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R Franco-Saenz

Publications and source records attributed to R Franco-Saenz.

At least 37 records · Page 2Linked to original sources
PubMed1991

Atrial natriuretic peptide inhibition of calcium ionophore A23187-stimulated aldosterone secretion in rat adrenal glomerulosa cells.

The effect of atrial natriuretic peptide (ANP) on calcium ionophore A23187-stimulated aldosterone secretion was investigated using collagenase-dispersed rat adrenal glomerulosa cell suspensions. A23187 treatment induced a dose-dependent stimulation of aldosterone secretion, exhibiting an EC50 of approximately 75 nM. In agreement with the presumed action of A23187 as a Ca2+ ionophore, stimulation was dependent on the extracellular Ca2+ concentration, being completely inhibited in nominally Ca(2+)-free medium. In such Ca(2+)-free medium, stimulation of aldosterone secretion by bath applied 25-hydroxycholesterol was not inhibited, indicating that cells and biosynthetic pathway enzymes were not inhibited by low extracellular Ca2+ levels. A23187-induced aldosterone secretion was also inhibited by more than 90% when cells were simultaneously treated with ANP. Maximal ANP inhibition of A23187-stimulated aldosterone secretion was not overcome by concentrations of A23187 up to 10 microM or by increasing the extracellular Ca2+ concentration from 1.25 to 5 mM in the presence of A23187 and ANP. Addition of A23187 to ACTH-, angiotensin II-, or K(+)-stimulated glomerulosa cells did not overcome ANP-induced inhibition of aldosterone secretion stimulated by these secretagogues. In contrast to ANP inhibition of Ca(2+)-dependent A23187 stimulation of aldosterone secretion, ANP inhibition of dBcAMP-stimulated aldosterone secretion was readily overcome by increasing the dBcAMP concentration. These results indicated that ANP selectively and noncompetitively inhibited an intracellular step necessary for Ca(2+)-dependent stimulation of the early pathway of aldosterone biosynthesis in rat adrenal glomerulosa cells.

Aldosterone↗
PubMed1991

Local generation of angiotensin II as a mechanism of aldosterone secretion in rat adrenal capsules.

Angiotensin-converting enzyme (ACE) is found in the adrenal gland, but the role of adrenal ACE in the formation of angiotensin II (AII) and subsequent stimulation of aldosterone is unclear. We examined the effect of adrenal ACE activity on aldosterone secretion by superfusing rat adrenal capsules with angiotensin I (AI) in the presence and absence of the ACE inhibitor, lisinopril. Angiotensin I (10 microM) stimulated aldosterone secretion from 914 +/- 41 to 1465 +/- 118 pg/min/capsule (P less than 0.05). Simultaneous superfusion of AI plus lisinopril (100 microM) inhibited the stimulation of aldosterone by 73% (P less than 0.05). Perfusion of the capsules with angiotensin II (1 microM) stimulated aldosterone from 893 +/- 180 to 1466 +/- 181 pg/min/capsule (P less than 0.01). In contrast, simultaneous superfusion of AII plus lisinopril (100 microM) did not inhibit the AII stimulation of aldosterone. The failure of lisinopril to inhibit AII stimulation of aldosterone argues against a toxic or nonspecific action of lisinopril. The inhibition of AI stimulation of aldosterone release by lisinopril is mostly due to lisinopril inhibition of ACE and resulting decreased conversion of AI to AII. These results demonstrate that adrenal ACE may generate AII from AI in the adrenal gland, and this locally produce AII stimulates aldosterone.

Adrenal Glands↗
PubMed1990

Role of the adrenal renin-angiotensin system on adrenocorticotropic hormone- and potassium-stimulated aldosterone production by rat adrenal glomerulosa cells in monolayer culture.

