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J Am Geriatr Soc. 1981 Aug;29(8):379-82.
Effect of age on active and inactive plasma renin in normal subjects and in patients with essential hypertension.

Nakamaru M, Ogihara T, Higaki J, Hata T, Maruyama A, Mikami H, Naka T, Iwanaga K, Kumahara Y, Murakami K.

The effect of age on the levels of active and trypsin-activatable inactive plasma renin was examined in 41 normal subjects and 54 patients with essential hypertension, during recumbency and after stimulation with furosemide and ambulation. Active renin levels in supine subjects and patients decreased with age. Inactive renin levels did not change with age in normal subjects, whereas in hypertensive patients they decreased with age. Following stimulation with furosemide and ambulation, the levels of active renin increased but the responsiveness to stimulus decreased with age in both groups. In contrast, inactive renin levels slightly increased after furosemide administration and ambulation, resulting in increased proportion of active to total renin. These data show that an acute stimulation with furosemide and ambulation affects mainly the active form of plasma renin, and the effect of age on inactive plasma renin in normal subjects may be different from that in patients with essential hypertension.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7021646&dopt=Abstract




J Lab Clin Med. 1981 Dec;98(6):929-37.
The effect of prostaglandin inhibition on renin release. A comparison of furosemide and low-sodium stimulation tests.

Goldiner WH, Valente WA, Hamilton BP, Mersey JH.

Furosemide administration is considered comparable to sodium restriction and upright posture as a stimulation test of PRA. This view can be questioned if different mechanisms of renin release are involved. Prostaglandins appear to be an important mediator of renin release. Using a prostaglandin antagonist, indomethacin, we attempted to assess the relative role of prostaglandins in the two renin stimulation tests. Eleven healthy volunteers on a high-sodium intake had PRA and PA measured in response to furosemide stimulation before and during indomethacin administration and then in response to sodium restriction combined with upright posture before and during indomethacin. Supine PRA was 0.41 ng/ml/hr on high sodium and 0.19 after indomethacin (p less than 0.05). On low sodium, the supine PRA was 2.07 ng/ml/hr and 0.98 after indomethacin (p less than 0.05). The increase in PRA (delta PRA) was 3.26 ng/ml/hr with furosemide stimulation and 1.23 after indomethacin (p less than 0.025). The PRA was 3.71 ng/ml/hr with low-sodium stimulation and upright posture and 2.53 after indomethacin (NS). PA paralleled PRA except that there was no suppression of supine values with indomethacin. We conclude that prostaglandins mediate baseline renin secretion and renin stimulation in response to furosemide. However, no comparable prostaglandin mediation could be demonstrated during renin stimulation secondary to sodium restriction. The two standard renin stimulation tests appear to involve different mechanisms of renin release.

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Artif Organs. 1982 May;6(2):220-4.
Furosemide-induced increase in urinary and peritoneal excretion of uric acid during peritoneal dialysis in patients with chronic uremia.

Grzegorzewska A, Baczyk K.

Intermittent peritoneal dialysis was performed in 17 patients with chronic uremia in order to observe the effect of furosemide added to the dialysate on urinary and peritoneal elimination of uric acid. Two kinds of dialysate were used: moderately hypertonic (osmolality, 431.2 mOsm/kg of water) and slightly hypertonic (osmolality, 368.9 Osm/kg of water). Significant increases in urine volume, urinary and peritoneal excretion of uric acid, and renal and peritoneal clearances were found. The increase in urinary excretion of uric acid exceeded that of urine volume. These findings were interpreted to be the result of furosemide action on renal function after being transferred through the peritoneum into the blood stream with the concomitant increase in the uric acid shift from the circulation into the peritoneal cavity. We concluded that the addition of furosemide is useful in increasing uric acid elimination in patients with chronic uremia.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7125968&dopt=Abstract













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