Atrial natriuretic factor (ANF) and renin-aldosterone in volume regulation of patients with cirrhosis

The role of the atrial natriuretic factor and of the main counteracting sodium-retaining principle, the renin-aldosterone system, in acute volume regulation of cirrhosis of the liver has been investigated. Central volume stimulation was achieved in 21 patients with cirrhosis, 11 without and 10 with ascites, and 25 healthy controls by 1-hr head-out water immersion. Immersion prompted a highly significant (p<0.001) increase of atrial natriuretic factor plasma concentrations in cirrhotic patients without ascites from 8.5 ± 1.3 fmoles per ml to 16.5 ± 2.6 fmoles per ml, comparable to the stimulation in control subjects (6.0 ± 0.6 fmoles per ml to 13.6 ± 2.6 fmoles per ml). In cirrhotic patients with ascites, atrial natriuretic factor increase (from 7.7 ± 1.3 fmoles per ml to 11.4 ± 2.3 fmoles per ml) was blunted (p<0.05). Plasma renin activity and plasma aldosterone concentration were elevated in cirrhotic patients, especially in the presence of ascites. Following immersion, plasma renin activity and plasma aldosterone concentration were reduced similarly in all groups. Water immersion induced a more pronounced natriuresis and diuresis in control subjects than in cirrhotic patients. Neither atrial natriuretic factor nor plasma renin activity nor plasma aldosterone concentration alone correlated to sodium excretion. However, atrial natriuretic factor to plasma aldosterone concentration ratios were closely correlated to basal and stimulated natriuresis in cirrhotic patients, particularly in those with ascites. These data suggest that atrial natriuretic factor and the renin-aldosterone system influence volume regulation in patients with cirrhosis

Influence of low and high pressure baroreceptors on plasma renin activity in humans

The effects of low and high pressure baroreceptors on plasma renin activity (immunoassay) were evaluated using graded lower body suction (LBS) in six healthy men. LBS at -10 and -20 mmHg for 10 min decreased central venous pressure without changing arterial pressure and thereby presumably reduced low but not high pressure baroreceptor inhibition of renin release. LBS at these levels produced forearm vasoconstriction, but did not increase renin. LBS at -40 mmHG decreased central venous and arterial pulse pressure and thus reduced both low and high pressure baroreceptor inhibition. LBS at this level produced forearm vasoconstriction and tachycardia and increased renin. In summary, reduction in low pressure baroreceptor inhibition in humans did not increase renin in the presence of physiological tonic inhibition from high pressure baroreceptors. Increases in renin did not occur until there was combined reduction of high and low pressure baroreceptor inhibition on plasma renin activity

Renin-Angiotensin-Aldosterone System, Glucose Metabolism and Incident Type 2 Diabetes Mellitus: MESA.

Background Mechanistic studies suggest that aldosterone impairs glucose metabolism. We investigated the cross-sectional associations of aldosterone and plasma renin activity with fasting plasma glucose, insulin resistance ( IR ), β-cell function, and longitudinal association with incident diabetes mellitus among adults in MESA (the multiethnic study of atherosclerosis) prospective cohort study. Methods and Results Homeostatic model assessment of IR ( HOMA 2- IR ) and HOMA 2-β were used to estimate IR and β-cell function, respectively. Incident diabetes mellitus was defined as fasting plasma glucose ≥126 mg/dL or anti-diabetic medication use at follow-up. Linear regression was used to examine cross-sectional associations of aldosterone with fasting plasma glucose, HOMA 2- IR and HOMA 2-β; Cox regression was used to estimate hazard ratios ( HR ) for incident diabetes mellitus with multivariable adjustment. There were 116 cases of incident diabetes mellitus over 10.5 years among 1570 adults (44% non-Hispanic white, 13% Chinese American, 19% Black, 24% Hispanic American, mean age 64±10 years, 51% female). A 100% increase in log-aldosterone was associated with a 2.6 mg/dL higher fasting plasma glucose, 15% higher HOMA 2- IR and 6% higher HOMA 2-β ( P&lt;0.01). A 1- SD increase in log-aldosterone was associated with a 44% higher risk of incident diabetes mellitus ( P&lt;0.01) with the greatest increase of 142% ( P&lt;0.01) observed in Chinese Americans ( P for interaction=0.09 versus other ethnicities). Similar cross-sectional findings for log-plasma renin activity existed, but log-plasma renin activity was not associated with incident diabetes mellitus after full adjustment. Conclusions Aldosterone is associated with glucose homeostasis and diabetes mellitus risk with graded associations among Chinese Americans and blacks, suggesting that pleiotropic effects of aldosterone may represent a modifiable mechanism in diabetes mellitus pathogenesis with potential racial/ethnic variation

