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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a result of effective beta adrenergic blockade with either propranolol or practolol, plasma renin activity was suppressed in all of 11 patients with cirrhosis and ascites. In contrast, the effect on the rate of renal excretion of aldosterone was variable, suggesting that factors other than the renin-angiotension system are responsible for the control of aldosterone secretion in cirrhosis. The changes in aldosterone could not be explained on the basis of changes in the plasma concentrations of potassium or sodium. The renal sodium excretion was inversely related to the values for aldosterone both before and after beta adrenergic blockade, indicating a major role for aldosterone in regulating sodium excretion. A number of patients had an abnormal intrarenal distribution of plasma flow with a relative hypoperfusion of the renin-secreting outer cortical nephrons. Plasma renin activity was inversely related to outer cortical plasma flow, suggesting that the reduced outer cortical flow may be a stimulus to increased renin secretion. Because the abnormal intrarenal hemodynamic pattern was not corrected by suppression of plasma renin activity, and presumably angiotension II concentrations, it is unlikely that it is attributable to the known renal vasonconstrictor effects of angiotensin II.
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PMID:Effect of beta adrenergic blocking drugs on the renin-aldosterone system, sodium excretion, and renal hemodynamics in cirrhosis with ascites. 1 38

Cardiovascular responsiveness to reflex impaired in patients with cirrhosis compared with control subjects. Peripheral vascular responses to exogenous noradrenaline were also impaired in cirrhotic patients, but peripheral vascular responses to infused adrenaline and to angiotensin II were similar in both groups. Impaired cardiovascular reactivity in patients with chronic liver disease could predispose them to circulatory failure after haemorrhage or surgery and should be considered when prescribing drugs which affect autonomic activity.
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PMID:Impaired cardiovascular responsiveness in liver disease. 5 Nov 90

[1-Sarcosine, 8-Isoleucine] angiotensin II was given to 8 patients with cirrhosis and ascites and 7 cirrhotic patients without ascites on a regular diet. The 3 ascitic patients with high plasma renin activity (PRA) gave a depressor response, but the other ascite patients with normal or low PRA gave a pressor response or no response. All the non-ascitic patients gave a pressor response. There was an inverse correlation between the PRA before infusion and the change in blood pressure induced by this compound. In the patient with the highest PRA, who had ascites of a few days' duration, a marked reduction in blood pressure was observed on infusion of this compound. These results suggest that the renin-angiotensin system might be involved in maintenance of a normal blood pressure in some patients with cirrhosis and ascites, whose ascites is presumably in an early stage.
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PMID:Blood pressure response to [1-sarcosine, 8-isoleucine] angiotensin II in patients with liver cirrhosis and ascites. 44 13

Plasma angiotensin II and plasma aldosterone was measured by radioimmunoassay in 78 patients with cirrhosis of the liver (group I: untreated, without ascites, n = 21; group II:untreated, with ascites, n = 25; group III: with ascites, during saluretic therapy, n = 32). From the obtained results it was concluded: (1) Excluding any pretreatment on the outpatient basis in most cirrhotics with or without ascites unaltered plasma levels of angiotensin II and aldosterone were found. (2) In contrast to previous suggestion secondary aldosteronism seems to be a minor determinant of hepatic ascites formation. (3) In untreated patients the 24-h-urinary excretion of electrolytes (Na+/K+ less than 1) represents an insufficient index of hyperaldosteronism. Obviously the kidney retains considerable amounts of sodium independent of circulating aldosterone levels. (4) Far above other mechanism hyperaldosteronism is most often induced by saluretic treatment of ascites and edema. The increased aldosterone secretion might indicate an adaptation phenomenon to restore total body sodium content. Certainly, the established concept of ascites therapy remains unimpaired by this physiological reaction.
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PMID:[Secondary hyperaldosteronism in patients with liver cirrhosis, frequently caused by therapy]. 45 75

