Effects of hormones on the rate of the triacylglycerol/fatty acid substrate cycle in adipocytes and epididymal fat pads.
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Biomedical subjects
Publications and source records attributed to B Brooks.
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Liver involvement is uncommon in secondary syphilis and may resemble liver disease from alcoholism or acute viral hepatitis. Liver biopsy usually indicates nonspecific reactive hepatitis with or without cholestasis. Jaundice may sometimes be absent although liver damage is present. The liver abnormalities can be resolved with antibiotic therapy, but penicillin therapy may cause Jarisch-Herxheimer reaction. Syphilitic hepatitis should be considered in the differential diagnosis of obscure liver disease.
A monolayer cell culture of juxtaglomerular cells (JGC) was derived from the renal cortex of neonatal rats. The JGC had the characteristics of those within the kidney, including peripheral dense bodies and myofibrils indicating a smooth muscle origin; rough ER containing fluffy material consistent with protein synthesis; a prominent Golgi apparatus for packaging granules, and granules having the characteristics of secretory granules and lysosomes. Transplants of the cultured cells into syngeneic recipients survived for 2 weeks or longer and retained the features of JGC. The JGC granules fluoresced when treated with a rabbit antibody against pure rat renin, followed by fluorescein isothyocyanate conjugated F(ab')2 fragment of goat antirabbit IgG (Fc fragment) heavy chain specific. The latter indicated the presence of renin. The JGC were lysed in the presence of DFP, captopril, leupeptin, and EDTA, and were extracted in the presence of pepstatin. The lysate contained renin activity that was inhibited by a specific renin antibody. Nonspecific proteases were excluded by the antibody and its pH optimum. Angiotensin I-converting enzyme was detected in the lysate prepared without the use of EDTA and captopril. Angiotensins I and II/III were derived from the extract by additional extractions, TLC, and RIA, using highly specific antibodies. The angiotensins were confirmed by chromatography monitored by authentic angiotensins. We concluded that the cultured JGC contained renin, angiotensin I-converting enzyme, and angiotensin I and II/III.
Cultured JGC contain renin, angiotensin I, angiotensin I-converting enzyme, angiotensin II, and, by implication, the entire RAS. JGC, as transplants, appear to secrete angiotensin II/III directly into the bloodstream to cause hypertension when the renal mass is reduced. There are two main phases of the hypertensive state, an angiotensin-dependent developmental phase and a non-angiotensin-dependent maintenance phase. This model may be useful in attempts to evaluate pro-hypertensive actions of angiotensin other than those due to direct systemic vasoconstriction. Certain of these actions appear to be intrarenal and include the stimulation of sodium reabsorption, a decrease in renopapillary blood flow, the stimulation of prostaglandin synthesis, and a constraint on the antihypertensive function of the RIC.
The ANRL was derived from the renal venous effluent as the kidney exerted its nonexcretory antihypertensive function. This was made possible by three developments: (1) improvement in the extraction of ANRL from fresh renal medulla; (2) the fact that purified ANRL caused an acute vasodepressor effect (acted as a vasodilator); and (3) experience with unclipping the one-kidney, one-clip hypertensive rat. Unclipping after an anastomosis between the ureter and the vena cava caused the MAP to return to normal levels in an average of 20 hr. At an average of 5 hr, when the MAP had dropped an average of 34 mm Hg (from approximately 190), an exchange infusion was started and blood was collected from the renal vein. The plasma was separated, lyophilized, and extracted for total lipids. The lipids were subjected to two TLC procedures and tested for vasodepressor activity. Renal venous effluent, under those conditions, yielded a considerable amount of vasodepressor lipid that was similar to that derived from fresh renal medulla. Controls (normal, nephrectomized, and hypertensive animals) yielded little or no such lipid. Indomethacin did not interfere with the derivation of the vasodepressor lipid. As the MAP was lowered and the ANRL-like lipid appeared in the renal venous blood, the RICs degranulated. The RICs appear to be the source of the antihypertensive lipid.
