[A case of aneurysmal cyst of the ethmoid sinus].
Aneurysmatic cyst occurs in the ethmoid sinus rarely. Basing upon the case of 5-year old boy, the authors discuss the diagnosis, treatment and course of the disease.
Bone Cysts, Aneurysmal↗
Biomedical subjects
J Gutkowska
Publications and source records attributed to J Gutkowska.
Reciprocity of hemodynamic changes during lower body negative and positive pressure.
Lower body negative pressure (LBNP) and lower body positive pressure (LBPP) are two opposite environments for the lower abdomen and lower extremities. We examined RR interval (RRI), blood pressure, forearm blood flow, cardiac output, plasma atrial natriuretic factor, and plasma catecholamines during sequentially administered LBNP and LBPP in order to define the cardiovascular and neuroendocrine reciprocity of these models of orthostasis (LBNP) and anti-orthostasis (LBPP). Six healthy young men were studied with a ramped onset of LBNP followed by a similarly ramped LBPP, spaced between periods of data acquisition during rest. Forearm blood flow decreased during LBNP and increased during LBPP. However, LBNP and LBPP did not produce reciprocal changes in cardiac output. No reciprocal changes were found in plasma catecholamines and plasma atrial natriuretic factor. The variability of RRI and systolic/diastolic blood pressures were analyzed within two bandwidths of interest: the low bandwidth, corresponding to the frequency of baroreflex-mediated variability (0.04 to 0.12 Hz), and the high bandwidth, representative of parasympathetically mediated variability at the frequency of respiration (0.22 to 0.28 Hz). The ratio of high to low bandwidth RRI variability was reciprocally diminished during LBNP and increased during LBPP, reflecting a relative decrease in the level of parasympathetic tone during LBNP and an increase during LBPP. In addition, the variability of the DBP within the low baroreflex bandwidth increased during LBNP and decreased during LBPP. The phase lag of RRI variability in relation to BP variability did not change reciprocally.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Participation of the ascending serotonergic system in the stimulation of atrial natriuretic peptide release.
Results obtained in our laboratories have provided evidence for the participation of the hypothalamic atrial natriuretic peptide (ANP) neuronal system in the regulation of water and electrolyte homeostasis. The anterior ventral third ventricular (AV3V) region, a site of the perikarya of the ANP neurons, receives important afferent input from ascending serotoninergic axons. We hypothesized that the ascending serotoninergic tract might be involved in control of the liberation of ANP. Therefore, electrolytic lesions were produced in the mesencephalic dorsal raphé nucleus (DRN), the site of perikarya of serotonin (5-HT) neurons whose axons project to the AV3V region. Rats with sham lesions constituted the control group. In a second group of animals, the serotoninergic system was depleted of 5-HT by lateral ventricular administration of p-chlorophenylalanine (PCPA), an amino acid that causes depletion of 5-HT from the serotoninergic neurons. Control animals were injected with an equal amount of isotonic saline. The DRN lesions induced an increase of water intake and urine output beginning on the first day that lasted for 1 week after lesions were produced. There was a concomitant sodium retention that lasted for the same period of time. When water-loaded, DRN-lesioned and PCPA-injected animals showed diminished excretion of sodium, accompanied by a decrease in basal plasma ANP concentrations, and blockade of the increase in plasma ANP, which followed blood volume expansion by intraatrial injection of hypertonic saline. The results are interpreted to mean that ascending stimulatory serotoninergic input into the ANP neuronal system in the AV3V region produces a tonic stimulation of ANP release, which augments sodium excretion and inhibits water intake. Therefore, in the absence of this serotoninergic input following destruction of the serotoninergic neurons by DRN lesions or intraventricular injection of PCPA, an antinatriuretic effect is obtained that is associated with increased drinking, either because of sodium retention per se or removal of ANP-induced inhibition of release of the dipsogenic peptide, angiotensin II. The serotoninergic afferents also play an essential, stimulatory role in volume expansion-induced release of ANP and the ensuing natriuresis.
Animals↗
Polyamine regulation of atrial natriuretic peptide in cultured cardiocytes.
