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P J Mulrow

Publications and source records attributed to P J Mulrow.

At least 19 recordsLinked to original sources
PubMed1992

Effect of atrial natriuretic peptide (8-33-Met ANP) in patients with hypertension.

In this pilot study we investigated the effects of a 4-h infusion of atrial natriuretic peptide (8-33 Met ANP) on hemodynamic, renal, and hormonal parameters in 12 patients with hypertension. Either 8-33 ANP in 5% mannitol (0.7 microgram/min [eight patients] and 1.05 micrograms/min [four patients]) or placebo (5% mannitol) was infused for 4 h on 2 consecutive days in a randomized double-blind crossover design. The plasma levels of ANP were not significantly different between the two doses of ANP and therefore the results from the two doses were combined. Plasma ANP increased from 61 +/- 24 pg/mL to 291 +/- 55 pg/mL after 2 h and to 288 +/- 40 pg/mL after 4 h. ANP caused a significant lowering of systolic blood pressure after 2 h of infusion from 148 +/- 5 mm Hg to 142 +/- 5 mm Hg (P less than .05) and to 128 +/- 6 after 4 h (P less than .01). Two hours after discontinuation of the infusion, systolic blood pressure was 126 +/- 6 and 135 +/- 7 mm Hg 4 h after the end of the infusion. Diastolic blood pressure did not change. Heart rate increased from 69 +/- 3 beats/min to 74 +/- 3 beats/min after 4 h and to 78 +/- 4 beats/min 2 h after termination of the infusion. Cardiac output did not change significantly. Urinary sodium and chloride increased significantly but creatinine clearance did not change. Plasma aldosterone decreased after 2 h of ANP infusion from 9.8 +/- 1.7 ng/dL to 6.7 +/- 0.9 ng/dL (P less than .01) and to 6.5 +/- 1.2 ng/dL after 4 h (P less than .05). Plasma renin activity decreased from 0.81 +/- 0.1 ng angiotensin I/mL/h to 0.57 +/- 0.1 after 2 h of infusion (P less than .05). There were no significant changes in plasma catecholamines or arginine vasopressin. Two patients developed severe hypotension and bradycardia and one of them had a sinus pause of 7.4 sec associated with loss of consciousness. Neither of these two patients had a significant increase in plasma catecholamines in response to the severe hypotension, suggesting that ANP may have inhibited their sympathetic response and increased their sensitivity to vagal cardioinhibitory reflexes. In conclusion, infusion of ANP in hypertensive patients causes prolonged lowering of systolic blood pressure with no change in diastolic pressure and cardiac output.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Changes in cholesterol levels after coronary artery bypass surgery.

To determine the factors responsible for the dramatic fall in cholesterol levels after coronary artery bypass surgery (CABG), the authors reviewed, in a retrospective study, the cholesterol levels of 36 patients who underwent CABG surgery during 1987 and compared their levels with those of a control group of 30 patients who underwent cholecystectomies during the same time. In a prospective study, the authors measured the lipids and the hematocrit levels of 15 patients undergoing CABG surgery before the initiation of cardiopulmonary bypass, after 5 minutes of extracorporeal circulation (ECC), and at the end of ECC. In the CABG group, the plasma cholesterol level fell from 211 +/- 63 mg/dl (mean +/- SE) to 70 +/- 48 mg/dl (p less than 0.01), a 77% decrease within 24 hours of surgery. In the cholecystectomy group, the plasma cholesterol fell from 192.3 +/- 8.9 mg/dl to 158 +/- 76 mg/dl (p less than 0.01), an 18% decrease within 24 hours of surgery. To estimate the contribution of hemodilution or blood loss to the fall in cholesterol, changes in hematocrit were recorded. In the CABG group, hematocrit fell from 39.5 +/- 0.7% to 23.5 +/- 0.7% 24 hours after surgery (41% decrease) (p less than 0.01), whereas in the cholecystectomy group hematocrit fell from 39.4 +/- 0.8% to 37.1 +/- 0.9% on the first postoperative day (6% decrease). There was a positive correlation between the fall in cholesterol and the fall in hematocrit in the CABG group (correlation coefficient 0.472), suggesting that hemodilution was a major factor in the decrease in cholesterol levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effect of angiotensin II on renin production by rat adrenal glomerulosa cells in culture.

