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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma renin activity (PRA) was subnormal or normal in the main strain of spontaneously hypertensive rats (SHR). PRA increased greatly in the stroke-prone substrain of SHR (SHRSP) at 20-30 weeks of age. Captopril (SQ 14,225) is an orally active angiotensin-converting enzyme inhibitor. The drug acutely decreased blood pressure moderately in SHR, and markedly in SHRSP. Participation of the renin-angiotensin system in the pathogenesis of hypertension in SHR may be limited. Etiology of hypertension in connection with renal excretory function and the central and peripheral nervous system is discussed.
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PMID:Blood pressure regulation by angiotensin in the spontaneously hypertensive rats. 39 Sep 89

1. Captopril (25 mg) reduced plasma angiotensin II (ANG II) by 53% (P less than 0.001) and mean brachial artery pressure (MBAP) by 18.7 mmHg (P less than 0.001) within 75 min in 26 hypertensive patients. After 2 months (on 150-600 mg/day) MBAP had decreased by 27.1 mmHg (n = 18) with no further change of plasma ANG II. delta MBAP was significantly related to control log plasm renin (PRA) and log ANG II in both conditions. 2. The acute depressor response to captopril was 11.2 mmHg greater (P less than 0.001) than delta MBAP during saralasin infusion (n = 12). 3. Heart rate slightly increased after acute administration of captopril (+3.3 beats/min; P less than 0.005), but cardiac output was not significantly affected; systemic vascular resistance decreased by 10% (P less than 0.01) with unchanged pulmonary vascular resistance. 4. During chronic administration, oxygen consumption, cardiac output and stroke volume increased by 15% (P less than 0.01), with unchanged heart rate; systemic vascular resistance had dropped by 30% (P less than 0.001). 5. Plasma ANG II and plasma aldosterone decreased, and PRA and ANG I increased acutely, with no further changes during chronic treatment.
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PMID:Haemodynamic effects of captopril in hypertensive patients: comparison with saralasin. 39 66

Pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), blood pressure (BP) were monitored before and after hypoxia, Captopril and Nitrendipine injected (7 mg/kg and 100 micrograms/kg) in group A(n = 9), and group B(n = 7) respectively results showed that during hypoxia PAP in all the pigs increased significantly (P < 0.05), compared with normoxia, and after captopril and nitrendipine intravenous injection, the PAP dropped significantly (from 3.76 +/- 0.25 to 3.43 +/- 0.1 kPa versus from 4.21 +/- 0.19 to 3.18 +/- 0.17 kPa. ACE in captopril group was significant reduced P < 0.05 (58.4 +/- to 27.0 +/- 3.0 mumol.min-1/L), but in nitrendipine group was not markedly changed (P > 0.05), we found that reducing the degree of PAP and its duration time, lowered the pulmonary vascular resistance (PVR) and right ventricle stroke index (RVSWI), also improved capacity of oxygen delivery. Nitrendipine was better than captopril, maybe it is an useful drug for patients with pulmonary hypertension.
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PMID:[Comparative studies between the effects of captopril and nitrendipine on the hemodynamics and angiotensin converting enzyme of pigs with acute hypoxic pulmonary hypertension]. 133 19

Acute hemodynamics of pimobendan were compared to captopril in a crossover trial in patients with chronic heart failure (NYHA II-III). Heart failure had been stabilized by conventional therapy with diuretics and digitalis for more than 2 weeks. Patients receiving vasodilators were excluded. The hemodynamics were analyzed using a Swan-Ganz catheter at the bedside during drug administration. Following an intravenous injection of 2.5 mg of pimobendan, there was a significant increase in heart rate and decrease in mean pulmonary artery pressure, total pulmonary resistance, mean arterial pressure, systemic vascular resistance and mean right atrial pressure 2 hours after the injection. Captopril (12.5 mg, orally) significantly decreased mean arterial pressure, systemic vascular resistance and double product 2 hours after administration. In this study, the inotropic effect was evaluated through the relation between the stroke volume index and diastolic pulmonary artery pressure, and also between the stroke volume index and mean arterial pressure. Although decreases of diastolic pulmonary artery pressure and mean arterial pressure were seen with both drugs, the differences in stroke volume index were not significant. In comparison with captopril, the acute hemodynamics of pimobendan are characterized as follows: 1) the systemic arteriovasodilating effects of the two drugs were equal, 2) the pulmonary arteriovasodilating effect of pimobendan was marked, 3) a venodilating effect, documented through a decrease of mean right atrial pressure, was seen only with pimobendan. This study concluded that pimobendan is a stronger arterio-venodilator than captopril.
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PMID:Acute hemodynamics of pimobendan in chronic heart failure. A comparative crossover study of captopril and pimobendan. 159 49