The rat zona glomerulosa has a renin-angiotensin system that appears to function as an autocrine or paracrine system in the regulation of aldosterone production. To further investigate dynamic changes of production of renin and aldosterone in vitro we developed a primary monolayer culture of rat adrenal glomerulosa cells in serum-free medium. Collagenase-dispersed glomerulosa cells were incubated in PFMR-4 medium containing 10% fetal calf serum for 48 hours; the medium was then replaced with serum-free PFMR-4 medium. The cell viability and the aldosterone secretion were stable over the additional 48 hours in the serum-free control medium. After incubation for 24 hours in the serum-free medium, the cells were exposed to high K+ or adrenocorticotropic hormone (ACTH) for another 24 hours. ACTH stimulated aldosterone secretion, and this increased secretion was associated with an increase in renin activity (cell active renin, from 15.56 +/- 0.71 to 45.75 +/- 5.69; cell inactive renin, from 0.67 +/- 0.54 to 8.75 +/- 3.40; medium inactive renin, from 5.58 +/- 1.16 to 106.20 +/- 14.01 pg angiotensin I (Ang I)/micrograms protein/3 hr). Aldosterone was also stimulated by high K+. This increase was also associated with an increase in active renin in the cells (from 15.08 +/- 1.80 to 23.26 +/- 2.15 pg Ang I/micrograms protein/3 hr) and an increase in inactive renin in the medium (from 10.87 +/- 1.62 to 21.37 +/- 3.20 pg Ang I/micrograms protein/3 hr). Addition of the angiotensin converting enzyme inhibitor lisinopril attenuated both ACTH- and high K(+)-stimulated aldosterone secretion significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1989

Hypodipsia and hypernatremia in congenital hydrocephalus.

The authors describe a case of hypodipsia and severe hypernatremia most probably secondary to hydrocephalus in a 22-year-old man in the absence of abnormalities of ADH secretion or metabolism. The patient became hypernatremic only in situations when the decreased spontaneous fluid intake was insufficient to replace that lost caused by sweating or vomiting. Adequate hydration returned the sodium value to normal.

Adult↗
PubMed1989

Regulation of adrenal renin messenger ribonucleic acid by dietary sodium chloride.

Zona glomerulosa (ZG) and zona fasciculata (ZF/M) poly(A)+ RNA were isolated from the adrenals of bilaterally nephrectomized female Sprague-Dawley rats and hybridized to a full-length 32P-labeled 1423-base pair (bp) renin cDNA as well as a 698-bp renin cDNA KpnI segment (corresponding to amino acids 92-325) by the dot blot procedure using Bio-Rad Zeta Probe membranes. Extensive hybridization was observed with ZG mRNA, and only slight binding was seen with ZF/M mRNA. These results extend earlier reports from this laboratory indicating that the enzymic activity for renin is predominantly localized in ZG cells. Hence, high message levels account for the high enzymic activity. Adrenal ZG poly(A)+ RNA was also isolated from rats maintained on normal and sodium-deplete diets for 15 days and was hybridized to the radiolabeled 698-bp renin probe. Essentially twice the amount of probe was bound to the message from salt-deplete ZG tissue compared to message from normal ZG per microgram mRNA. Hybridization was proportional to the amount of poly(A)+ RNA employed over the range of 0-1 microgram, suggesting the applicability of this procedure for approximate quantitation purposes. The membranes were freed from the 32P-labeled renin cDNA and subsequently rehybridized with a 32P-radiolabeled 1200-bp beta-actin cDNA probe. It was observed that ZF/M poly(A)+ RNA contained more beta-actin message than ZG poly(A)+ RNA, indicating a greater transcription rate for beta-actin in ZF/M tissue in contrast to transcription of the renin gene.

Adrenal Glands↗
PubMed1989

Production of renin, angiotensin II, and aldosterone by adrenal explant cultures: response to potassium and converting enzyme inhibition.