In the following investigation, we have studied the role of polyamines in the regulation of atrial natriuretic peptide (ANP) using ventricular cardiocytes which in culture synthesize and secrete ANP. Polyamines are cellular cations ubiquitous in eukaryotes, and ANP is a hormone synthesized and secreted by the cardiac atria in adult animal. The cardiocytes were isolated from neonatal rat hearts by enzymatic dissociation using trypsin and collagenase. The functional role of polyamines in regulation of ANP was assessed by exposing the cardiocytes to difluoromethylornithine (DFMO) which is an inhibitor of ornithine decarboxylase, an initial rate-limiting enzyme in the biosynthesis of polyamines. The results showed that DFMO reduced the levels of putrescine (diamine) and spermidine (triamine) in cultured cardiocytes, and it decreased the levels of ANP in media and cellular extracts of cardiocytes as a function of its dose. An addition of putrescine (100 microM) restored within 5-15 min the levels of ANP in media of both control and polyamine-depleted cardiocytes. These results suggest that polyamines are one of the cellular factors involved in regulation of ANP secretion in cultured cardiocytes.
Animals↗
Atrial natriuretic factor in ovine pregnancy: plasma levels, molecular forms and biological activity.
Pregnancy is associated with hypervolemia and elevated plasma ANF, but the time course over which ANF increases and the mechanisms that control plasma ANF levels are unclear. Plasma ANF was measured in 12 nonpregnant and 16 pregnant sheep at various gestational ages. ANF was elevated at 30-35 days of pregnancy (15.7 +/- 1.4 vs. 22.9 +/- 3.4 fmol/ml, P = 0.04), but did not increase further with the advance of gestation. Tissue content of ANF was unchanged in the right atrium, left atrium, renal cortex, renal medulla, adrenals and lungs, but ovarian ANF content was increased during pregnancy (9.2 +/- 2.2 vs. 67.2 +/- 23.2 fmol/mg protein, P = 0.003). However, the ovarian tissue ANF concentration was less than 0.2% of that in the atria during pregnancy. HPLC of plasma from both nonpregnant and pregnant ewes revealed the presence of a single peak that elutes in parallel with synthetic human ANF. HPLC of atrial and lung tissue homogenates revealed multiple peaks that may represent different molecular forms of ANF. The biological activity of ANF in the plasma of pregnant ewes was reduced to 23% of nonpregnant levels. ANF in lung tissue was also biologically active, but that activity was reduced to 13% of nonpregnant levels. These data suggest that elevated plasma ANF in pregnancy is not secondary to increased atrial, renal, adrenal, ovarian or pulmonary contribution. Since we have previously shown that the metabolic clearance of ANF is not decreased, other extra-atrial sites may contribute to the increased plasma ANF during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of prostaglandin inhibition on the renal function curve during ovine pregnancy.
OBJECTIVE: This study was designed to assess the influence of prostaglandins on the steady-state relationship of mean arterial pressure and urinary sodium excretion. STUDY DESIGN: Ten nonpregnant and nine pregnant ewes were chronically prepared with indwelling catheters and maintained in metabolism cages. All the ewes received a continuous intravenous infusion of indomethacin (5 mg/kg/day) for 24 days. Step increases in sodium intake (20, 100, 400, and 1200 mmol per day), each maintained for 6 days, were administered as a fixed dietary (20 mmol) component with the balance infused intravenously. Mean arterial pressure was continuously monitored. The renal function curves were constructed from the steady-state mean arterial pressure-urinary sodium excretion relationships after sodium balance was attained. RESULTS: Indomethacin inhibited urinary excretion of prostaglandin E2 by 62% +/- 4% in nonpregnant and 47% +/- 6% in pregnant ewes, and 6 keto-prostaglandin F1 alpha, the stable metabolite of prostaglandin I2, by 55% +/- 4% and 65% +/- 6% in nonpregnant and pregnant ewes, respectively. Blood volume was not affected by indomethacin or salt in either group. Plasma angiotensin II was suppressed less in pregnant ewes (60% vs 80%) by increases in salt intake. Chronic treatment with indomethacin did not alter the renal function curves of either nonpregnant or pregnant ewes. CONCLUSIONS: These results suggest that prostaglandins do not influence the steady-state relationship between mean arterial pressure and urinary sodium excretion in either nonpregnant or pregnant sheep.
