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Biomedical subjects

R J Grekin

Publications and source records attributed to R J Grekin.

67 records · Page 4Linked to original sources
PubMed1981

Hormonal adaptation to the stresses imposed upon sodium balance by pregnancy and lactation in the Yanomama Indians, a culture without salt.

The Yanomama Indians of northern Brazil and southern Venezuela have been identified as a "no-salt" culture. In this study, data were obtained to determine in this population the adjustments of sodium-related hormones to the stresses imposed upon sodium balance by pregnancy and prolonged lactation. Controls against the possibility that findings in the Yanomama were ethnic rather than dietary were provided by similar observations in the Guaymi Indians of Panama, who have free access to salt. Urinary concentrations of sodium were approximately 1 mEq/l in male and female Yanomama, with 24-hour excretion rates in the males averaging 1 mEq, similar to our prior observation. The pregnant Yanomama had exceeding high urinary concentrations of aldosterone. These were associated with higher plasma renin activities and serum aldosterone concentrations than in all other subjects. Although pregnant Guaymi had elevations of serum and urinary aldosterone, these were significantly lower (p < 0.001) than those of the Yanomama. Prolonged lactation in the Yanomama was associated with elevation of plasma renin activity and serum and urinary aldosterone concentration compared with the Guaymi, but were not higher than those in nonlactating Yanomama females. The findings suggest that pregnancy in a salt-poor environment is associated with an exaggerated augmentation of hormonal responses that enhance positive sodium balance.

Adult↗
PubMed1981

Aldosterone receptor measurements during changes in dietary sodium.

Type I aldosterone receptors were measured in rat kidney cytosol preparations after alterations in dietary sodium and aldosterone injection. Changes in sodium intake had no effect on receptor number or affinity in adrenalectomized rats. Intact rats had decreased receptor numbers after a low sodium diet compared to those after a high sodium diet (P less than 0.005), and the decrease in receptor number was significantly correlated with the corresponding rise in serum aldosterone (r = -0.65; P less than 0.01). In adrenalectomized rats, injection of aldosterone was associated with a decrease in receptor number, and serum aldosterone correlated inversely with receptor number (r = 0.64; P less than 0.01). We conclude that increases in serum aldosterone decrease the number of available cytoplasmic aldosterone receptors, but changes in sodium intake have no direct effect upon aldosterone receptor number or affinity.

Adrenalectomy↗
PubMed1981

The relationship of adrenal iodocholesterol uptake to adrenal zona glomerulosa function.

Dexamethasone suppression adrenal scintigraphy is routinely used in the clinical assessment of patients with aldosteronism. To determine the relation between adrenal iodocholesterol uptake and aldosterone secretory activity, iodocholesterol uptake in dexamethasone-suppressed dogs was measured during salt loading and salt depletion. Sodium loading resulted in decreases in both serum aldosterone and adrenal iodocholesterol uptake. Sodium depletion was associated with increases in both serum aldosterone and iodocholesterol uptake. From these studies we calculate that under basal conditions, approximately 10% of adrenal iodocholesterol uptake is angiotension dependent, and approximately 50% is ACTH dependent. The administration of dexamethasone results in an increase in the sensitivity of adrenal scintiscanning in the assessment of adrenal zona glomerulosa function.

19-Iodocholesterol↗
PubMed1980

Angiotensin II-induced aldosterone stimulation in man is not dependent upon adrenocorticotropin.

To document a possible role of ACTH in the aldosterone response to angiotensin II, we measured plasma aldosterone levels during physiological increments in plasma angiotensin II in normal male volunteers on two occasions, once with suppression of endogenous ACTH secretion (dexamethasone or hydrocortisone) and again without ACTH suppression. The subjects were studied under standardized conditions of dietary sodium (40 mmol/day) and potassium (100 mmol/day) intake and controlled body posture. Glucocorticoid pretreatment did not alter the plasma levels of angiotensin II attained during incremental infusions (0.5, 1, 2, and 4 ng/kg . min) of the octapeptide. Baseline plasma aldosterone levels were significantly lowered by glucocorticoid pretreatment. However, aldosterone responsiveness to infused angiotensin II (change and percentage of change from baseline levels) was not altered by suppression of endogenous ACTH production. Serum potassium levels were not increased by the administration of angiotensin II. The results demonstrate that in normal males on a sodium-restricted diet, baseline aldosterone levels are controlled in part by ACTH. The aldosterone response to angiotensin II, however, is not dependent upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH, or a rise in serum potassium.