1. The antihypertensive neutral renomedullary lipid (ANRL) is a natural product derived from fresh renal medulla and from venous blood. 2. ANRL appears to be an antihypertensive hormone secreted when the kidney exerts its antihypertensive function after unclipping. 3. The kidney appears to be the main source of ANRL, maintaining a basal rate of secretion of ANRL. 4. The kidney of the one-kidney, one-clip hypertensive rat appears to secrete an inappropriate amount of ANRL. Thus a deficiency of the secretion of the antihypertensive hormone may play a role in the pathogenesis of the one-kidney, one-clip hypertensive model. 5. Degranulation of the renomedullary interstitial cells (RIC) occurs as the kidney exerts its antihypertensive action after unclipping, supporting these cells as the source of ANRL. 6. Channels between collecting duct cells may encourage water reabsorption while the clip is in place; conversely, the closure of these channels when the clip is removed may encourage the diuresis that is observed.
The role of vasopressin in the pathogenesis of partial nephrectomy (PN)-salt hypertension was examined in the rat. Hypertension was produced by reducing renal mass 70% and substituting 1% saline for drinking water 2 to 4 days after surgery. PN alone resulted in an increase in systolic blood pressure. Subsequent salt loading led to a further large increase in arterial pressure. On the second to third day after substitution of saline for drinking water, urinary vasopressin excretion (UADHV) was increased six-fold and the plasma vasopressin concentration was increased two and one-half-fold. UADHV then fell to a level that was three-fold greater than control values 5 days later. Although there was a marked stimulation of vasopressin release during the period of salt loading, a vasopressin pressor antagonist had only a small effect on arterial pressure. This suggests vasopressin is not a major pressor agent in PN-salt hypertension.
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The kidney exerts both prohypertensive and antihypertensive functions. Part of the anti-hypertensive function of the kidney is mediated by the renomedullary interstitial cells (RIC), as an endocrine-type function. Six experimental models of hypertension and their relation to the antihypertensive function of the RIC are discussed. It is proposed that the anti-hypertensive function of the RIC may be deficient by the three mechanisms: 1) absence of the cells (as in the renoprival state); 2) severe damage to the cells (as in partial nephrectomy-salt hypertension of the rat and late malignant hypertension of the rabbit); and 3) constraint of the function of these cells (as in angiotensin-salt hypertension due to a lower salt intake). The constraint may result from excessive angiotensin, either by a direct effect or via a hemodynamic mechanism. The converting enzyme inhibitors (CEI) fail to exert their antihypertensive function when the RIC are absent or damaged. Conversely, the CEI are effective in those models associated with intact RIC. CEI appear to exert their antihypertensive action partly through an effect on RIC.
Four types of lipids with potential antihypertensive properties have recently been derived from the kidney. These consist of prostaglandins (PG), a renin inhibitor, a neutral lipid, and alkyl ether analogs of phosphatidylcholine. PGI2, mostly renocortical, and PGE2, mostly renomedullary, may aid the antihypertensive function of the kidney by decreasing renal vascular resistance and shunting blood toward the juxtamedullary zone and the renal papilla, where the renomedullary interstitial cells (RIC) are located. Several analogs of the renin inhibitor are available. The neutral lipid is a natural product derived from fresh renal medulla and from RIC grown as monolayer tissue culture. The alkyl ether analogs of phosphatidylcholine (formerly designated as the antihypertensive polar renomedullary lipid or APRL) are orally active vasodilators. They cause a prolonged depressor effect due to a decrease in peripheral vascular resistance. The latter may be partly due to alpha-adrenergic antagonism.
Allied health educators are expected to have exemplary clinical skills. Opportunities to practice are often limited in the academic setting. One method for insuring the maintenance of clinical skills among allied health faculty is a professional practice clinic. The University of Texas School of Allied Health Sciences at Houston, in conjunction with a teaching affiliate, Hermann Hospital, has opened a free-standing nutrition clinic on a fee-for-service basis. Reasons for establishing a clinical practice included: 1) to provide opportunities for faculty to practice; 2) to provide a teaching laboratory; 3) to provide a community service; 4) to provide a mechanism for research with defined groups; and 5) to facilitate faculty development with fee-generated income. A partnership model between the university and hospital was proposed which included the organizational structure, description of services, fee schedule, and funding base. Evaluation areas will include: impact on educational program, effectiveness as health counselors, faculty and staff growth, and generated income as profit.