6-Ketoprostaglandin F1 alpha↗
Clinical relationships of cyclic GMP.
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Cyclic GMP↗
Indirect hypertensive actions of long-term intracarotid angiotensin II infusion during ovine pregnancy.
Angiotensin II (AngII) influences the regulation of mean arterial pressure (MAP) through numerous mechanisms, including an action of circulating AngII on the brain to alter autonomic activity. We have obtained evidence that the relative importance of this effect is increased during pregnancy. Consequently, these studies were undertaken to assess the effects of bilateral infusion of AngII (0.35 ng.kg-1.min-1.artery-1) into the internal carotid arteries (ica) of sheep for 13 days. Six non-pregnant (NP) and six 105- to 125-day pregnant (PG) ewes were maintained in large metabolism cages, where MAP was continuously monitored. By day 10 of ica AngII infusion in NP ewes, MAP was increased from 83.9 +/- 1.6 to 92.9 +/- 2.8 mmHg (1 mmHg = 133.3 Pa) (p = 0.001). Twenty-four hour urine volume (UV, 2664 +/- 341 to 1583 +/- 228 mL; p = 0.005) and sodium excretion (UNaV, 190 +/- 5 to 113 +/- 19 mmol/day; p = 0.005) were decreased. 51Cr-tagged blood volume (BV) was increased on day 13 (3643 +/- 187 to 4379 +/- 446 mL; p = 0.05). In contrast, by only day 6 of ica AngII infusion in PG ewes, MAP increased from 79.1 +/- 1.9 to 84.1 +/- 1.4 mmHg (p = 0.03) in association with a BV expansion from 3999 +/- 274 to 4207 +/- 275 mL. These changes were preceded by decreases in UV (2813 +/- 413 to 2198 +/- 362 mL; p = 0.01) and UNaV (190 +/- 15 to 118 +/- 26 mmol/day; p = 0.01). By day 13, MAP had plateaued at 93.0 +/- 1.2 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin II↗
Renal perfusion pressure and renin secretion in bilaterally renal denervated sheep.
To further investigate the influence of renal nerves on renin secretion, the renin secretion responses to step reductions of renal perfusion pressure (RPP) were studied in conscious sheep with innervated kidneys (n = 5) and with bilaterally denervated kidneys (n = 5). The average basal level of RPP in sheep with denervated kidneys (82 +/- 4 mmHg; 1 mmHg = 133.3 Pa) was similar to that in sheep with innervated kidneys (83 +/- 3 mmHg). RPP was reduced in four sequential 15-min steps, to a final level of 54 +/- 2 mmHg in sheep with innervated kidneys and to 57 +/- 1 mmHg in denervated sheep. The renin secretion rate was increased as RPP was reduced in sheep with innervated kidneys. Baseline peripheral plasma renin activity was reduced and there was almost no response of renin secretion rate to reduction of RPP in sheep with denervated kidneys. Also, baseline renal blood flow, urine flow rate, sodium excretion rate, and potassium excretion rate were higher in sheep with denervated kidneys than those with innervated kidneys. Baseline plasma angiotensin II was similar in both groups of sheep. As RPP was decreased, plasma angiotensin II was increased in sheep with innervated kidneys, but was not RPP or renal denervation. In conclusion, hormonal factors, such as angiotensin II and atrial natriuretic factor, do not account for the dramatic suppression of renin secretion in response to the reduction of RPP in sheep with bilateral renal denervation. Renal nerves are a necessary component in the control of renin secretion during reduction of RPP and may contribute to the regulation of baseline plasma renin activity and sodium excretion rate in conscious ewes.
Angiotensin II↗
Metabolic clearance of atrial natriuretic factor in ovine pregnancy.
