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Biomedical subjects

R Franco-Saenz

Publications and source records attributed to R Franco-Saenz.

At least 55 records · Page 3Linked to original sources
PubMed1986

Mechanisms by which nephrectomy stimulates adrenal renin.

Renin has been identified in the adrenal gland by several investigators. Nephrectomy is the most potent stimulator of adrenal renin, and in the present study we investigated the mechanism by which nephrectomy stimulates adrenal renin. The pituitary plays a permissive role since hypophysectomy abolished the response of adrenal renin to nephrectomy (from 117.3 +/- 14.55 to 10.37 +/- 1.63 ng angiotensin I/mg protein/hr) and adrenocorticotropic hormone (ACTH) treatment restored the response to nephrectomy in hypophysectomized rats to 120 +/- 20.62 ng angiotensin I/mg protein/hr. However, large doses of ACTH given to intact rats did not increase adrenal renin to the high level observed after nephrectomy. Potassium also plays an important role, since prevention of hyperkalemia after nephrectomy by treatment with a cation exchange resin, sodium polystyrene sulfonate (Kayexalate), significantly reduced the adrenal renin response to nephrectomy. A third factor involved is the lack of negative feedback by plasma angiotensin II. Infusion of angiotensin II intraperitoneally prevented the rise in adrenal renin after nephrectomy (from 65.25 +/- 7.60 to 9.27 +/- 0.99 ng angiotensin I/mg protein/hr) despite an increase in plasma potassium and corticosterone. In conclusion, three factors influence the response of adrenal renin to nephrectomy: 1) the pituitary through the release of ACTH, 2) a direct stimulation by high plasma potassium levels, 3) the lack of angiotensin II feedback inhibition. Whether the high adrenal renin contributes to the high aldosterone observed in rats after nephrectomy remains to be established.

Adrenal Cortex↗
PubMed1986

Suppression of adrenal renin in Dahl salt-sensitive rats.

We previously showed that adrenal renin is highest in the rat zona glomerulosa (ZG) and that low sodium or high potassium and nephrectomy increase adrenal ZG renin and aldosterone. Dahl salt-sensitive rats (S) have been shown to have lower plasma renin activity and plasma aldosterone and higher plasma 18-hydroxy-11-deoxycorticosterone than Dahl salt-resistant rats (R). In this study we assess the possible role of adrenal ZG renin in the suppression of aldosterone in S rats. Adrenal ZG renin was significantly decreased in S as compared with R rats even at 6 weeks of age, when both S and R rats are still normotensive (S = 7.2 +/- 0.2, R = 18.0 +/- 1.6 ng angiotensin I/mg protein/hr). Adrenal ZG aldosterone was also significantly lower in S than in R rats (S = 21.1 +/- 4.3, R = 39.5 +/- 3.6 ng/mg protein). Furthermore, the rise in adrenal ZG renin and aldosterone after nephrectomy in S rats was significantly less than that in R rats. To determine if the suppressed adrenal ZG renin of S rats is due to volume expansion, we studied the effect of a sodium-deficient diet on adrenal ZG renin in S and R rats. After 2 weeks of a sodium-deficient diet S rats had significantly lower basal adrenal ZG renin than did R rats (S = 7.6 +/- 0.4, R = 21.7 +/- 1.9 ng angiotensin I/mg protein/hr) and a marked blunting of the adrenal ZG renin response to nephrectomy (S = 13.6 +/- 1.1, DR = 167 +/- 16.1 ng angiotensin I/mg protein/hr).(ABSTRACT TRUNCATED AT 250 WORDS)

18-Hydroxydesoxycorticosterone↗
PubMed1986

Effects of dietary linoleic acid on blood pressure and renal function in subtotally nephrectomized rats.

