Renal Autoexplantation and Protection Against Renoprival Hypertensive Cardiovascular Disease and Hemolysis *

282

116

Platelet-activating factor (PAF) acetylhydrolase has been recognized as an enzyme that inactivates PAF. We developed a convenient and reproducible method for determining human serum PAF acetyihydrolase activity. The assay was based on measurement of 1I4Clacetate produced from 1-O-alkyl-2-1'4C]-acetyl-sn-glycero-3-phosphocholine upon precipitation of the complex of radioactive substrate and albumin with TCA. The apparent Km value of PAF acetylhydrolase (near the physiological concentration of serum protein) was 1.5 X 10-4 M PAF. 32 subjects with serum PAF acetylhydrolase deficiency were found among 816 healthy Japanese adults. The low PAF acetylhydrolase activity in the deficient serum might not be due to the presence of enzyme inhibitor. Both the sensitivity to PAF and the metabolism of PAF in platelets from PAF acetylhydrolase-deficient subjects were almost the same as those of normal subjects. Deficiency in serum PAF acetylhydrolase appeared to be transmitted by autosomal recessive heredity among five Japanese families. Among healthy adults, healthy children, and asthmatic children, who were grouped into five classes on the basis of respiratory symptoms (remission, wheezy, mild, moderate, and severe groups), the probability of PAF acetylhydrolase deficiency was significantly higher in groups with severe symptoms (moderate and severe) (P < 0.01). These results suggest that deficiency of serum PAF acetylhydrolase might be one of the factors leading to severe respiratory symptoms in asthmatic children.

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of serum platelet-activating factor (PAF) acetylhydrolase. Correlation between deficiency of serum PAF acetylhydrolase and respiratory symptoms in asthmatic children.

Miwa¹,

Miyake²,

Yamanaka³

et al. 1988

282

116

“…In 1965 Lee, Covino, Takman, and Smith (1) presented evidence that prostaglandin E2 (PGE2),1 and medullin, Received for publication 19 October 1972 and in revised form 20 December 1972. lAbbreviations used in this paper: PGA, prostaglandin A, later renamed prostaglandin A2 (PGA2) were present in the renal medulla, the portion of the kidney known to have vasodepressor properties (2). Nissen (3) demonstrated that a period of salt repletion in salt-depleted rats induced an increase in the number of lipid droplets in renal medullary interstitial cells.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Chronic Sodium Loading and Sodium Restriction on Plasma Prostaglandin A, E and F Concentrations in Normal Humans

Rm¹,

Spector²,

Bv³

et al. 1973

A B S T R A C T It has been suggested that prostaglandins may be involved in the control of sodium homeostasis. Prostaglandin A and prostaglandin E have been shown to increase renal blood flow and urinary sodium excretion and prostaglandin A has been shown to stimulate aldosterone release. The purpose of this study was to determine the effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations.Seven normal human volunteers were placed on three sodium intake diets: (a) ad lib. sodium intake, (b) high sodium intake, and (c) low sodium intake. Plasma prostaglandin A, E, and F concentrations were measured by radioimmunoassay.Mean prostaglandin A levels on the ad lib. diet were 1.60 ng/ml. Prostaglandin A levels decreased 49% to 0.82 ng/ml on the high sodium intake and increased 34% to 2.14 ng/ml on the low sodium intake. Prostaglandin A levels increased 161% on the low sodium diet in comparison with levels on the high sodium diet. Plasma prostaglandin E and F concentrations did not change significantly during variation in sodium intake.These results show that dietary sodium content markedly effects plasma prostaglandin A levels and that prostaglandins may play a role in the physiologic mechanism of sodium homeostasis.

“…The renal medulla appears to contribute to the renal antihypertensive function through a nonexcretory action as indicated by results with three experimental models (15)(16)(17)(18)(19)(20)(21). As a consequence of these observations, antihypertensive and vasoactive lipids were extracted from renomedullary tissue (22)(23)(24)(25)(26) and certain of these depressor lipids were demonstrated to belong to the prostaglandin family of compounds, namely, prostaglandins E and A2 (27)(28)(29)(30).…”

mentioning

confidence: 99%

Renomedullary Antihypertensive Function in Accelerated (Malignant) Hypertension

Muirhead¹,

Brooks²,

Pitcock³

et al. 1972

Self Cite

A B S T R A C T The antihypertensive function of the renal medulla was tested on accelerated (malignant) hypertension of the rabbit. A procedure for the development of accelerated hypertension of the rabbit of lethal proportions within 3 wk was established. This procedure consisted of the application of a rigid clip with a fixed and unyielding gap to the left renal artery and removal of the right kidney. Three additional manipulations, other than simple nephrectomy, were performed on the right kidney after application of the rigid clip to the left renal artery. These were: (a) a sham operation, (b) removal of the kidney and separation of the renal cortex and its autotransplantation in a fragmented state, and (c) removal of the kidney and separation of the renal medulla and its autotransplantation in a fragmented state. After the shamoperated kidney and autotransplanted renal medulla, the standardized accelerated hypertension did not develop, whereas after autotransplanted renal cortex it did. After a period of protection against accelerated hypertension, removal of either the sham-operated kidney or the renomedullary transplants was followed by a prompt rise in arterial pressure and death of the animal.