Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal prostaglandins have several potential functions in renal physiology. Perhaps their best documented role is the maintenance of renal blood flow during renal ischemia, although they are apparently not essential to blood flow autoregulation in the absence of ischemia. Alterations in sodium excretion parallel the hemodynamic changes induced by prostaglandin infusions and prostaglandin inhibition with indomethacin. A direct action on sodium balance is unproven. Numerous studies, in vivo and in vitro, have convincingly demonstrated that prostaglandins or their precursors stimulate renin release and prostaglandin inhibition blunts renin release independent of hemodynamic and electrolyte balance. These functions of prostaglandins have implicated them in the manifestations of Bartter's syndrome, the nephropathy of liver cirrhosis, renovascular hypertension, and other nephropathies.
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PMID:Prostaglandins: renin release and renal function. 72 86

Infusion of the angiotensin-II-antagonist saralasine led in one patient with Bartter's syndrome and one patient with decompensated hepatic cirrhosis, both of whom had a markedly raised plasma renin activity, to a fall in systolic and diastolic blood pressure. The results indicate that in normotensive patients a raised angiotensin II concentration in blood is haemodynamically important for the level of blood pressure if plasma renin activity is raised. In normotensives with normal plasma renin activity saralasine in the usual dosage (4.2 mug/kg-min) does not influence the blood pressure.
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PMID:[The influence of saralasine on blood pressure and renal function in Bartter's syndrome and decompensated hepatic cirrhosis (author's transl)]. 95 92

1-Sarcosine, 8-isoleucine angiotensin II (Sar1-Ile8-AII) was infused intravenously in 5 normal volunteers and 66 subjects with various hypertensive, fluid and electrolyte disorders. Changes of blood pressure (BP), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were studied. In normal subjects, Sar1-Ile-AII showed pressor (agonistic) activity, which was related to both dosage and sodium intake. Hyporeninaemic hypertensive subjects (pirmary aldosteronism) showed pressor responses to a smaller dose of this compound than the dose employed in normal subjects. Hyporeninaemic hypertensive subjects and normal volunteers after 3 days of high sodium intake showed significant elevations of BP and PAC and reduction of PRA. Changes of BP, PAC and PRA in normoreninaemic subjects including those with Bartter's syndrome, renal tubular acidosis or liver cirrhosis with ascites showed reduction of BP and PAC and elevation of PRA. The results indicate that the compound has both agonistic and antagonistic activities for blood pressure; which of these is obtained apparently depends upon endogenous angiotensin II levels, as well as the dosage employed. The results in subjects with high and low PRA suggest that the compound has antagonist and agonist actions at 3 sites of angiotensin II action, i.e. peripheral vascular bed, renin release mechanism from juxta-glomerular apparatus and the zona glomerulosa of the adrenals.
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PMID:Changes of blood pressure, plasma renin activity and plasma aldosterone concentration following the infusion of Sar1-Ile8-angiotensin II in hypertensive, fluid and electrolyte disorders. 101 63

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

The renin-angiotensin-aldosterone system (RAAS) is characterized by a circadian rhythm (CR) whose acrophase is detectable early in the morning. The prorenin and angiotensin converting enzyme (ACE) show a CR as well. However, while the prorenin is in phase with the RAAS the ACE shows its circadian acrophase in the afternoon suggesting a negative feed-back. The RAAS CR is influenced by many factors. Its mesor is modified by sodium intake. The physical activity and rest affect both the mesor and acrophase. The variations in mesor amplitude and acrophase in aged subjects are conditioned by sex and physical activity. Moreover, the RAAS CR seems to be influenced by the race. In addition, it is abolished by the beta-adrenergic blockade, suggesting the existence of an adrenergic clock. Interestingly, the RAAS CR seems not to be a pacemaker for the blood pressure CR, whose acrophase is early in the afternoon. The RAAS CR is not substantially modified has in essential hypertension. However, the CR of plasma renin activity is disappeared in the low-renin essential hypertension, while the CR of plasma aldosterone is detectable. On the contrary, the aldosterone CR is not detectable in ascitic liver cirrhosis; but, it is restored when the ascites is removed by peritoneal-jugular shunt. No significant variation of the RAAS CR seems to occur in obesity and Cushing's syndrome. The RAAS CR has disappeared in Conn's disease as well as in Bartter's syndrome and Liddle's syndrome. The administration of indomethacine in Bartter's syndrome and of triamterene in Liddle's syndrome is able to restore the RAAS CR. Finally, the RAAS CR is not detectable in the heart or kidney transplanted patients; such a phenomenon could be attributed to cyclosporine and corticosteroids administration and to the denervation of the transplanted organs.
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PMID:[Circadian rhythm of the renin-angiotensin-aldosterone system: a summary of our research studies]. 1555 56