The effect of a high linoleic acid diet on blood pressure, renal function, and urinary prostaglandin excretion was studied in rats with decreased renal mass. Subtotally nephrectomized (5/6 nephrectomy) male rats received either a 15% linoleic acid (high linoleic acid, HLA) diet containing 20% safflower oil or a 0.28% linoleic acid (low linoleic acid, LLA) diet containing 20% coconut oil. Sham-operated rats were also placed on either HLA or LLA diet. The subtotal nephrectomized rats developed similar degrees of hypertension during the first 3 weeks after subtotal nephrectomy. However, 4 weeks after subtotal nephrectomy, the rats on HLA diet had significantly lower blood pressure than the rats on LLA diet [HLA 152 +/- 3 (mean +/- SE) mm Hg versus LLA 171 +/- 3 mm Hg]. This difference persisted until termination of the experiment at 7 weeks after subtotal nephrectomy (HLA 159 +/- 7 mm Hg versus LLA 192 +/- 6 mm Hg). The GFR measured 7 weeks after subtotal nephrectomy was significantly lower in both of the subtotally nephrectomized groups. However, the HLA subtotal nephrectomized rats had significantly higher GFR than the LLA-treated rats (HLA 0.23 +/- 0.05 ml/min 100 g versus LLA 0.12 +/- 0.02 ml/min/100 g, P less than 0.05). There was no difference in the GFR or blood pressure in the sham-operated rats treated with HLA or LLA diet. PGE2 excretion was lower in the two groups of subnephrectomized rats, but there was no difference between the HLA and LLA treated rats. Urinary 6-ketoPGF1 alpha was not decreased by subtotal nephrectomy and there was no difference between the dietary groups. However, TXB2 excretion was higher in the groups with subtotal nephrectomy, but there was no difference between the two dietary groups. In conclusion, the HLA diet attenuates the rise in blood pressure after subtotal nephrectomy in the rat and preserves renal function. There was no difference in urinary excretion of PGE2, 6-keto-PFG1 alpha, or thromboxane B2 between the two dietary groups.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effect of indomethacin on the adrenal renin response to nephrectomy in the rat.

The role of prostaglandins in the control of adrenal renin in vivo was evaluated in nephrectomized rats. Nephrectomy increased adrenal renin from 13.2 +/- 1.37 ng angiotensin I/mg protein/hr to 166.5 +/- 17.3 ng angiotensin I/mg protein/hr. Indomethacin treatment significantly suppressed the adrenal renin response to nephrectomy. (47.8 +/- 5.22 ng angiotensin I/mg protein/hr). Adrenal aldosterone was also suppressed by indomethacin. Adrenal prostaglandin E2 increased after nephrectomy and decreased after indomethacin. Plasma corticosterone and serum potassium did not change after indomethacin. These data indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the adrenal renin response to nephrectomy, suggesting that prostaglandins may play a role in the adrenal response to nephrectomy.

Adrenal Glands↗
PubMed1985

Effect of atrial peptides on aldosterone production.

This study examines the effects of the synthetic atrial peptides (atriopeptin I, II, and III) on aldosterone and corticosterone production by rat adrenal cell suspensions. Furthermore, we studied the effect of atriopeptin II infusion on the plasma aldosterone response to angiotensin II in the rat in vivo. Atriopeptin I, II, and III decreased aldosterone release from zona glomerulosa cells in a dose-dependent fashion. 10 pM atriopeptin II inhibited basal aldosterone release significantly (P less than 0.01), and 10 nM atriopeptin II or III lowered it by 79%. Atriopeptin II decreased the sensitivity of the glomerulosa cells to adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin II had no effect on basal or ACTH-stimulated corticosterone release by fasciculata-medullary cells. In vivo infusions of angiotensin II with or without simultaneous infusions of atriopeptin II showed that atriopeptin II significantly inhibited the aldosterone response to angiotensin II. This inhibition by atriopeptin II was independent of any effect on plasma renin activity, serum potassium, or ACTH. These data raise the possibility that the atrial natriuretic peptides may affect sodium excretion by the kidney, not only directly, but also indirectly through the inhibition of aldosterone production.

Adrenal Glands↗
PubMed1985

Sites of action of beta-melanocyte stimulating hormone in aldosterone biosynthesis in the rat.

The sites of action of beta-melanocyte stimulating hormone (beta-MSH) on aldosterone biosynthesis were studied using collagenase-dispersed adrenal glomerulosa cells from rats maintained on either normal or sodium-deficient diets for 2 weeks. Isolated cells were treated with a cyanoketone derivative (WIN 19,578) to isolate the early and late steps in aldosterone biosynthesis. WIN 19,578 (1 microM) completely blocked aldosterone production stimulated by sodium depletion, AII, ACTH, and beta-MSH. beta-MSH (1 microM) significantly stimulated pregnenolone production (early step) and the conversion of corticosterone to aldosterone (late step) in aldosterone biosynthesis. The effect of beta-MSH was similar to AII and ACTH. Sodium depletion enhanced the effect of beta-MSH only on the late step in aldosterone biosynthesis. In conclusion, beta-MSH stimulates both the early and late steps of aldosterone biosynthesis. These results suggest that beta-MSH or peptides containing beta-MSH may play a role in the regulation of aldosterone production.

Adrenal Glands↗
PubMed1984

Inhibition of aldosterone production by an atrial extract.

Crude extracts of rat atria reduced the basal amount of aldosterone released from rat zona glomerulosa cells and partially inhibited aldosterone stimulation by adrenocorticotropic hormone and angiotensin II. The destruction of this activity by trypsin suggests that the active factor is a peptide, possibly atrial natriuretic factor. These data suggest that atrial natriuretic factor affects sodium excretion by the kidneys both directly and through the inhibition of aldosterone production.