Plasma atrial natriuretic factor (ANF) is normally released into the circulation primarily by volume expansion and atrial distension, but we have shown that plasma ANF is elevated in pregnant sheep before volume expansion. Because alterations in the metabolic clearance of ANF could lead to elevated plasma ANF levels, the present study was designed to determine the pharmacokinetics of plasma ANF in pregnant sheep. Chronically instrumented nonpregnant and pregnant sheep received intravenous injections of monoiodinated human ANF (125I-hANF). Plasma decay curves of 125I-hANF followed a biexponential function in both groups. High-performance liquid chromatography (HPLC) revealed the accumulation of smaller degradation products by 2 min postinjection, and by 30 min no intact ANF was present. Because HPLC identification of ANF and its metabolites was shown to be more efficient than precipitation with 10% trichloroacetic acid (TCA) or extraction by Sep-Pak cartridges, ANF kinetic parameters were calculated from HPLC-corrected plasma decay curves. Injected ANF was rapidly distributed in an initial distribution volume (IDV) that was expanded in pregnant sheep. Metabolic clearance rate (MCR) was greater in pregnant sheep (2.8 +/- 0.3 vs. 6.8 +/- 1.2 l/min, P = 0.002), while plasma half-life (t1/2) was not altered (2.2 +/- 0.5 vs. 2.4 +/- 0.4 min). The data demonstrate that during pregnancy, the t1/2 of ANF is not altered but the MCR of ANF is enhanced. These findings imply that plasma ANF is increased by mechanisms other than reduced clearance in pregnant sheep.
Animals↗
Increased plasma atrial natriuretic peptide after acute injection of alcohol in rats.
A number of mechanisms may be involved in the protective effect of low ethanol (ETOH) consumption on the development of the age-dependent hypertension in both human and experimental animals. It was the objective of the present study to test the hypothesis that acute administration of low doses of ETOH would increase the plasma content of atrial natriuretic peptide (ANP), a hormone known to decrease blood pressure. Plasma ANP levels were increased significantly within 15 min after the i.p. injection of 1 or 2 g of ETOH/kg b.wt. The increase in plasma ANP was more pronounced and longer lasting after the i.p. injection of 2 rather than 1 g of ETOH/kg b.wt. This increase in plasma ANP level was associated with a rapid decrease of atrial ANP, but not of ventricular ANP which on the contrary was significantly elevated at 120 min postinjection. It has been suggested that opioids could play a significant role in controlling ANP release. In fact, circulating levels of beta-endorphin were also rapidly increased after the ETOH injection, with a time-course pattern similar to that of ANP. Furthermore, a highly positive correlation was found between the ETOH-induced changes of plasma ANP and beta-endorphin contents. Significant increases in plasma corticosterone and adrenocorticotropic hormone, but not aldosterone contents, were observed after the i.p. injection of 2 g of ETOH/kg b.wt., whereas plasma arginine vasopressin levels were significantly decreased at 15 but not at 120 min postethanol. There was no significant elevation in blood pressure during the 120-min experimental period, although a small tachycardia did develop in the ETOH-treated animals. Thus, acute in vivo administration of ETOH increased plasma ANP content in a dose-dependent manner and may play a role in the "protective" effect of low ETOH consumption in the development of the age-dependent hypertension.
Adrenocorticotropic Hormone↗
Hypothalamic control of water and salt intake and excretion.
This article provides a personal and historical review of research concerning the hypothalamic control of water and salt intake and excretion. The following major points will be considered: 1. Electrical, osmotic, cholinergic, alpha-adrenergic and peptidergic stimulation of the hypothalamus. 2. Determination of the pathways involved in these neuroendocrine responses. 3. The participation of ANP in the control of thirst and salt excretion. 4. The participation of the brain ANPergic neuronal system in ANP release. 5. The role of hypothalamic ANPergic neurons and of sinoaortic and renal baroreceptors in the regulation of volume expansion-induced release of ANP. 6. Effects of the brain ANP system on other hormones.
Angiotensin II↗
Essential role of hypothalamic muscarinic and alpha-adrenergic receptors in atrial natriuretic peptide release induced by blood volume expansion.
