial baroreceptors (strong LBNP). We found that during mild LBNP systemic blood pressure was maintained after acute and chronic ACE inhibition, as in control studies; however, the decrements in forearm blood flow and the increments in forearm vascular resistance caused by LBNP were diminished after ACE inhibition (the latter by 69 and 67%, respectively, in acute and chronic studies), in spite of the fact that the falls in central venous pressure and the increases in noradrenaline (NA) were similar to those observed in control conditions. During strong LBNP, the fall in systemic blood pressure was greater after acute and chronic ACE inhibition than in control conditions and was associated with a reduction in the response of forearm vascular resistance similar to that observed during mild LBNP, while the increments in NA were again superimposable to those seen before ACE inhibition. These alterations in the haemodynamic responses to LBNP induced by ACE inhibition were associated with significant increments in basal plasma renin activity and with marked reductions in Ang II. These findings suggest that even in the sodium-replete state, Ang II exerts a facilitatory action on adrenergic function that is physiologically relevant for the regulation of forearm blood flow and the maintenance of blood pressure during the application of gravitational stresses.
...
PMID:Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium-replete patients with essential hypertension. 268 17

We examined the effects of antihypertensive therapy with captopril, an angiotensin converting enzyme inhibitor, on exercise tolerance and humoral factors in 19 elderly patients (greater than 60 years old) with essential hypertension. Captopril (37.5-75 mg/day) was administered for 8 weeks. Fourteen of the 19 patients in whom captopril was effective took a treadmill exercise test according to Kattus' protocol. Exercise tolerance was increased in all patients (from 13.1 +/- 1.3 to 16.5 +/- 1.0 min, P less than 0.01). Captopril attenuated the rise in blood pressure during the exercise test but did not affect the heart rate. Resting values of plasma adrenaline decreased by 47% and noradrenaline by 17%, with no significant changes in plasma renin activity (PRA) or aldosterone. The change in mean blood pressure showed an inverse relationship to pretreatment plasma noradrenaline (r = -0.73, P less than 0.01). The results show that captopril is effective in the treatment of hypertensive elderly patients, and suggest that the sympathetic nervous system is involved in the mechanism of the antihypertensive response to captopril therapy.
...
PMID:Effects of treatment with captopril on exercise tolerance and plasma catecholamines in elderly hypertensives. 269 59

The haemodynamic and neurohormonal responses to the angiotensin converting enzyme (ACE) inhibitor captopril were studied in 12 patients with primary autonomic failure; seven had multiple system atrophy and five had pure autonomic failure. Basal supine mean arterial blood pressure was higher in the patients with multiple system atrophy than in those with pure autonomic failure and the normal subjects. Basal plasma noradrenaline levels were normal in the patients with multiple system atrophy, but lower in those with pure autonomic failure. Captopril lowered the mean arterial pressure in the patients with multiple system atrophy and pure autonomic failure but not in the normal subjects. In the patients with multiple system atrophy and pure autonomic failure, captopril lowered the cardiac output and the stroke volume. Forearm vascular resistance was unchanged. No significant changes occurred in the normal subjects. Plasma renin activity was unchanged after captopril in the patients with autonomic failure, but rose in the normal subjects. Plasma noradrenaline was unchanged in all groups after the administration of captopril. We conclude that captopril lowers the mean arterial pressure in patients with multiple system atrophy and pure autonomic failure. After the administration of captopril there is a reduction in cardiac output, secondary to a fall in stroke volume. The vasodepressor response to captopril in patients with autonomic failure is not related to the basal level of plasma renin activity or sympathetic nervous activity, indicating that the hypotensive effects of bradykinin or prostaglandins, or both, may contribute.
...
PMID:Angiotensin converting enzyme inhibition lowers blood pressure in patients with primary autonomic failure independently of plasma renin levels and sympathetic nervous activity. 269 48