Adrenocorticotropic Hormone↗
PubMed1984

Idiopathic aldosteronism. A possible disease of the intermediate lobe of the pituitary.

A 37-year-old woman with documented primary aldosteronism died of a cerebral hemorrhage. At postmortem examination she was found to have bilateral, adrenal hyperplasia and nodular basophilic hyperplasia of the anterior and intermediate lobe of the pituitary. Based on these findings and experimental evidence suggesting the existence of a pituitary factor that stimulates aldosterone secretion, we postulate that idiopathic aldosteronism is caused by an abnormality of the intermediate lobe of the pituitary gland leading to overproduction of non-adrenocorticotropic hormone peptides derived from pro-opiomelanocortin that increase aldosterone production and cause hyperplasia of the adrenal glands.

Adrenal Glands↗
PubMed1984

Primary myelolipoma of mediastinum.

Myelolipoma is a benign nonepithelial neoplasm composed of mature marrow elements and fat cells. This rare neoplasm is usually discovered by pathologists incidentally at autopsy, and, with rare exceptions, usually occurs in the adrenal glands. One of these exceptional anatomic sites is the mediastinum, and only three cases of primary mediastinal myelolipomas have been documented in the English-language literature (1-3). We are presenting a primary myelolipoma involving the posterior mediastinum that was discovered on routine chest radiographs and successfully resected. Computed tomography (CT) scan findings of this rare mediastinal tumor are also presented. This is the first case report in the English language of primary myelolipoma in the mediastinum that was detected clinically and resected successfully.

Humans↗
PubMed1984

Biphasic alteration of renin release by calcium.

The effects of calcium reintroduction on renin release were examined. Calcium reintroduction to calcium-deprived rat renal cortical slices caused an initial stimulation of renin release (30-40 min) followed by a period of suppression of release (4.5 hr). With ouabain present the initial stimulation was enhanced but the subsequent fall in release was more pronounced. Our results suggest that although renin release from juxtaglomerular cells can be both stimulated and inhibited by raising intracellular calcium, it is the inhibition of release that is the more persistent effect.

Animals↗
PubMed1984

Inhibition of aldosterone production by atrial natriuretic factor.

Extracts of rat atrial muscle lowered basal aldosterone release from rat adrenal glomerulosa cell suspensions, and partially inhibited the stimulation of aldosterone release by adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin I, an atrial peptide with natriuretic, diuretic and smooth muscle relaxant activities, significantly decreased basal aldosterone release at 1 pM concentrations. Also, atriopeptin I decreased the sensitivity of the glomerulosa cells to adrenocorticotropin and angiotensin II. These data suggest that peptides contained in mammalian atria affect sodium excretion not only by a direct effect on the kidney, but also indirectly through inhibition of aldosterone production.

Adrenal Glands↗
PubMed1983

Electron microscopic study of testicular tumor in congenital adrenal hyperplasia.

Ultrastructural features of bilateral testicular biopsy materials, obtained from both tumor and nontumor areas of the testis of a 27-year-old man with congenital adrenal hyperplasia, revealed a number of pathologic changes. Germ cell hypoplasia and extratubular cellular hyperplasia were noticed in the nontumor portion of the testis. In some areas of the tumor, dense collagenous materials surrounded the compressed degenerative seminiferous tubule. In other areas at least three different types of cells were identified: 1) branched, irregular giant cells, 2) small cells in clusters, and 3) modified myoid or smooth muscle cells. It is suggested that these three types of cells have different origins. The concept that these types of tumor cells originate from "pluripotential cells" is supported.

Adrenal Hyperplasia, Congenital↗
PubMed1983

Reexamination of the effect of urinary kallikrein on renin release: evidence that kallikrein does not release renin but protects renin from destruction.

Previously, we showed that superfusion of rat kidney slices by rat urinary kallikrein stimulated renin release. The resin measurements were performed on superfusion samples which we stored frozen at -20 C for 24 h. In this study we investigated the effect of freezing on the renin concentration of superfusion samples in the control period. The renin concentration measured immediately without freezing was 9.8 +/- 2.4 ng angiotensin I/10 ml . 3 h/mg tissue, while the concentration in the samples frozen for 24 h was 2.9 +/- 1.0 ng angiotensin I/10 ml . 3 h/mg. The renin concentration of the superfusion samples during the kallikrein perfusion period was the same as that of the nonfrozen control samples. It appeared, therefore, that kallikrein acted as if it stimulated renin release from kidney slices, when the renin was measured in frozen samples. To clarify this phenomenon, we added kallikrein, inactivated kallikrein, and albumin to superfusion samples of the control period and froze the samples for 24 h. After freezing, the renin concentration of the control samples decreased to about 20% of that of nonfrozen samples, except in those samples to which the various proteins were added. In these samples, the loss of renin activity was prevented. The addition of Trasylol, a specific inhibitor of kallikrein, blocked the protective effect of both kallikrein and albumin. These data suggest that the renin released into the superfusion media of kidney slices is destroyed by freezing and that kallikrein or BSA prevents this destruction. These data negate previous data indicating that kallikrein stimulates renin release.

