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)

The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, arginine vasopressin (AVP) and plasma renin activity during morphine withdrawal in chloralose-anesthetized rats. Dependence was induced by s.c. morphine base pellets. Adrenal, renal and splanchnic SNA and SNA from the lumbar sympathetic chain were recorded before and after i.v. injections of naloxone. Baroreceptor function was examined with phenylephrine-induced increases in mean arterial pressure. In separate experiments, arterial plasma norepinephrine, epinephrine, dopamine, plasma renin activity and AVP were measured before and after naloxone-precipitated withdrawal. Naloxone administration elicited an increase in mean arterial pressure and heart rate. Although renal SNA was inhibited by approximately 50%, adrenal SNA and lumbar SNA increased by approximately 400 and 80%, respectively. Splanchnic SNA did not change significantly. The baroreceptor-mediated inhibition of adrenal SNA was facilitated while that for renal SNA was attenuated. The arterial plasma level of norepinephrine was doubled and epinephrine increased almost 20-fold. AVP increased about 15-fold, whereas plasma renin activity showed only a minor increase after naloxone. This study shows that a marked differentiation of the SNA response occurs during morphine withdrawal in rats, which suggests an interaction between opioid receptors and the control of regional sympathetic output. Furthermore, large amounts of AVP and epinephrine are released, which probably contribute to the cardiovascular changes seen in the withdrawal phase.
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PMID:Regional changes in sympathetic nerve activity and baroreceptor reflex function and arterial plasma levels of catecholamines, renin and vasopressin during naloxone-precipitated morphine withdrawal in rats. 218 76

In 78 patients with ischaemic heart disease prior to and after treatment with obsidan the authors examined relationship between the indices of activity of the sympatho-adrenal and renin systems. A correlation analysis was made between the data adrenalin excretion, noradrenalin, dopamine and DOPA in the urine and renin activity in the blood. After obsidan treatment the excretion of adrenaline and renin activity in blood plasma diminish. After obsidan treatment different links of activity of the sympato-adrenal system function more conjointly. Change in the activity of one of the links produces corresponding changes in the activity of the others. Dependence of renin activity is shown to exist on the activity of the sympatho-adrenal system after treatment as compared to their levels prior to treatment . The initial background recorded prior to treatment influences significantly the final result of treatment. A negative correlation exists between the activity of the sympatho-adrenal system and renin which is regarded as evidence of protective compensatory reaction of the body. It is suggested that the increase of noradrenalin secretion, causing rise of the blood pressure is associated with the compensatory decrease of renin activity.
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PMID:[Indices of sympathetic-adrenal system and renin activity in ischemic heart disease before and after obzidan treatment]. 704 44

We examined the relation between change in renal plasma flow (RPF) and change in glomerular filtration rate (GFR) in healthy humans on a low-salt diet during direct renin inhibition with aliskiren. We measured the renal hemodynamic response to acute dosing of 300mg aliskiren by mouth to 19 healthy normotensive subjects (age, 33+/-3 years; baseline RPF, 575+/-23; GFR, 138+/-14mL/min/1.73m(2)) on a low-sodium diet (10mmol/day). GFR and RPF were measured by the clearance of inulin and para-aminohippurate. There was a marked increase in average RPF (169+/-24mL/min/1.73m(2)) and a small rise in average GFR (1.4+/-5mL/min/1.73m(2)) from baseline in response to aliskiren. There was a clear correlation between the change in RPF and the change in GFR between subjects (r=0.65; P < .003). A substantial increase in RPF was accompanied by a rise in GFR. Dependence of GFR on RPF was identified in healthy humans after RPF rose significantly with aliskiren. The responsible mechanism likely involves intravascular oncotic pressure along the glomerular capillary resulting in greater surface area available for filtration.
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PMID:Renal plasma flow: glomerular filtration rate relationships in man during direct renin inhibition with aliskiren. 2040 74