Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting. This hypertension increases myocardial oxygen consumption and can be prevented by application of vasodilators. A possible cause is activation of the renin angiotensin system. Magnesium is a potent vasodilator and has a beneficial effect after myocardial ischaemia. The study was performed to analyse the influence of magnesium infusion on the haemodynamic status and plasma renin activity in patients undergoing aortocoronary bypass grafting. METHODS. Eighteen patients (NYHA classification II-III) undergoing bypass surgery were divided into two groups, a magnesium and a control group. The magnesium group (n = 9) received 0.8 mEq/kg per h magnesium aspartate as an infusion for 15 min while still awake. After induction of anaesthesia, the magnesium infusion was reduced to 0.2 mEq/kg per h and stopped after aortic cannulation was completed. Plasma magnesium levels and concentrations within erythrocytes were measured. Anaesthesia was induced by flunitrazepam (0.01 mg/kg), fentanyl (0.005 mg/kg) and pancuronium (0.1 mg/kg). After intubation, patients were normoventilated with N2O/O2 = 1:1 and isoflurane (0.5-1.0 vol%). Additional doses of fentanyl (0.0025 mg/kg) were injected before the incision and before sternotomy. Mean arterial pressure, heart rate, cardiac index, total peripheral resistance, pulmonary vascular resistance, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, left ventricular stroke work index, right ventricular stroke work index, intrapulmonary shunt and plasma renin activity were evaluated at five predefined points: (1) prior to magnesium infusion; (2) after magnesium infusion; (3) 10 min following induction of anaesthesia under steady-state conditions; (4) after sternotomy; (5) after aortic cannulation. RESULTS. Concerning the haemodynamic parameters (MAP, RAP, PAP, PCWP) no significant difference between the two groups could be demonstrated. In the control group peripheral resistance (TPR) was higher following sternotomy and aortic cannulation than in the magnesium group. Magnesium prevented decrease of the cardiac index (CI) under steady-state conditions, during sternotomy and following aortic cannulation. Left and right ventricular stroke work indexes (LVSWI and RVSWI) were higher in the magnesium group. Plasma renin levels were not significantly different between the two groups. CONCLUSION. Patients undergoing cardiac surgery benefit from magnesium administration in the pre-bypass phase. Due to its vasodilating effect, magnesium lowers the output impedance of the left ventricle and improves cardiac pumping function. It opposes detrimental cardiovascular responses to sternotomy and following aortic cannulation. Also of importance is the advantageous effect of magnesium on cardiac arrest elicited by cardioplegia and for reactivation of the ischaemic myocardium.
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PMID:[Hemodynamics of coronary surgery patients following magnesium aspartate infusion]. 148 73

To test the efficacy of exogenous prostaglandins for vasodilator therapy in heart failure, we studied the effects of the prostacyclin-derivative iloprost (1.5-150 ng/kg/min) in seven conscious dogs before and after induction of heart failure by right ventricular pacing (250/min. 10 days). In healthy dogs, iloprost (150 ng/kg/min) decreased mean arterial blood pressure (MAP) (-45%) by a decrease in total peripheral resistance (TPR) (-55%), and increased cardiac output (CO) (+24%) and heart rate (HR) (+20%) with no effect on right atrial and pulmonary arterial pressures (RAP, PAP). Plasma norepinephrine (NE) (+47%), renin (+351%), and aldosterone (+126%) were increased. Urine flow (-70%) and Na excretion (-53%) were decreased. Iloprost (15 ng/kg/min) increased renal blood flow (RBF) (+29%), but did not change glomerular filtration rate (GFR). In dogs with heart failure, iloprost decreased arterial BP (-31%), TPR (-42%) and pulmonary vascular resistance (-28%) and increased CO (+29%), with no change in RAP and PAP. Plasma NE (+34%), renin (+385%), and aldosterone (+146%) were increased. RBF was unchanged. GFR (-24%) and filtration fraction (FF) (-30%) were decreased, as was urine flow (-65%). In experimental heart failure, iloprost is a potent arteriolar dilator, increasing CO with no preload effect. These beneficial effects are limited, however, by further neurohumoral activation and deterioration of renal function.
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PMID:Hemodynamic, hormonal, and renal effects of the prostacyclin analogue iloprost in conscious dogs with and without heart failure. 170 1