Animals↗
PubMed1983

Effect of sodium deficiency on beta-melanocyte-stimulating hormone stimulation of aldosterone in isolated rat adrenal cells.

The effect of sodium deficiency on the adrenal sensitivity to beta MSH was studied using collagenase-dispersed rat adrenal cells from rats maintained on a normal sodium or a sodium-deficient diet for 2 weeks. In the cells prepared from adrenals of rats fed a normal sodium diet, angiotensin II (AII) and ACTH caused a dose-dependent increase in aldosterone production by glomerulosa cells at a threshold concentration of 10(-10) M and induced a maximal response at 10(-8) M. beta MSH also stimulated aldosterone production at a threshold of 10(-8) M and a maximum at 10(-6) M. However, in the cells from sodium-depleted rats, the threshold for AII was 10(-11) M and the maximum was 10(-8) M, while the threshold for ACTH and beta MSH was 10(-10) M. The shift to the left of the dose-response curve for beta MSH during sodium depletion was greater than that for AII or ACTH. The aldosterone levels obtained with maximal doses of beta MSH and AII were similar during sodium depletion. Sodium depletion did not affect the corticosterone response of decapsular cells to all three stimulators. In conclusion, sodium deficiency enhances the sensitivity of the adrenal glomerulosa cells to beta MSH, causing significant stimulation of aldosterone production by doses of beta MSH within the physiological range. These data suggest that beta MSH or peptides containing beta MSH may play a role in the regulation of aldosterone secretion during sodium deficiency in the rat.

Adrenal Glands↗
PubMed1983

Adrenal renin: a possible regulator of aldosterone production.

We have confirmed the presence of adrenal renin and have shown that the concentration is much higher in the glomerulosa cells. The renin concentration of these cells is influenced by changes in sodium balance and after nephrectomy, while the renin of the fasciculata-medullary tissue is not. There is a positive correlation between adrenal renin and aldosterone concentration. The data suggest that adrenal renin may be a local hormone that plays a role in the regulation of aldosterone production.

Adrenal Glands↗
PubMed1981

Stimulation of aldosterone production by beta-melanotropin.

Experimental and clinical evidence suggests that a non-ACTH pituitary factor(s) is important in the regulation of aldosterone secretion in certain conditions. Earlier studies have suggested that beta-melanotrophin (beta-MSH) has only weak steroidogenic potency on the adrenal gland in the rat, but recently Challis et al.5 and Rudman et al.6 have reported that alpha- and beta-MSH have a trophic action on fetal adrenal gland. However, little is known about the effect of beta-MSH on aldosterone production. We recently reported that beta-lipotropin (beta-LPH) stimulates aldosterone production in rat capsular cells. As the amino acid sequence of beta-MSH is contained within the beta-LPH structure, we have now investigated the aldosterone-stimulating activity of synthetic beta-MSH. Our results indicate that beta-MSH causes a dose-dependent increase in aldosterone production in rat capsular cells which is blocked by a synthetic beta-MSH analogue. The synthetic hormone does not increase corticosterone production in decapsular cells.

Aldosterone↗
PubMed1981

Effects of indomethacin on plasma renin activity in the conscious rat.

The role of prostaglandins in the control of renin release in vivo was evaluated in the conscious rat. Indomethacin suppressed urinary prostaglandin E2 (PGE2) excretion from 5.3 +/- 0.5 to 2.6 +/- 0.5 ng/3 h (P less than 0.001). Basal plasma renin activity (PRA) fell from 6.20 +/- 1.07 to 2.98 +/- 0.45 ng . ml-1 . h-1 (P less than 0.02). Indomethacin suppressed PRA stimulated by furosemide, insulin-induced hypoglycemia, hydralazine, isoproterenol, arachidonic acid, and sodium-free diet, whereas PRA stimulated by PGE2 was not suppressed by indomethacin. The suppression of PRA by indomethacin in the sodium-deplete state rules out sodium retention as the mechanism of action of indomethacin. These results indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the renin response to several of the known stimulators, suggesting that prostaglandins may play a pivotal role in the control of renin release.

Animals↗