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)

In 31 patients with essential hypertension (EH) and in 21 healthy subjects, the influence of water immersion (WI) on arterial blood pressure, plasma renin activity, plasma aldosterone and atrial natriuretic peptide was examined after administration of captopril. In other 15 patients with EH and 25 healthy subjects, the influence of WI without captopril pretreatment on the above mentioned parameters was assessed. Plasma renin activity and plasma aldosterone concentration did not differ in patients with EH and in healthy subjects. In contrast, plasma atrial natriuretic peptide concentration was significantly higher but its response to WI-induced "central hypervolemia" significantly less marked in patients with EH than in healthy subjects. Results obtained in this study do not confirm presence of a tight interrelationship between atrial natriuretic peptide secretion and activity of the renin-angiotensin-aldosterone system both in patients with EH and in healthy subjects.
Kardiol Pol 1991
PMID:[Effects of water immersion and captopril on secretion of atrial natriuretic peptide and the activity of the renin-angiotensin system in essential hypertension]. 183 78

Left ventricular hypertrophy in arterial hypertension occurs in over 50% of patients. The detection of such high incidence has been facilitated by the introduction of echocardiography into diagnostic studies. Both earlier electrocardiographic findings and later echocardiographic results show that cardiac hypertrophy leads to an increased mortality and predisposes to cardiac arrhythmias, ischemic heart disease including myocardial infarction and heart failure. The development of hypertrophy is mediated by hemodynamic factors such as elevated blood pressure due to increased peripheral vascular resistance, ejection fraction, increased cardiac output, blood viscosity, as well as by non-hemodynamic factors. Of the latter ones the contribution of a genetic factor is discussed, whereas the role of para- and autocrine cardiac function manifested by local production and action of catecholamines as well as the renin-angiotensin system has been proved. Blockade of these systems makes possible prevention of the development of cardiac hypertrophy or its regression. Such results have been obtained both in experimental studies and in humans with hypertension treated with selected drugs. Regression of hypertrophy is accompanied by an improvement in systolic and especially diastolic cardiac function, the impairment of which is usually diagnosed prior to the detection of hypertrophy. The improvement in cardiac function and possibility of preventing consequences of hypertrophy help us to evaluate the efficacy of hypotensive drugs and their preferential use in this regard. There are also changes in recently recommended models of pharmacological treatment in arterial hypertension.
Kardiol Pol 1991
PMID:[Hypertrophy and function of the left heart ventricle in hypertension]. 183 84

In 12 patients with chronic renal failure (CRF) treated with haemodialyses and in 21 healthy controls plasma renin activity (PRA) and the concentrations of aldosterone and atrial natriuretic peptide (ANP) were determined in serum before and after blockade of the angiotensin converting enzyme with captopril. The study was carried out under conditions of the so called bed rest test (BR) and water immersion test (WI). After captopril administration a significant rise of PRA was noted in both groups with a drop of aldosterone level which was significant only in the control group. Captopril administration had no effect on serum ANP level. The results of the study are not suggesting the presence of a close relationship between ANP secretion and the activity of the RAA system in healthy controls and in CRF patients.
Mater Med Pol
PMID:Activity of the renin-angiotensin-aldosterone (RAA) and secretion of the atrial natriuretic peptide (ANP) in patients with chronic renal failure. 184 98

In 12 patients with acute non-inflammatory renal failure (ANRF) and in 21 healthy persons the relationship was studied between the activity of the renin-angiotensin-aldosterone (RAA) system and vasopressin secretion. The study was carried out during the so called bed rest test and during water immersion (WI) after captopril-induced blockade of the angiotensin-converting enzyme. The results of these experiments suggest the absence of a close functional relationship between the activity of the RAA system and vasopressin secretion in patients with ANRF and in healthy controls.
Mater Med Pol
PMID:The activity of the renin-angiotensin-aldosterone (RAA) system and vasopressin secretion in patients with acute non-inflammatory renal failure. 184 99

An effect of the long-term prazosin therapy on sympathetic activity, renin plasma activity and beta-endorphin and lipid blood levels was investigated in 23 patients with the primary arterial blood hypertension. Group A included 18 patients treated with prazosin, and group B - 5 patients treated with prazosin combined with propranolol. Mean daily dose of prazosin in group A was 3.0-10.0 +/- 1.3 mg in different phases of therapy whereas in group B mean daily dose of prazosin was 3.0-6.5 +/- 1.8 mg and propranolol 50-80 mg. Significant decrease in diastolic and systolic blood pressure (p < 0.01) was achieved in both groups. Additionally significant decrease in pulse rate (p < 0.01) was seen in group B. It was found that prazosin produced significant increase in plasma noradrenaline in group A and decrease in 4-hydroxy-3-methoxyglycol excretion with the urine (p < 0.05) in both groups. Moreover, negative correlation between a decrease in blood pressure (diastolic) and noradrenaline excretion with the urine (p < 0.05) was noted in group A. No effect of prazosin therapy on plasma renin activity, beta-endorphin and lipids blood levels was observed in both groups. These results suggest that prazosin therapy in patients with the primary blood hypertension exerts an effect on sympathetic activity and does not change plasma renin activity or blood beta-endorphin and lipids levels.
Pol Tyg Lek
PMID:[Effect of long-term prazosin treatment on certain humoral and metabolic factors in patients with primary hypertension]. 184 64