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Captopril (SQ 14225), a converting enzyme inhibitor, significantly lowered the arterial pressure (AP) of rats with angiotensin-salt hypertension, a hypertensive state associated with sodium retention, volume expansion, and suppression of both renin and aldosterone secretion. While captopril was acting, there was no increase in sodium, potassium, or water excretion. Thus, the antihypertensive effect was not due to natriuresis or diuresis. Moreover, as the AP was lowered, there was no change in plasma renin concentrtion, the pulse rate was lowered, and the lack of potassium retention suggested minimal or no effect on aldosterone secretion. The mechanism of action of captopril in a sodium-volume-expanded, renin-aldosterone-suppressed state is unknown.
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Obligatory urinary and fecal nitrogen losses and urinary urea nitrogen and creatinine excretion levels were determined in 11 young women (four of whom used oral contraceptives), eight older men, and five young men. Values for obligatory nitrogen losses in the young women who did not use oral contraceptives were similar to those observed previously in young women and lower than those reported for young men. Our values for older men were lower than previously reported values for obligatory losses observed in young and elderly men, but similar to previously reported values for young women and to values for our women who did not use oral contraceptives. The four oral contraceptive users had significantly higher levels of total urinary and fecal obligatory nitrogen losses than the nonusers in our study. When values from our study and values from other recent studies are considered, variations in obligatory nitrogen losses appear to be larger among individuals within an age-sex group than the observed differences between groups. When the intakes of protein recommended as safe by the Food aculated from obligatory nitrogen losses per se, the recommended levels appear to be only marginally adequate.
A case of an extrarenal Wilms tumor arising in the inguinal region of a 2-month-old boy is described. A review of the literature indicates that nine well-documented cases of extrarenal Wilms tumor have previously been described. Four of these tumors arose within teratomas. The remaining five cases, in which no teratomatous components were encountered, probably arose in embryologic rests of renal tissue.
Transplants and lipid extracts of the same monolayer tissue culture of renomedullary interstitial cells from murine renal medulla exerted a similar antihypertensive action in rats having hypertension of the sodium-volume-dependent-type. The antihypertensive action resembled that caused by lipid extracts of rabbit renal medulla and extracts of lapine renomedullary interstitial cells grown in tissue culture. The recession of the arterial pressure of the hypertensive animals usually occurred slowly and steadily to a maximum within 6 to 12 hours. On occasions, a substantial acute depressor effect preceded the slow and steady decline of the pressure. As the pressure was lowered, there was either minimal or no change in the pulse rate. The lowering of the hypertensive pressure before there was vascularization of the transplant appears to support the view that the transplanted cells secreted and/or liberated an antihypertensive substance(s) that seeped out and was absorbed by nearby capillaries and/or lymphatics and circulated and acted in the manner of a hormone. The extracted and purified lipid from the same cells as used for transplantation is proposed as a candidate for such hormonal action. Evidence is presented that minimizes the possibility of the classic renomedullary prostaglandins as this antihypertensive lipid. The findings add support to the concept that the kidney exerts a hormonal antihypertensive action that opposes the well known hormonal prohypertensive renal actions.
1. Allogenic transplants of cultured renomedullary interstitial cells exert a powerful anti-hypertensive action. The blood pressure of hypertensive animals usually drops slowly over 8-12 h whereas the pulse is unchanged or reduced. 2. Lipids derived from the cultured cells exert a similar anti-hypertensive action. 3. The anti-hypertensive action of transplanted cultured cells almost certainly results from the secretion of a substance(s) that acts in the manner of a hormone. The tissue culture lipid is a prime candidate hormone. 4. The relationship of the kidney to the hypertensive state is considered to entail pro- and anti-hypertensive actions. The pro-hypertensive actions include (a) activation of the renal pressor system (mainly renin-angiotensin), (b) failure to prevent sodium and fluid overloading because of either an injured or absent kidney or the excessive action of mineralocorticoids (mainly aldosterone). The antihypertensive actions of the kidney include (a) the relief of sodium and fluid overloading through diuresis-natriuresis and (b) the action of the reno-medullary interstitial cell hormone (the antihypertensive renomedullary hormone).