Adrenocorticotropic Hormone↗
PubMed1979

Disorders of chloriuretic hormone secretion.

Experimental evidence supports the existence of a circulating substance, natriuretic hormone, which augments electrolyte excretion. Because such a hormone probably acts by inhibiting chloride reabsorption in the thick, ascending limb of the loop of Henle it would more accurately be called chloriuretic hormone. Chloriuretic hormone must have an action which resembles that of loop diuretics such as frusemide and ethacrynic acid. An excess of chloriuretic hormone could explain all the manifestations of Bartter's syndrome, whereas a deficiency could account for Gordon's syndrome. Hyporeninaemic hypoaldosteronism may develop in subjects who are unable to increase chloriuretic hormone concentrations appropriately in response to progressive impairment of renal function.

Aldosterone↗
PubMed1979

Adrenal imaging with iodomethyl-norcholesterol (I-131) in primary aldosteronism.

Twenty consecutive patients with primary aldosteronism (PAl) underwent dexamethasone suppression (DS) imaging with 6beta-[131I]-iodomethyl-19-norcholesterol (NP-59): A) to establish the value of the adrenal scan in distinguishing aldosteronomas from bilateral hyperplasia; b) to determine its ability to locate aldosteronomas when present; and c) to compare the efficacy of NP-59 in this current series against that reported previously with NM-145 in PAl. Ten of twenty patients had an aldosteronoma, five had histologically confirmed hyperplasia, and five had presumed hyperplasia. With NP-59, nine of ten tumors were correctly located (90%) , correct distinction between tumor and hyperplasia was possible in 90%, and a locating DS scan was specific for tumor in 90%. In a combined series of different patients with PAl imaged with NM-125, 21 of 25 tumors were correctly located (84%), tumor was distinguished from hyperplasia in 86%, and the specificity of the localizing scan was 92%. The imaging delay required from tracer injection to attainment of an interpretable scan averaged 2.7 days with NP-59 and 4.8 days with NM-145. In summary, no significant differences were noted in the clinical results achieved with these two agents. The preferred agent is NP-59, since the study can be completed with less average time delay than is possible with NM-145.

Adosterol↗
PubMedDate not supplied

Electrolyte and hormonal effects of deoxycorticosterone acetate in young pigs.

Balances of sodium, potassium, and water were studied in the growing male pig as hypertension developed in response to subcutaneous implantation of deoxycorticosterone acetate (DOCA). Serum sodium, potassium, deoxycorticosterone (DOC), aldosterone, and plasma renin activity (PRA) were determined. These variables were observed in a total of 10 experimental and nine control pigs. All animals were uninephrectomized and fed a diet of Purina Pig Chow and tap water ad libitum. No salt was added to the food or water. Serum DOC levels rose dramatically on the day of the implantation, then gradually declined but remained approximately 10 times greater than control levels 40 days after implant. Plasma renin activity was suppressed rapidly and completely, whereas aldosterone fell only slowly to about half its control value. Sodium retention was maximum during the first 24 hours. Therefore an "escape" process became operative, causing sodium balance to return to normal after the third day, at which time the major rise in arterial pressure occurred. A marked increase in water turnover (intake and output) also began after the third day and persisted throughout the experimental period. Water balance remained normal during this period of increased turnover. Hypokalemia developed in the absence of kaliuresis, suggesting that potassium moved into the cells. Except for the potassium retention, these changes parallel the abnormalities seen in other states of mineralocorticoid excess.

Animals↗