Angiotensin II (Ang II) inhibits renin secretion and production from the kidney, but the effect of Ang II on adrenal renin is not clear. Nephrectomy, via elevated plasma adrenocorticotropic hormone (ACTH) and potassium, is a strong stimulator of adrenal renin production in the rat. This stimulation is inhibited by the infusion of Ang II, suggesting a negative feedback between Ang II and adrenal renin. In the present study, we examined the effect of Ang II on adrenal renin using a primary culture of rat glomerulosa cells. Cells were exposed to ACTH (10(-11) M), high potassium (8 and 12 mM), db-cyclic AMP (db-cAMP), (10(-3) M), or Ang II (10(-11) to 10(-5) M) for 24 hours, and active renin and inactive renin were measured. Active renin was predominant in the cells, whereas inactive renin predominated in the medium. Ang II stimulated renin production in a dose-dependent fashion (cell-active renin, 1.21 +/- 0.20 to 2.39 +/- 0.16; medium-inactive renin, 2.59 +/- 0.40 to 6.14 +/- 0.49 ng Ang I/10(6) cells). Both ACTH and db-cAMP significantly stimulated active renin in the cells (ACTH, 1.73 +/- 0.14 to 9.44 +/- 0.98; db-cAMP, 1.45 +/- 0.16 to 3.96 +/- 0.71 ng Ang I/10(6) cells) and inactive renin in the medium (ACTH, 4.98 +/- 0.38 to 43.7 +/- 5.63; db-cAMP, 3.80 +/- 0.32 to 33.55 +/- 5.62 ng Ang I/10(6) cells). The addition of Ang II (10(-7) M) blunted the stimulation of renin production by both ACTH and db-cAMP by 60%. High potassium-stimulated renin production was not inhibited by Ang II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1992

Regulation of renin gene expression in rat adrenal zona glomerulosa cells.

Our previous studies indicated that the amount of renin present in cultured adrenal zona glomerulosa cells increased after stimulation with adrenocorticotropic hormone or potassium. In the present study, we investigated the effects of adrenocorticotropic hormone or potassium on renin gene expression in cultured rat adrenal zona glomerulosa cells. The amount of rat renin messenger RNA (mRNA) was measured by complementary DNA synthesis and the competitive polymerase chain reaction method. The effects of adrenocorticotropic hormone or potassium on adrenal zona glomerulosa cell renin activity and renin mRNA content were compared with the activity and content of control cells. After 1 and 4 hours of stimulation by adrenocorticotropic hormone or potassium, total renin in the medium increased slightly; at the same time, the percent change in the amount of renin mRNA was 281% and 291%, respectively, in the adrenocorticotropic hormone-stimulated group and 218% and 348%, respectively, in the potassium-stimulated group. Twenty-four hours after adrenocorticotropic hormone or potassium stimulation, total renin in the medium increased significantly, by 689% and 220%, respectively; percent change in the renin mRNA content was 754% and 278%, respectively. These results demonstrate that adrenocorticotropic hormone and potassium increased the activity of adrenal renin through an increase in the level of renin mRNA.

Adrenocorticotropic Hormone↗
PubMed1992

Regulation of the adrenal renin angiotensin system in cultured bovine zona glomerulosa cells: effect of catecholamines.