The existence of renin in a number of extrarenal tissues has been well documented, but the physiological role of extrarenal renin remains unknown. To study the physiological role of adrenal renin, we developed a serum-free culture system for adrenal capsular/zona glomrulosa explants. Explants showed good viability in culture (greater than 80%), and demonstrated net production of aldosterone, angiotensin II, and prorenin. Aldosterone production was consistently stimulated by an increase in potassium (6 mM) in the culture medium. Both aldosterone and angiotensin II production could be attenuated by adding the angiotensin converting enzyme inhibitor lisinopril to the culture medium (0.1 mM). These data suggest that rat adrenal explants are capable of producing all of the components of a functional renin-angiotensin-aldosterone system and that these components can interact in response to physiological stimuli. These findings support the hypothesis that a local adrenal renin system may play a physiological role in the control of adrenal aldosterone production.

Adrenal Glands↗
PubMed1989

Effect of posture on the plasma levels of atrial natriuretic factor.

Atrial natriuretic factor (ANF) is a peptide with potent natriuretic, diuretic and vasorelaxant activities. Stretching of the right atria causes release of ANF into the circulation. Therefore, changes in central blood volume or acute volume expansion are likely to change the plasma levels of ANF. In this study we investigated the effects of changes in posture on the plasma levels of ANF, plasma renin activity (PRA) and plasma aldosterone (aldo). Eight male and five female volunteers ranging in age from 23 to 26 years were placed on a normal sodium intake and on the experimental day blood was obtained for ANF, PRA, and aldo after 30 minutes of lying supine, 30 minutes of 10 or 20 degrees head-down tilt, and 30 minutes of standing. Plasma ANF increased significantly after 30 minutes of head-down tilt from the supine value of 33.7 +/- 5.2 pg/ml to 47.7 +/- 7.7 pg/ml (p less than 0.02) and suppressed to 14.1 +/- 0.02) after 30 minutes of standing. PRA did not change significantly with head-down tilt, (supine 1.64 +/- 0.44 ngAI/ml/h vs. 30 minutes tilt 1.28 +/- 0.32 ngAI/ml/h (p = NS). Plasma aldosterone decreased by head-down tilt from 11.2 +/- 1.2 ng/ml to 8.4 +/- 0.8 ng/dl (p less than 0.02) and returned to the supine level after standing. In conclusion ANF levels change significantly with posture. Increase in central blood volume by head-down tilt increases ANF levels and suppresses plasma aldosterone with no effect on PRA. Standing decreases ANF significantly. These results suggest that for proper interpretation of plasma levels of ANF, posture at the time of sampling has to be standardized.

Adult↗
PubMed1989

Effect of atrial natriuretic factor on renin and aldosterone.

Atrial natriuretic factor (ANF) inhibits basal and stimulated aldosterone production in vitro and in vivo. Infusions of ANF have been reported to inhibit renin release in several species, including humans. A 4-h infusion of ANF into 12 patients with mild hypertension reduced plasma aldosterone at 2 and 4 h, with a rebound increase 2 h after the end of the infusion. Plasma renin activity also showed a mild but significant reduction at 2 h with a rebound increase at 6 h. The effect of ANF on renin release in vitro is controversial. Using a superfusion system of rat renal cortical slices and of dispersed juxtaglomerular (JG) cells, we found that ANF did not affect basal or isoproterenol-stimulated renin release by the kidney slices or dispersed JG cells. These studies suggest that ANF does not inhibit renin release by a direct effect on the JG cells and that the inhibition of renin release found in vivo studies may be mediated through a macula densa mechanism. Since calcium plays an important role in aldosterone secretion, we investigated the effect of ANF on calcium fluxes in rat adrenal glomerulosa cells. ANF did not affect either calcium influx or calcium efflux in rat adrenal glomerulosa cells. These studies suggest that the inhibitory effect of ANF on aldosterone production is distal to the calcium messenger system.

Aldosterone↗
PubMed1988

Adrenal renin: a possible local hormonal regulator of aldosterone production.

The complete renin-angiotensin system is present in the adrenal cortex: prorenin, renin, angiotensinogen, angiotensin I and II, and converting enzyme. Most of the renin found is probably synthesized there since the renin concentration increases after nephrectomy, and the mRNA for renin is present. The renin-angiotensin system has the highest activity in the zona glomerulosa cells, the site of aldosterone formation. A low-sodium diet or a high-potassium diet, or nephrectomy markedly increases the adrenal renin concentration in the zona glomerulosa cells without any effect on the fasciculata-medullary cells. There is a close correlation between adrenal renin and aldosterone production. The adrenal renin angiotensin system may be a local regulator of aldosterone production.