1. Left ventricular myocardial infarction was induced in female Wistar rats by ligation of the left anterior descending coronary artery. 2. One month following operation, rats with infarcts developed marked cardiomegaly compared to sham operated rats, indicating the presence of chronic left ventricular failure. 3. The ratio of the noradrenaline metabolite 3,4-dihydroxyphenylethylene glycol (DHPG) to noradrenaline (NA) was elevated in the right ventricle of rats with heart failure one month following infarction, suggesting a chronic increase in cardiac sympathetic activity. 4. Perindopril therapy for one month commenced 4 weeks after infarction returned cardiac weights to normal and significantly reduced right ventricular DHPG/NA ratios. 5. The results suggest that ACE inhibition with perindopril reduces elevated levels of cardiac sympathetic activity in rats with chronic left ventricular failure and leads to regression of cardiomegaly.
...
PMID:Cardiac 3,4-dihydroxyphenylethylene glycol (DHPG) and catecholamine levels during perindopril therapy of chronic left ventricular failure in rats. 272 98

1. The effects of the angiotensin-converting enzyme (ACE) inhibitor lisinopril on plasma vasoactive intestinal polypeptides (VIP) and plasma noradrenaline, adrenaline and dopamine were studied in 12 patients with congestive heart failure over two consecutive 48-hr periods. The first day in each period served as a treatment day and the second as a control day. 2. A parallel monitoring was made of various hormonal parameters related to the renin-angiotensin-aldosterone system, and a right-heart catheter was used to monitor haemodynamics at rest. 3. Potent inhibition of the renin-system (as demonstrated by decreases in angiotensin converting enzyme (ACE) activity, angiotensin II and plasma aldosterone) together with improved haemodynamics (decreases in mean right atrial pressure, mean pulmonary arterial pressure, mean pulmonary capillary wedge pressure and mean systemic arterial pressure) were recorded. 4. Plasma VIP was significantly increased by a mean of 20.3% (P less than 0.01) on the lisinopril treatment days compared with the control days, whereas circulating catecholamines showed no significant pattern of change. 5. It is postulated that the potent vasodilatory neuromodulator VIP is implicated in the ACE inhibitor effects. 6. The ACE is a non-specific peptidase that previously has been implicated in the potentiation of other vasoactive endogenous systems (kinins and enkephalins).
...
PMID:Increase in vasoactive intestinal polypeptides (VIP) by the angiotensin converting enzyme (ACE) inhibitor lisinopril in congestive heart failure. Relation to haemodynamic and hormonal changes. 282 21

1. A double-blind, four period crossover study was undertaken to test for an interaction between single oral doses of nifedipine retard (20 mg) and lisinopril (20 mg) in normal subjects. 2. Side effects with both drugs were mild and the incidence was additive. 3. Blood pressure (BP) was lowered by nifedipine for 4 h, by lisinopril for 48 h and the combination showed simply additive effects. Standing heart rate was higher after the combination than after single treatment. 4. Plasma angiotensin converting enzyme (ACE) and renin activity (PRA), aldosterone, noradrenaline and adrenaline levels showed no evidence of an interaction. 5. The pharmacokinetics of lisinopril were unaltered by nifedipine and vice versa. 6. There is no evidence of a pharmacokinetic or pharmacodynamic interaction between single oral doses of nifedipine and lisinopril.
...
PMID:Lisinopril and nifedipine: no acute interaction in normotensives. 283 20