Pulmonary hypertension (PH) is one of the evolutive complications in respiratory diseases leading to chronic respiratory insufficiency (CRI). In most cases PH is mild, but acute worsening can happen and especially during exercise, during sleep (particularly during rapid-eye-movement sleep) and during acute respiratory failure. Usually, pulmonary artery pressure finds again the level observed prior to the worsening. Although PH is usually mild, it is of prognostic value in CRI and particularly in patients with chronic obstructive pulmonary disease (CODP): the survival rate is significantly lower in patients with PH compared with those without PH and the higher PAP is the lower the survival rate. In general, long-term changes in PAP in COPD patients are mild. Long-term oxygen therapy can reverse the progression of PH and increase the survival rate. PH can lead with more or less delay to cor pulmonale and right heart failure (RHF). Oedema can be due to RHF but in some cases they can also be explained by the stimulation of the renin-angiotensin system with increasing of the aldosterone level, due to the fall in renal blood flow. These renal hemodynamic changes are related to arterial blood gas changes (hypercapnic acidosis, hypoxemia).
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PMID:[Pulmonary artery hypertension in chronic respiratory diseases]. 185 23

It has been speculated that ACE inhibitors may have beneficial effects in patients with coronary artery disease not only by their vasodilator properties but also by an effect on an assumed local renin-angiotensin system in atherosclerotic coronary arteries. Thus, the aim of the present study was to evaluate the effect of a single intravenous infusion of captopril on haemodynamics and coronary diameter at rest and during myocardial ischaemia induced by rapid atrial pacing. The study was performed in 12 patients with coronary artery disease and exertional angina pectoris despite medical therapy. Central haemodynamics (PAO, PAP) and left ventricular end-diastolic pressure were measured. Biplane cineventriculography and coronary arteriography were performed during control pacing (10% above the normal heart rate) before and after 15 min of captopril infusion, as well as during angina pectoris induced by rapid atrial pacing before and after captopril (six patients 0.15 mg kg-1, six patients 0.3 mg kg-1). Mean aortic pressure was not significantly decreased by either 0.15 mg kg-1 or 0.3 mg kg-1, whereas mean pulmonary pressure was significantly reduced by captopril by 28% at rest and 34% during rapid atrial pacing. Neither the endsystolic volume index nor left ventricular ejection fraction was significantly affected by captopril. Left ventricular end-diastolic volume index was reduced by 9% at rest and 7% during pacing-induced angina. Left ventricular end-diastolic pressure decreased from 11 +/- 9 mmHg to 4.8 +/- 4.1 mmHg at rest after captopril, and from 10 +/- 11 mmHg to 5.1 +/- 5.0 mmHg during pacing-induced angina after captopril.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial and coronary effects of captopril during pacing-induced ischaemia in patients with coronary artery disease. 219 7

Diuretic effects of aminophylline in patients after cardiac surgery were studied by using the local renal thermodilution catheter (Goodman Co. Ltd.). The subjects were 11 patients who underwent cardiac surgery in our hospital. All patients had shown almost normal renal and endocrine function. On the day of operation, we indwelld renal thermodilution catheter into the left renal vein under fluoroscopy. After operation, when the urinary volume decreased below 1 ml.kg-1.hr-1, we administered aminophylline at a rate of 2 ml.kg-1.hr-1. We measured HR, BP, CO, PAP, CVP, renal blood flow, urinary volume, urinary electrolytes, plasma renin activity, angiotensin II, aldosteron, ADH and alpha hANP just before and after infusion of aminophylline. The urine volume, renal blood flow and renal blood flow distribution rate showed significant increases of about 70%, 40% and 35% respectively. But hemodynamic parameters including HR, mean BP and CO increased for 5%, 10% and 8% respectively after administration of aminophylline. In the endocrine system, only angiotensin II increased significantly but aminophylline did not cause any change in endocrine system. The results suggest that diuretic effect of aminophylline is mainly achieved by increasing renal blood flow.
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PMID:[Diuretic effects of aminophylline in patients after cardiac surgery]. 223 25

Diethylstilbestrol (DES) treatment of a male Syrian hamster resulted in the development of a renal tumor and its widely scattered serosal metastases. Cells in both the primary tumor and metastatic nodules contained secretory granules. The tumors were transplanted serially into DES-supported and non-DES-supported host hamsters until DES-independent tumors developed. Rabbit antiserum to mouse salivary renin and rabbit antiserum to rat kidney resin were reacted with sections of the primary tumor, metastatic nodules, and all transport tumors. The sections were stained by the PAP and Vector-ABC-AP procedures. Renin-positive material was observed in all tumors. Plasma renin activity (PRA) was determined for the host hamsters carrying the renal tumor transplants and compared to the PRA values that had been determined for normal non-DES-treated male and female hamsters. It was found that the average PRA values of host hamsters carrying the tumor transplants were significantly higher than the normal PRA values.
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PMID:Immunohistochemical renin study of DES-induced renal tumor in the Syrian hamster. 305 27