Plasma renin activity (PRA), plasma renin concentration (PRC), angiotensinogen, angiotensin II (AT II) and plasma aldosterone were determined by radioimmunoassay in 77 patients with cirrhosis of the liver [group I: with ascites, untreated (n=23); group II: patients with ascites during treatment (n=32); group III: after removal of fluids, but under further spironolactone therapy (n=10); group IV: untreated subjects without ascites (n=12)]. With the exception of decreased angiotensinogen values in all groups ranging between 39% (group IV) and 73% (group III) no significant changes of the other parameters of the RAAS were found in untreated patients. A highly significant increase of PRA, PRC, AT II and plasma aldosterone was observed in treated cirrhotics with (group II) or without (group III) ascites. In the total series of patients AT II was closely related to PRA, PRC and aldosterone emphasizing aldosterone secretion. Plasma sodium was inversely correlated to PRA, PRC, AT II and aldosterone, but no relationship was detected between these parameters of the RAAS and plasma potassium. Our results indicate that hyperaldosteronism in cirrhosis appears unlikely to be the major determinant of avid renal sodium retention and ascites formation. An increased activity of the RAAS is most often initiated by therapeutic factors and/or markedly altered electrolyte metabolism. Therefore, basal conditions of the patients to be studied must be well defined to exclude any artificially induced stimulation of the RAAS.
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PMID:Studies on the activity of the renin-angiotensin-aldosterone system (RAAS) in patients with cirrhosis of the liver. 64 12

Arterial and venous plasma concentrations of total immunoreactive angiotensin II (AT II), its bioactive hepta-octapeptide fraction and its inactive hexapeptide were measured in normal subjects (n=16), in patients with acute viral hepatitis (n=12), and in treated (n=16) and untreated (n=17) patients with cirrhosis of the liver and ascites. Independent of normal or increased values of total immunoreactive AT II, the ratio between the hepta-octapeptides and the hexapeptide remained unchanged. This might indicate continuous octapeptide generation and balanced metabolite turnover throughout the systemic circulation. Moreover, a significant arterio-venous peptide gradient was lacking. It has to be concluded that total venous plasma AT II sufficiently reflects both the arterial hormone concentration and its major fraction of hepta-octapeptides in arterial (79%) and venous (76%) blood.
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PMID:Total immunoreactive angiotensin ii, its hepta-octapeptide fraction, and its hexapeptide in patients with liver disease. 64 13

In an attempt to evaluate the role of renin-angiotensin system in the contols of blood pressure and aldosterone secretion in the patients with cirrhosis and asictes, 7 patients were infused of an antagonist of angiotensin II, Sar-1 Ile-8 angiotensin II, intravenously to inhibit the action of renin-angiotensin system and to observe changes in arterial pressure and plasma aldosterone. In 1 patient with recent onset of severe ascites and high plasma renin activity, blood pressure and plasma aldosterone decreased during the infusion. In contrast, mild rise in blood pressure and various changes in plasma aldosterone were observed in the other 6 patients with normal plasma renin activity. These results suggest variable angiotensin dependency in the controls of blood pressure and plasma aldosterone in the patients with cirrhosis and ascites according to the stage of the disease, the states of sodium and water balance and/or palasma renin activity.
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PMID:Role of renin-angiotensin system in the controls of blood pressure and aldosterone in patients with cirrhosis and ascites. 73 36

1-Sar-8-ala angiotensin II (saralasin) was infused intravenously in graded doses of from 0.1 to 10 mug/kg/min to five patients with cirrhosis and ascites after three days of restricted sodium intake. In each patient blockade of AII by saralasin produced a marked fall in blood pressure, a rise in plasma renin activity (PRA) and plasma renin concentration (PRC) and, in four of the five, a fall in plasma aldosterone (PA). The rise in PRA and PRC correlated poorly with changes in blood pressure. The effects of saralasin rapidly reversed after cessation of the infusion. Plasma volume was normal or high in each case. Three patients were mildly hypotensive in the control state, and all five were resistant to the pressor effect of infused AII. After three days of salt loading, the above effects of saralasin were diminished but not abolished. In four normal subjects, after salt depletion, saralasin infusion induced qualitatively similar but much smaller changes in blood pressure, PRA and PRC. In two cirrhotic patients without ascites, after salt depletion, saralasin infusion caused a rise in blood pressure with no significant changes in PRA, PRC or PA. These results provide evidence that in patients with cirrhosis and ascites circulating AII is active in support of blood pressure, in direct suppression of renal renin release, and in stimulation of aldosterone release.
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PMID:Effect of blockade of angiotensin II on blood pressure, renin and aldosterone in cirrhosis. 94 Feb 84

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


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