Zero gravity and cardiovascular homeostasis. The relationship between endogenous hyperprolactinemia and plasma aldosterone

Prolactin, thyrotropin and aldosterone were measured by radioimmunoassay and plasma renin activity by the radioimmunoassay of angiotensin I in normal women before and after the intravenous injection of 200 micrograms of thyrotropin releasing hormone. Prolactin increased at 15 minutes following thyrotropin releasing hormone. Plasma renin activity was not different from control levels during the first hour following the administration of thyrotropin releasing hormone, nor did the plasma aldosterone concentration differ significantly from the control levels during this period. However, with upright posture, an increase in aldosterone and in plasma renin activity was noted, demonstrating a normal capacity to secrete aldosterone. Similarly, no change in aldosterone was seen in 9 patients with primary hypothyroidism given thyrotropin releasing hormone, despite the fact that the increase in prolactin was greater than normal. These data demonstrate that acutely or chronically elevated serum prolactin levels do not result in increased plasma aldosterone levels in humans

Acute Alteration of Plasma Renin Activity by Large Doses of Intravenous Prednisolone

Large doses of intravenous glucocorticoids have been used in an attempt to reverse homograft rejection. The intravenous administration of 1 g prednisolone over 1 hr resulted in a significant acute reduction of plasma renin activity in 5 normal subjects tested and in 11 out of 15 patients bearing renal homografts. No definite explanation for failure to respond nor the mechanism of this prednisolone effect is readily at hand. An acute decrease in renin activity could be salutary for the chronically or acutely rejecting patient in that it could reduce vasopressor and salt-retaining effects. However, several of the non-responders had an increase in renin activity which could have been detrimental. © 1972, SAGE Publications. All rights reserved

Variations in Arterial Blood Pressure after Kidney Transplantation

The course of hypertension within the first 2 months after kidney transplantation was correlated with renal function, plasma renin activity (PRA), and the daily maintenance dose of prednisone in 18 homograft recipients. During acute rejection blood pressure (BP) closely correlated with PRA. Patients with normal homograft function showed an increase in BP early after transplantation which in most returned to normal 3-8 weeks later. In the latter group no correlation could be found between the level of BP and PRA, however the BP correlated closely with the dose of prednisone. These observations suggest that during acute rejection the increase in BP may at least partly be mediated by a renal pressor mechanism, whereas with normal renal function the high dose of glucocorticoids may play an important role in the development of hypertension.</jats:p

Rebound Rise in Renin Concentrations after Cessation of Salicylates

Salicylates are widely used in the treatment of rheumatic disorders, and they have been shown to induce minor changes in renal function. One of the major mechanisms of action of salicylates is the suppression of prostaglandin synthetase activity, and in animal rnodels renal prostaglandin production is closely related to renin release and the regulation of renal blood flow. Indomethacin has been shown to decrease the glomerular filtration rate and to lower plasma renin activity in human beings, and to reduce the antihypertensive effectiveness of cer¬tain beta-adrenoreceptor-blocking agents. We there-fore studied the effects of aspirin, another commonly prescribed non-steroidal anti-inflammatory agent, on plasma renin concentration, both during administra¬tion and after withdrawal

Hypokalemic rhabdomyolysis: a rare manifestation of primary aldosteronism

Rhabdomyolysis is a rare presentation of hypokalemia, although muscle weakness is a well-known manifestation of hypokalemia. Primary aldosteronism is characterized by hypertension, suppressed plasma renin activity, increased aldosterone excretion and hypokalemia with metabolic alkalosis. Rhabdomyolysis is not common in primary aldosteronism. We present here a 40-year-old woman presenting with rhabdomyolysis accompanied by severe hypokalemia as heralding symptom of primary aldosteronism

Measurement of renin in both renal veins: its use in diagnosis of renovascular hypertension

THE RECENT development of a simple reliable method for measuring plasma renin activity, together with the availability of a safe procedure for obtaining samples of blood from both renal veins, has prompted us to assess the utility of such measurements in the diagnosis of surgically correctable renovascular hypertension. Previous studies of this type have been reported by McPhaul,1 Fitz,2 Kirkendall,3 and Ueda,4 and their associates. A series of 22 patients, diagnosed by conventional measures as having renovascular hypertension, were subjected to operative treatment. Proof of the diagnosis was considered to be established if there was unquestionable improvement in blood pressure after corrective surgery. This is a report of the measurements of renin activity in blood plasma specimens obtained from both renal veins preoperatively and, whenever possible, postoperatively. In addition, plasma renin activity in effluent blood from both kidneys was measured in 13 patients with "essential" hypertension, who were not subjecte