Concentration of free serotonin, adrenaline, noradrenaline, aldosterone and plasma renin activity have been assayed in blood of 18 patients with the primary arterial hypertension (WHO stage I) and in 10 healthy volunteers. It was found that blood free serotonin and noradrenaline are increased in hypertensive patient. No difference in adrenaline and aldosterone levels and plasma renin activity was seen. No significant correlation between free serotonin and assayed hormones was noted.
Pol Tyg Lek
PMID:[Digoxin-like substance in blood and hypertension in dialysed patients with chronic renal failure]. 184 88

Influence of blockade converting enzyme on plasma renin activity (PRA), aldosterone and vasopressin secretion in 12 hemodialyzed patients with chronic renal failure and in 21 healthy subjects was observed. Our observation were provided during bed rest and water immersion tests. We didn't observe statistically significant influence PRA (increase after converting enzyme blockade) on vasopressin secretion in patients with chronic renal failure and in healthy subjects. Correlation between PRA and vasopressin secretion was absent.
Pol Arch Med Wewn 1991 May
PMID:[Renin-angiotensin-aldosterone system (RAA) and vasopressin secretion in patients with chronic renal failure]. 189 92

The kidney possesses an extensive sympathetic innervation of both vascular and tubular elements and their functional role is only now becoming apparent. There is a graded recruitment of effects when the nerves are stimulated, with neurogenically mediated renin release being initially observed, at higher levels of activation there is a concomitant increase in tubular sodium reabsorption, while at very high frequencies there are marked reductions in renal blood flow and glomerular filtration rate. There is evidence that under normal physiological circumstances the renal nerves have a relatively low activity and it is likely that their primary action is to modulate renin release and sodium and water retention. Reflex neural regulation of kidney function can be exerted by a number of systems; the cardiovascular system, via the carotid sinus baroreceptor reflex, and the receptors of the heart and lungs; the somatosensory system, by receptors in the skin, muscle and joints; via the visceral system, by means of receptors in the gut; as well as mechano- and chemo-receptors within the kidneys themselves. These actions of the renal nerves are mediated by a range of adrenoceptors at the different neuro-effector junctions. There is a good consensus that at the granular renin-containing cells of the juxtaglomerular apparatus, beta 1-adrenoceptors mediate the release of renin. By contrast, at the vasculature alpha 1-adrenoceptors are involved in causing vasoconstriction although there is evidence that post-synaptic alpha 2-adrenoceptors may also contribute. Finally, at the tubular epithelial cells themselves, alpha 1-adrenoceptors are activated to stimulate sodium reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)
Pol Arch Med Wewn 1991 Mar
PMID:The physiology and pharmacology of the renal nerves. 205 15

In the presence of NADPH cytochrome P-450-dependent monooxygenases oxidize arachidonic acid giving rise to four epoxyeicosatrienoic acids (EETs) which are hydrolyzed enzymatically to dihydroxyeicosatrienoic acids (DHETs). EETs generate vasodilators. Allylic oxidation forms hydroxyeicosatetraenoic acids, of which 12(R)HETE is an inhibitor of Na(+)-K(+)-ATPase and renin release. Finally, omega and omega-1 hydroxylation of arachidonic acid generates 20- and 19-HETEs which are involved in the development of hypertension in SHR rats.
Pol J Pharmacol Pharm
PMID:Cytochrome P-450 metabolites of arachidonic acid: implications for blood pressure regulation. 212 86

In 16 children with steroid-responsive nephrotic syndrome (with minimal changes in the glomeruli) the plasma renin activity and aldosterone level were determined during recurrence of the nephrotic syndrome at the stage of oedema increase (FEN alpha 0.25%) and in early period of remission. Plasma renin activity was raised in all cases suggesting presence of hypovolaemia. Since it was not possible to establish a correlation between plasma renin activity and albumin level, as well as between this activity and aldosterone level, and aldosterone level and sodium excretion it may be surmised that the renin-angiotensin-aldosterone system has no decisive role in the pathogenesis of the nephrotic syndrome. The mechanism of oedema development is doubtlessly more complex.
Pol Arch Med Wewn
PMID:[Renin activity and aldosterone level in the plasma of children with lipoid nephrosis]. 225 Dec 9


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