Adrenal Glands↗
PubMed1988

Effect of atrial natriuretic factor on calcium fluxes in adrenal glomerulosa cells.

We studied the effect of atrial natriuretic factor (ANF) on calcium influx and efflux in rat adrenal glomerulosa cells stimulated by angiotensin II (Ang II) or potassium ion, and observed how ANF inhibits the initial and sustained phases of the aldosterone response to Ang II or K+ using a superfusion system of dispersed adrenal glomerulosa cells. K+ (8 mM) significantly increased Ca2+ influx rate compared with basal rate (0.91 +/- 0.10 vs 0.42 +/- 0.04 nmol/min/10(6) cells; p less than 0.01). ANF (10(-8) M) did not inhibit the K+-induced increase in Ca2+ influx rate (0.99 +/- 0.18 nmol/min/10(6) cells). Ang II (10(-9) and 10(-8) M) stimulated Ca2+ influx rate (10(-9) M Ang II, 0.62 +/- 0.02; 10(-8) M Ang II, 0.71 +/- 0.09 vs basal, 0.44 +/- 0.03 nmol/min/10(6) cells; p less than 0.05), while ANF (10(-8) M) did not change the Ca2+ influx rate increased by Ang II (ANF + 10(-9) M Ang II, 0.62 +/- 0.06; ANF + 10(-8) M Ang II, 0.69 +/- 0.14 nmol/min/10(6) cells). In the Ca2+ efflux study ANF (10(-8) M) was perfused through the cells 10 minutes before the start of perfusion with Ang II (10(-9) M) or K+ (12 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1988

Effect of atrial natriuretic peptide on renin release in a superfusion system of kidney slices and dispersed juxtaglomerular cells.

The effect of atrial natriuretic peptide (ANP) on renin release is controversial. Several reports state that ANP inhibits renin secretion, while others have shown no effect. We investigated the effect of synthetic rat ANP with 24 amino acids (atriopeptin III) on renin release in vitro in a dynamic superfusion system of renal cortical slices as well as collagenase-dispersed juxtaglomerular cells. In the superfusion system of kidney slices, isoproterenol (5 x 10(-8) M) clearly stimulated renin release from kidney slices, while angiotensin II (AII; 10(-5) M) suppressed renin release. ANP (10(-10)-10(-6) M) did not inhibit basal renin release or blunt the stimulatory effect of isoproterenol. The suppression of renin secretion by AII was never modified in the presence of ANP. The superfusion system of juxtaglomerular cells demonstrated greater sensitivity of renin release in responses to isoproterenol and AII. In this system, ANP (10(-6) M) did not alter renin release from the cells stimulated by isoproterenol (5 x 10(-8) M) or inhibited by AII (10(-8) M). However, basal renin release was slightly stimulated in the late phase of ANP superfusion and for 20 min after the ANP perfusion was stopped. Similarly, 8 bromo-cGMP (10(-6) M) did not inhibit, but, rather, stimulated basal renin release slightly. These results suggest that ANP does not inhibit renin release by a direct effect on the juxtaglomerular cell in the rat.

Angiotensin II↗
PubMed1988

Effects of dibutyryl adenosine 3',5'-monophosphate, angiotensin II, and atrial natriuretic factor on phosphorylation of a 17,600-dalton protein in adrenal glomerulosa cells.