The renin-angiotensin system consists of two main enzymes, renin and angiotensin-converting enzyme, which lead to the formation of angiotensin-II. Angiotensin-II is a potent vasoconstrictor and stimulates the production of aldosterone. In this study we examined the effect of ACTH, potassium, (Bu)2cAMP (dbcAMP), and catecholamines on the adrenal renin-angiotensin system. To study the production of renin and aldosterone in vitro, we developed a monolayer culture of bovine zona glomerulosa cells in serum-free medium. Collagenase-dispersed zona glomerulosa cells were incubated in Pasadena Foundation for Medical Research-4 medium containing 10% fetal calf serum for 72 h, and the medium was replaced with serum-free medium for the next 24 h of the experimental period. The cells during this 24 h were exposed to various doses of ACTH, potassium, dbcAMP, and sympathomimetic agents. ACTH and dbcAMP stimulated aldosterone secretion, and this secretion was associated with an increase in renin activity in cells and medium. Aldosterone was also stimulated by high doses of potassium, and potassium had a stimulatory effect on the secretion of renin in medium. Catecholamines had a weak stimulating effect on aldosterone secretion and were potent stimulators of adrenal renin activity in cells and medium. Dopamine had no significant effect on basal aldosterone secretion or renin activity in cells and medium. In conclusion, these data indicate that adrenal renin is synthesized in bovine zona glomerulosa cells in vitro, and that ACTH and dbcAMP stimulate adrenal renin and aldosterone production. Furthermore, adrenal renin, like renal renin, may be under the control of the sympathetic nervous system.

Adrenocorticotropic Hormone↗
PubMed1992

Transforming growth factor-beta 1 inhibits aldosterone and stimulates adrenal renin in cultured bovine zona glomerulosa cells.

Transforming growth factors-beta (TFG beta s) are multifunctional peptides that affect proliferation, differentiation, and many other functions in a variety of cell types. In this study we examined the effect of TGF beta 1 on aldosterone and adrenal renin production using cultured bovine adrenal zona glomerulosa cells. Collagenase-dispersed zona glomerulosa cells were incubated in PFMR-4 medium containing 10% fetal calf serum for 72 h, and the medium was replaced with serum-free medium for the next 24 h. The cells during this 24-h period were exposed to TGF beta 1, ACTH, and (Bu)2cAMP (dbcAMP). It was observed that TGF beta 1 at 1 nM 1) inhibited basal aldosterone secretion from 680.0 +/- 40.0 to 270.0 +/- 10.0 pg/10(6) cells.h, 2) inhibited ACTH- and dbcAMP-stimulated aldosterone production, 3) increased levels of active renin in the cells from 17.8 +/- 2.5 to 70.7 +/- 4.4 pg angiotensin-I/10(6) cells.h and prorenin from 270.0 +/- 5.0 to 970.0 +/- 90 pg angiotensin-I/10(6) cells.h, 4) stimulated prorenin in the medium synergistically in combination with ACTH and dbcAMP, and 5) had no significant effect on basal cAMP production, but significantly inhibited the ACTH-stimulated production of cAMP. These observations show that TGF beta 1 is a potent inhibitor of basal and ACTH- and cAMP-stimulated aldosterone production and inhibits ACTH-stimulated cAMP production. Contrary to its effect on aldosterone, TGF beta 1 stimulates the synthesis and release of adrenal renin and prorenin. TGF beta 1 may act as an autocrine or paracrine regulator of aldosterone production.

Adrenocorticotropic Hormone↗
PubMed1992

Zonal distribution and regulation of adrenal renin in a transgenic model of hypertension in the rat.