The role of angiotensin system in the development of hypoxic pulmonary hypertension, in nine pigs (50 +/- 8 kg) were studied. A Swan-Ganz Catheter and an arterial catheter were inserted into the pulmonary artery and aorta, pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), Cardiac output (CO) and arterial blood gases were monitored before and after hypoxia and captopril injection (7.3 mg/kg.iv). Plasma renin activity (PRA) and angiotensin II (AT-II) were measured by RIA. Angiotensin converting enzyme (ACE) was measured by fluorometry. Results showed that during hypoxemia (PaO2 6.3 +/- 0.2 kPa, PaCO2 5.4 +/- 0.2 kPa), PAP increased from 2.43 +/- 0.17 to 3.76 +/- 0.2 kPa, (P less than 0.05) and right ventricle stroke work index (BVSWI) from 55.7 +/- 7.2 to 91.3 +/- 9.3 mJ/m2 (P less than 0.05). PRA increased from 0.56 +/- 0.19 to 1.28 +/- 6.30 mol. L-1/h (P less than 0.02) and AT-II from 62.4 +/- 17.4 to 133.3 +/- 31.8 ng/L (P less than 0.01); but ACE decreased from 77.6 +/- 5.6 to 58.4 +/- 4.2 mumol.min-1/L (P less than 0.02). After Captopril injection ACE was reduced to 26.7 +/- 3.4 mumol.min-1/L (P less than 0.001) and AT-II dropped to 61.9 +/- 15.5 ng/L (P less than 0.01), as compared with those during hypoxemia. There was significant correlation between PAP and PRA (r = 0.5643 P less than 0.01). We surmise that angiotensin system may play a part in acute hypoxia-induced pulmonary hypertension, and captopril Inhibits AT-II, leading to the drop of pulmonary arterial pressure.
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PMID:[Effect of captopril on hypoxia-induced pulmonary hypertension in pigs]. 164 28

In the present study we examined whether the angiotensin I converting enzyme inhibitor, captopril, would protect stroke-prone spontaneously hypertensive rats (SHRSP) from stroke and renal pathology over a 26-week period. In the control group of six untreated SHRSP fed Stroke-Prone Rodent Diet and 1% NaCl drinking solution, all animals developed severe hypertension and stroke by 16.1 weeks of age. In eight salt-loaded SHRSP treated with oral captopril (50 mg/kg/day) beginning at 8.4 weeks of age, systolic blood pressure was slightly but temporarily suppressed and then continued to rise; by 12 weeks of age systolic blood pressure reached levels of severe hypertension, 240 +/- 8 mm Hg, and did not differ from that of untreated SHRSP. No deaths or brain lesions were noted in captopril-treated SHRSP despite severe hypertension maintained through 26 weeks of age when the study ended. Captopril treatment prevented increases in urinary protein excretion (14 +/- 2 v 63 +/- 16 mg/day at 11.7 weeks of age, P less than .01) and the severe brain, renal, and cardiac vascular lesions observed in untreated SHRSP. When maintained on Stroke-Prone Rodent Diet and saline, plasma renin activity of untreated SHRSP surviving until 14.5 weeks of age was markedly increased (29.1 +/- 9.4 ng Ang I/mL/h) compared with either untreated SHRSP (9.2 +/- 2.5 ng Ang I/mL/h, P less than .01) or Wistar-Kyoto rats (3.5 +/- 1.0 ng Ang I/mL/h, P less than .01) maintained on standard diet and water.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic benefit of captopril in salt-loaded stroke-prone spontaneously hypertensive rats is independent of hypotensive effect. 193 Aug 50

To evaluate the role of angiotensin system in the development of hypoxia induced pulmonary hypertension, nine pigs (50 +/- 8 kg) were studied. A Swan-Ganz Catheter and an arterial catheter were inserted into the pulmonary artery and aorta. Pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO) and arterial blood gases were monitoring before and after hypoxia and captopril injection (7.0 mg/kg). Plasma renin activity (PRA) and angiotensin II (ATII) were measured by RIA. Angiotensin converting enzyme (ACE) by fluorometry. Results showed during hypoxemia (PaO2 6.2 +/- 0.3 kPa, PaCO2 5.3 +/- 0.2 kPa): PAP increased from 2.4 +/- 0.2 to 3.8 +/- 0.3 kPa, (P less than 0.05) and right ventricle stroke work index (RVSWI) from 55.7 +/- 7.2 to 91.3 +/- 9.3 mJ/m2 (P less than 0.05); mean-while PRA increased from 0.6 +/- 0.2 to 1.3 +/- 0.3 mol.L-1/h (P less than 0.05) and ATII from 62.4 +/- 17.2 to 133.3 +/- 31.8 ng/L (P less than 0.01). But ACE decreased from 77.6 +/- 5.2 to 58.4 +/- 4.2 mumol.min-1/L (P less than 0.05). After Captopril injection ACE was remarkably reduced to 26.7 +/- 3.4 mumol.min-1/L (P less than 0.001) and ATII dropped to 61.9 +/- 15.5 ng/L (P less than 0.01) compared with those during hypoxemia. There was significant correlation between PAP and PRA (r = 0.564, P less than 0.01). We speculate that angiotensin system may play a part in acute hypoxia induced pulmonary hypertension and captopril inhibits the production of ATII leading to the decrease of pulmonary arterial pressure.
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PMID:[Effect of captopril on the activities of angiotensin II and angiotensin converting enzyme during hypoxia induced pulmonary hypertension]. 196 75