Rat adrenal glomerulosa cells were incubated with [32P]phosphate and (Bu)2AMP (dbcAMP), angiotensin II, and atrial natriuretic factor (ANF). Incorporation of [32P]phosphate into cellular proteins was analyzed by one-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. dbAMP stimulated phosphorylation of a 17.6K protein, while angiotensin II did not stimulate it. ANF did not affect the protein phosphorylation, whether the cells were in the basal state or stimulated by dbcAMP or angiotensin II. On the other hand, ANF markedly inhibited angiotensin II-stimulated aldosterone production, but only slightly inhibited dbcAMP-stimulated aldosterone. These results suggest that in rat adrenal glomerulosa cells phosphorylation of the 17.6K protein may have a relationship with the stimulatory effect of cAMP on aldosterone production; however, neither angiotensin II nor ANF affected the phosphorylation of this protein, and phosphorylation of the 17.6K protein is not an obligatory step in the regulation of aldosterone production.

Aldosterone↗
PubMed1987

Inhibitors of aldosterone secretion.

Aldosterone secretion may be inhibited by potassium depletion, inhibitors of the renin-angiotensin system, dopamine and atrial natriuretic factor. The latter appears to be an important physiological regulator of aldosterone secretion. ANF inhibits basal, ACTH, Angiotensin II and potassium-stimulated aldosterone production in vitro by a direct action on the adrenal gland. In vivo data also support a direct inhibitions of aldosterone. The stimulation of aldosterone secretion by infusions of Angiotensin II and potassium is inhibited by simultaneous infusions of ANF. Infusions of ANF lower the basal aldosterone secretion in man. The mechanism by which ANF inhibits aldosterone is not known. No unifying first step has been identified to explain ANF's ability to inhibit all stimuli. In vivo, part of the lowering of aldosterone levels may be due to inhibition of renin secretion. This effect of ANF upon renin is inconsistent and appears to depend upon the experimental conditions.

Adrenal Glands↗
PubMed1987

Endocrine cardiomyocytes.

A short review of the history related to the identification and classification of cardiac hormones shows that long before the development of modern scientific technology these substances had been predicted. It is an outstanding example of how meticulous observation, even with simple instruments, coupled with creative imagination, sound logic, and far reaching vision, may bring about marvelous accomplishments. The fast changing field and numerous contributions are responsible for the unsettled nomenclature and not completely settled concepts of the heart as a pump and as an endocrine organ. Although the bulk of knowledge amassed prior to the advent of the electron microscope is amazing, it was, however, only after the biological application of electron microscopy that the morphological evidence of the cardiac elements responsible for the endocrine function of the heart could have been provided. As usual, although not always the case, it was the anatomical, specifically the subcellular, description of the endocrine cardiomyocytes that caused the recent extraordinary advances in the recognition of another function of the heart. In a broad sense, the extension of internal secretion and its subcellular morphological background to other structures allow one to add endocrinosity as a general principle of construction and function of the human body. Our selective, obviously incomplete review, may not include publications that a different subjective approach might have included. While the Authors count on the indulgence of the readers, they emphasize that what is missing is not necessarily less important. The main aims of this publication have been to concentrate on early historical developments and to be able to repeat, once again, how much the mind can accomplish, even without the wonders of modern technology. Once the latter is made available, however, it obliges scientists to use their ingenuity at a higher level, providing the scientific and technological revolutions that occur from time-to-time. The recent history of medicine is replete with such events, which have proven so beneficial for mankind.

Animals↗
PubMed1986

Effect of atrial natriuretic factor on the plasma aldosterone response to potassium infusion in rats--in vivo study.

Previous in vitro studies have shown that atrial natriuretic factor inhibits the secretion of aldosterone stimulated by AII, ACTH, and potassium in adrenal cell suspensions. The present study investigated the effects of atriopeptin II on the plasma aldosterone response to a potassium infusion in conscious unrestrained rats in vivo. The infusion of potassium chloride solution increased plasma aldosterone level from 20.4 +/- 3.7 to 168.4 +/- 27.3 ng/dl. The simultaneous administration of atriopeptin II reduced the increase in plasma aldosterone level (16.0 +/- 2.1 to 63.3 +/- 10.4 ng/dl). There was no significant difference in the plasma renin activity, corticosterone, or serum potassium levels between the two groups. These results suggest that atriopeptin II may be important in the regulation of aldosterone secretion.

Aldosterone↗