The present light (LM) and transmission electron microscopic (TEM) studies were carried out to further document the anatomy of the 'superficial' juxtamedullary nephrons (SJMNs) located on the inside cortical surface of the rat kidney. TEM revealed that SJMNs possess all vascular and tubular cell types constituting the juxtaglomerular apparatus (JGA) in typical cortical and juxtamedullary nephrons (JMNs). Proximal to the glomeruli, epithelioid cells filled with secretory granules predominated in the media of afferent arterioles. The presence of renin in the granules was immunocytochemically demonstrated by the protein A-gold method. Further upstream from the glomeruli, epithelioid cells alternated with plain smooth muscle cells. The use of renin and angiotensin II antisera revealed similar arteriolar distributions of renin and angiotensin II positive cells in SJMNs as well as in typical JMNs. Numerous nerve terminals were found along afferent and efferent arterioles, suggesting a dense innervation of these vessels. The distribution of renin-containing (i.e., epithelioid) cells in the preglomerular arterioles was assessed in various nephron populations by LM using the PAP method and renin antiserum. In SJMNs, most renin-positive cells were found in the vicinity of the JGA along a mean arteriolar length of 35 +/- 3 micron (range 7-107 micron). In JMNs, renin-positive cells had a similar distribution along a mean arteriolar length of 35 +/- 1 micron. Scattered renin-positive cells were observed up to a maximal arteriolar length of 173 and 238 micron in SJMNs and JMNs, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renin status of the afferent arteriole and ultrastructure of the juxtaglomerular apparatus in 'superficial' juxtamedullary nephrons from rats. 329 64

The PAP-technique and antibodies to myosin were used to demonstrate the prerequisites for vasoconstriction in the juxtaglomerular part of the preglomerular arteriole as compared with its proximal segment in rats and mice. In contrast with the myosin-positive/renin-negative proximal part of the afferent arteriole no myosin-like activity could be demonstrated in its distal, renin-positive part. In accordance, no thick myofilaments were found in fully differentiated juxtaglomerular epithelioid cells replete with mature secretory granules. Stimulation of the renin-angiotensin system was followed by an increase of the renin-positive/myosin-negative portions of the preglomerular arteriole. Marked interspecies and internephron variations in the length of this vessel segment under control and stimulated conditions were observed. The juxtaglomerular part of the preglomerular arteriole close to the macula densa seems therefore to have only limited capabilities for vasoconstriction. This finding may be of importance regarding the tubulo-glomerular feedback, a mechanism allegedly triggered by the so-called 'macula densa-signal'. It is suggested that this non-contractile segment of the afferent arteriole may represent the renal vascular receptor responsible for the increase of renin secretion during pressure reduction. Unlike the afferent arterioles, most of the efferent arterioles showed the highest level of their weak but distinct myosin-like immunoreactivity in the juxtaglomerular region, indicating some efferent juxtaglomerular vasoconstrictive ability.
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PMID:Myosin content and vasoconstrictive ability of the proximal and distal (renin-positive) segments of the preglomerular arteriole. 330 Sep 94

In an attempt to localize components of the renin angiotensin-system in the pineal gland of rats, immunocytochemical studies using the PAP-technique were performed with antisera against angiotensin I, angiotensin II and angiotensinogen. The staining pattern thus obtained was not only the same for the three antisera, but was also identical to that shown for many other peptide-antisera in the literature. In those studies, the immunocytochemical staining had been ascribed to a distinct pineal cell population or to cell processes. However, by examining adjacent semithin and ultrathin sections by immunocytochemistry and electron microscopy, respectively, we could identify the extracellular perivascular compartment and its flocculent material as the site of staining. This unexpected localization and the observation of "immunoreactivity" of some preimmunesera in the same compartment as well as several additional findings and arguments are taken to suggest that likelihood of "pseudopositive" immunostaining, typical for the pineal gland.
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PMID:Neuropeptides in the pineal gland? A critical immunocytochemical study. 616 95

The PAP-method was used for immunocytochemical investigations with antisera against angiotensin (ang) I, ang II and renin in kidneys of rats and mice. In 14 rats, ang II was found in the media of the afferent arteriole - both in the region of the JGA and upstream until the interlobular artery. Serial sections alternately reacted for ang II and renin revealed that the octapeptide is contained in the well known renin positive epitheloid cells of the afferent arteriole and, beyond that, together with renin probably in the same "specific" granules. Fixation conditions were critical for the visualization of immunoreactivity With ang I antisera, comparable in terms of titer and affinity to the ang II antisera, specific immunoreactivity could not be found in the kidneys of rats. With horse radish peroxidase and ferritin as tracers it could be shown that the epitheloid cells of the JGA have the ability to pinocytize and incorporate macromolecules into their granules. It is suggested that ang II is taken up by these cells through the same route, Intracellular generation of ang II appears unlikely as an explanation. Functionally the selective uptake of ang II by epitheloid cells might be a specific process, possibly connected with the negative feedback of the octapeptide on renin secretion. Negative results in mice may be explained by a small uptake or more rapid degradation of ang II by the epitheloid cells.
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PMID:Angiotensin II in epitheloid (renin containing) cells of rat kidney. 617 Jun 18


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