After myocardial infarction, the renin-angiotensin system is found to be activated. While this response may be beneficial in acute failure, it could be detrimental in chronic stages. Therefore effects of captopril therapy were investigated during early and later phases after myocardial infarction in conscious rats, chronically instrumented for hemodynamic measurements. Hemodynamics were measured at baseline and after stimulating the heart by a volume load (cardiac function curve). Myocardial infarction decreased baseline cardiac output and impaired cardiac function, without effects on baseline mean arterial pressure, central venous pressure and heart rate. Captopril given 3 to 5 weeks after infarction improved cardiac function in a dose-dependent manner by increasing stroke volume, whereas stroke work was not affected. In contrast, captopril given from 1 to 21 days after infarction did not lead to improved cardiac function; instead, tachycardia together with a decreased stroke volume suggested deterioration, rather than improvement, of cardiac function. These data indicate that captopril therapy in chronically infarcted conscious rats improved cardiac function when treatment was started after completion of the healing process, but that early treatment not only failed to improve ventricular function, but may have a deleterious effect of the heart.
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PMID:Delayed but not immediate captopril therapy improves cardiac function in conscious rats, following myocardial infarction. 206 27

Angiotensin-converting enzyme inhibition has proven to be a successful approach for the long-term treatment of patients with congestive heart failure. This investigation compared the acute hemodynamic changes after sublingual administration of the angiotensin-converting enzyme inhibitor captopril with those after nitroglycerin. A total of 24 patients with severe left heart failure (New York Heart Association classes III and IV) were given 25 mg captopril and 0.8 mg nitroglycerin sublingually in this randomized, cross-over study. Hemodynamic monitoring revealed a clear improvement in pre- and afterload parameters for both drugs (P less than 0.01 and P less than 0.001), while captopril induced a higher increase in cardiac index (+49.2% vs. +25%), stroke volume index (+53.5% vs. +25.7%), and stroke work index (+55% vs. +28%) than nitroglycerin (P less than 0.001). Although not statistically significant, the onset of change for most hemodynamic parameters was measured earlier after nitroglycerin (after 12-19 vs. 16-22 minutes). Captopril revealed later peak effects (after 47-84 vs. 25-55 minutes, P less than 0.001) and a longer sustained improvement in hemodynamic values (return to baseline values after 117-162 vs. 68-120 minutes, P less than 0.001). No side effects occurred after either captopril or nitroglycerin in this study. Thus, these results indicate there is an early improvement in hemodynamic parameters after the sublingual administration of both drugs in patients with severe congestive heart failure, and that captopril induces a more pronounced and prolonged improvement than nitroglycerin.
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PMID:Sublingual administration of captopril versus nitroglycerin in patients with severe congestive heart failure. 211 16

The chemistry, pharmacology, pharmacokinetics, adverse effects, and dosages of the three currently available angiotensin-converting enzyme (ACE) inhibitors are reviewed. This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. The ACE inhibitors, therefore, are capable of lowering blood pressure primarily by promoting vasodilatation and reducing intravascular fluid volume. Captopril, the first orally active, commercially available ACE inhibitor, is a sulfhydryl-containing compound. Captopril was followed by the introduction of enalapril and lisinopril, two non-sulfhydryl ACE inhibitors. The pharmacokinetic profiles of these three ACE inhibitors differ. Captopril has rapid onset with relatively short duration of action, whereas enalapril and lisinopril have slower onset and relatively long duration of action. Captopril is an active ACE inhibitor in its orally absorbable parent form. In contrast, enalapril must be deesterified in the liver to the metabolite enalaprilat in order to inhibit the converting enzyme; this accounts for its delayed onset of action. Lisinopril does not require metabolic activation to be effective; however, a slow and incomplete absorption pattern explains the delay in onset of activity. Captopril and its disulfide metabolites are primarily excreted in the urine with minor elimination in the feces. Approximately two-thirds of an administered enalapril dose is excreted in the urine as both the parent drug and the metabolite enalaprilat; the remainder of these two substances are excreted in the feces. Lisinopril does not undergo measurable metabolism and approximately one-third is excreted unchanged in the urine with the remaining parent drug being excreted in the feces. The ACE inhibitors lower systemic vascular resistance with a resultant decrease in blood pressure. Their efficacy is comparable to diuretics and beta-blockers in treating patients with mild, moderate, or severe essential and renovascular hypertension. In those patients with severe congestive heart failure (CHF) the ACE inhibitors produce a reduction in systemic vascular resistance, blood pressure, pulmonary capillary wedge pressure, and pulmonary artery pressure. These drugs may produce improvement in cardiac output and stroke volume and, with chronic administration, may promote regression of left ventricular hypertrophy. The antihypertensive effects of the ACE inhibitors are enhanced when these agents are combined with a diuretic. Captopril and enalapril have been shown to be of particular benefits as adjunctive therapy in patients with congestive heart failure, both in terms of subjective improvement of patient symptoms, and in improving overall hemodynamic status.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors: a comparative review. 218 39


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