The hypertensive transgenic rat [TGR (mRen-2)27] is a genetic model of hypertension in which transfection of the Ren-2 mouse renin gene into rats results in severe hypertension. These transgenic rats express a high level of renin in the adrenal gland, and the hypertension is ameliorated by treatment with angiotensin-converting enzyme inhibitors. In this study we investigated the distribution of adrenal renin in the TGR rat and examined the regulation of adrenal renin in a monolayer culture of adrenal cells. High concentrations of active renin and prorenin were found in the adrenal capsular (glomerulosa) and decapsular (fasciculata-medullary) portions of the TGR adrenal. This is in contrast with the Sprague-Dawley (S-D) rat, in which adrenal renin is found mostly in the active form and located primarily in the glomerulosa cells. The zonal distribution of aldosterone was also different in the TGR, with substantial amounts of aldosterone in the zona fasciculata as well as in the glomerulosa, while in the S-D rat, aldosterone is limited to the zona glomerulosa. In the primary monolayer culture of glomerulosa cells, TGR cells had significantly higher levels of active renin and prorenin and showed an increased response to ACTH and high potassium in the medium. Renin activity in the medium was predominantly in the form of prorenin and significantly higher than that in the S-D rat. Cultured fasciculata cells from TGR also produce renin that is stimulated by ACTH, but not by a high potassium concentration. Renin activity in the adrenal homogenate, medium, and plasma from TGR rats was completely inhibited by the renin inhibitor (CP 71362; 1 microM), but only slightly inhibited (12.3 +/- 3%) by a monoclonal antibody that inhibits renin activity from S-D rat tissues by 79.2 +/- 2.5%, suggesting that renin in the plasma and adrenal glands from TGR appears to derive primarily from mouse renin. In conclusion, the TGR (mRen-2)27 rats have higher than normal levels of adrenal renin, and the cultured cells show an exaggerated renin response to ACTH and potassium. The distribution of the renin enzyme in the adrenal zones of the TGR is similar to the distribution of mouse adrenal renin.

Adrenal Glands↗
PubMed1992

Adrenal renin: regulation and function.

Extrarenal renin has been identified in a variety of tissues. All of the components of the renin-angiotensin system have been detected in some organs, including the adrenal gland. A number of hypotheses have been expressed regarding the physiological function of these extrarenal renin systems, but no specific function has been clearly identified. This review focuses on the renin system in the adrenal cortex. Renin has been found in a variety of species, including the human adrenal cortex and adrenal tumors. Our investigations have focused on the renin-angiotensin system in the adrenal cortex of the rat, and have shown that renin is mainly present and synthesized in the zona glomerulosa cells. Renin production is under physiological control and can be altered by changes in electrolyte intake, adrenocorticotrophic hormone (ACTH), and the genetic background of the rat. In these experiments, a positive correlation between adrenal renin and aldosterone concentration is found. Furthermore, in primary culture of zona glomerulosa cells, a converting enzyme inhibitor can reduce the aldosterone stimulation by ACTH and potassium. However, these studies by themselves are not convincing evidence of the physiological role of the adrenal renin system. Further investigations are necessary to determine its role, if any, in adrenal function.

Adrenal Cortex↗
PubMed1991

Guanabenz-induced inhibition of aldosterone secretion from isolated rat adrenal glomerulosa cells.

The authors examined the effects of the alpha 2-adrenergic agonist guanabenz and other alpha-adrenergic ligands on aldosterone secretion and cyclic nucleotide content in isolated rat adrenal glomerulosa cells. Guanabenz inhibited aldosterone secretion stimulated by potassium, angiotensin II (AII), and adrenocorticotropic hormone (ACTH), exhibiting IC50 values of 35 microM, 43 microM, and 58 microM for stimulation by 10 mM K+, 1 nM AII, and 10 pM ACTH, respectively. Guanabenz did not affect the cGMP content of purified adrenal glomerulosa cells but inhibited ACTH stimulation of cAMP accumulation. Guanabenz inhibition of ACTH-induced cAMP may represent a mechanism for inhibition of aldosterone secretion, however, guanabenz also inhibited aldosterone secretion stimulated by the cAMP analog dibutyryl cAMP. The effect of guanabenz on the early and late pathways of steroidogenesis was tested in the isolated rat glomerulosa cells using 25-OH cholesterol and steroid precursors to aldosterone. Guanabenz inhibited the steroidogenic response to 25-OH cholesterol stimulation of aldosterone secretion but induced a much smaller inhibition of the steroidogenic response to exogenous pregnenolone, progesterone, and 11-deoxycorticosterone. These results suggested that guanabenz inhibited aldosterone secretion primarily through inhibition of the early component of the steroidogenic pathway prior to pregnenolone formation. The effects of guanabenz were not mimicked by other alpha-adrenergic ligands suggesting that these effects of guanabenz were not mediated through activation of alpha-adrenergic receptors.

Adrenocorticotropic Hormone↗
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

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↗