Spirally cut strips of human saphenous vein and pulmonary artery preincubated with 3H-noradrenaline were superfused in the presence of corticosterone and desipramine or cocaine. In the saphenous vein angiotensin I, angiotensin II and angiotensin III concentration-dependently increased the electrically (2 Hz) evoked tritium overflow (relative order of potency: angiotensin II greater than angiotensin I greater than angiotensin III). The angiotensin receptor antagonist saralasin displaced the concentration-response curve of angiotensin II to the right, and also blocked the facilitatory effect of angiotensin III. Captopril, an inhibitor of angiotensin converting enzyme, did not modify the concentration-response curve of angiotensin I and did not significantly diminish the release-increasing effect of the nonselective beta-adrenoceptor agonist isoprenaline, whereas saralasin attenuated the facilitatory effect of the beta 2-adrenoceptor agonist procaterol. In the pulmonary artery the angiotensin receptor agonist Val5-angiotensin II-Asp1-beta-amide also increased the electrically evoked tritium overflow in a concentration-dependent manner. It is concluded that the sympathetic nerve fibres of the human saphenous vein (and probably of the human pulmonary artery as well) are endowed with facilitatory presynaptic angiotensin receptors. Angiotensin I exerted its facilitatory effect in the saphenous vein probably via direct stimulation of angiotensin receptors but not by conversion to angiotensin II. Furthermore, the beta 2-adrenoceptor-induced facilitation of noradrenaline release may in part be mediated by local stimulation of angiotensin II synthesis, which may occur by increased formation or activation of renin and/or increased availability of angiotensinogen.
...
PMID:Facilitatory presynaptic angiotensin receptors on the sympathetic nerves of the human saphenous vein and pulmonary artery. Potential involvement in beta-adrenoceptor-mediated facilitation of noradrenaline release. 284 3

1. Isolated preparations of rat anococcygeus muscle were incubated with [3H]-noradrenaline and the efflux of radioactivity induced by stimulation of intramural sympathetic nerves was used as a measure of release of transmitter noradrenaline. Isometric contractile responses were also measured. 2. Angiotensin I (0.03 microM) and angiotensin II (0.03 microM) produced non-sustained contractile responses and enhanced the stimulation-induced (S-I) effluxes of radioactivity as well as the contractile responses to electrical stimulation. These effects were blocked by the angiotensin II receptor antagonist saralasin (0.03 microM), and the effect of angiotensin I, but not angiotensin II, was blocked by the angiotensin converting enzyme inhibitor captopril (0.1 microm). 3. The findings indicate that there are both pre- and postjunctional receptors for angiotensin II and that angiotensin I is converted to angiotensin II in the anococcygeus muscle preparation. 4. Isoprenaline (0.1 microM) slightly enhanced the S-I efflux of radioactivity, and produced a greater enhancement after neuronal uptake blockade with desipramine (0.03 microm) and alpha-adrenoceptor blockade with phentolamine (1 microM). 5. The facilitatory effect of isoprenaline on S-I efflux of radioactivity was abolished by propranolol (0.3 microM), but was not affected by low concentrations of saralasin (0.03 microM) or captopril (0.1 microM) which abolished the effect of angiotensin I. The findings suggest that isoprenaline acts directly on prejunctional beta-adrenoceptors to enhance S-I noradrenaline release, rather than indirectly by releasing angiotensin II from within the tissue. Higher concentrations of saralasin (0.1 microM) or captopril (5 microM) did block the facilitatory effect of isoprenaline. The significance of this finding is not clear.
...
PMID:Facilitation of noradrenaline release from sympathetic nerves in rat anococcygeus muscle by activation of prejunctional beta-adrenoceptors and angiotensin receptors. 285 20

Haemodynamic and humoral effects of captopril were studied in patients with essential and renovascular hypertension. Captopril decreased significantly both systolic and diastolic blood pressure and moderately, it reduced also the heart rate. On the basis of the haemodynamic effects our patients could be divided into two groups: in patients where the total peripheral resistance (TPR) exceeded 2000 dyn x sec x cm-5 during rest, captopril exerted its hypotensive effect by decreasing TPR. In patients in whom TPR was lower, the hypotensive action could be attributed to the reduction of cardiac output (CO). Captopril increased plasma renin activity, and decreased the activity of angiotensin converting enzyme (ACE) in the plasma. In acute study captopril did not influence plasma noradrenaline level but increased it during long-term administration. It did not affect dopamine or adrenaline levels. Captopril had no effect on plasma beta-endorphin concentration, moreover, the opiate antagonist, naloxone, failed to antagonize its antihypertensive effect. Comparing the acute effects of Capoten (Squibb, USA) and Tensiomin (EGIS, HUNGARY) no significant differences were found.
...
PMID:Clinical studies with captopril treatment of hypertensive patients. 285 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---