Expansion of the blood volume induces natriuresis, which tends to return the blood volume to normal. This response is mediated at least in part by the release of atrial natriuretic peptide (ANP) into the circulation. Previous experiments have shown the participation of the anterior ventral third ventricular (AV3V) region of the hypothalamus in the ANP release that follows volume expansion. When injected into the AV3V region, the cholinergic drug carbachol induces natriuresis and the release of ANP. In the present experiments, microinjection of norepinephrine into the AV3V region induced natriuresis and an increase in plasma ANP. To determine whether cholinergic and alpha-adrenergic pathways are crucial to the volume expansion-induced release of ANP, certain receptor-blocking drugs were injected into the AV3V region of conscious rats. Thirty minutes later blood volume was expanded by intravenous injection of 2.0 ml/100 g of body weight of hypertonic saline (0.3 M NaCl). Microinjection of isotonic saline (2 microliters) into AV3V region of control animals 30 min prior to volume expansion had no effect on the 3-fold increase in plasma ANP concentrations measured 5 min after volume expansion. In contrast, although the receptor-blocking drugs did not alter the initial concentrations of plasma ANP 30 min later, just prior to volume expansion, blockade of muscarinic cholinergic receptors by intraventricular injection of 5 nmol (2 microliters) of atropine sulfate or methylatropine markedly reduced the response to volume expansion but did not obliterate it. Microinjection of the alpha receptor blocker phentolamine (5 nmol) into the AV3V 30 min prior to volume expansion also markedly suppressed the ANP response. Intraperitoneal (i.p.) injection of methylatropine (0.01 mmol/100 g of body weight), which does not cross the blood-brain barrier, also did not affect the basal levels of ANP 30 min after i.p. injection. But, in striking contrast with the blockade of the response to volume expansion induced by intraventricular injection of methylatropine, the response to volume expansion was markedly enhanced by i.p. injection of methylatropine. The results therefore indicate that hypothalamic muscarinic and alpha-adrenergic synapses are essential to release of ANP in response to volume expansion. These results are consistent with a hypothetical pathway for physiological control of ANP release which involves distension of baroreceptors within the right atria, carotid and aortic sinuses, and kidney which alters afferent input to brain stem noradrenergic neurons with axons projecting to the AV3V region. There they activate cholinergic interneurons by an alpha 1-adrenergic synapse. The cholinergic neurons in turn stimulate ANP neurons in this brain region via muscarinic receptors. The stimulation of these neurons activates efferent pathways which induce the release of ANP.
Animals↗
Effect of morphine on urine output: possible role of atrial natriuretic factor.
We examined the possible role of atrial natriuretic factor (ANF) in morphine-induced diuresis. Morphine (20 micrograms/20 microliters) administered intracerebroventricularly (i.c.v.) in conscious, normally hydrated Sprague-Dawley rats significantly increased urine output from 0.22 +/- 0.16 ml/h/rat to 2.07 +/- 0.46 ml/h/rat, 3 h after injection. Morphine injection also significantly increased the plasma ANF level to a maximum of 364 +/- 46 pg/ml compared to control animals (33 +/- 7 pg/ml) in which 20 microliters of saline was injected i.c.v. (P < 0.001). This peak increase occurred 1 h after morphine administration, however, it continued to remain significantly elevated (171 +/- 36 pg/ml vs. 39 +/- 8 pg/ml in control animals; P < 0.001) 2 h later. The maximal diuresis observed 3 h after administration of morphine i.c.v. was abolished by pretreatment of the animals with 0.8 mg of naloxone given intravenously (i.v.) and also by anti-rat ANF serum (0.4 ml i.v.). A short, transient increase in blood pressure, occurred 2-5 min after morphine administration, but it is unlikely that this increase accounted for the increase in plasma ANF. We conclude that the diuresis induced by i.c.v. administration of morphine is due to enhanced release of ANF.
Animals↗
Immunocytochemical localization of atrial natriuretic factor (ANF)-like peptides in the brain and heart of the treefrog Hyla japonica: effect of weightlessness on the distribution of immunoreactive neurons and cardiocytes.
The localization of atrial-natriuretic factor (ANF)-like immunoreactivity was investigated in the brain and heart of the treefrog Hyla japonica by the indirect immunofluorescence technique. Concurrently, the effect of weightlessness on the distribution of ANF-containing neurons and cardiocytes was studied in frogs that were sent into space for 9 days on the space station "MIR." In control animals, the amygdala contained the most prominent group of ANF-immunoreactive cells and fibers. ANF-positive neurons and nerve processes were also detected in other areas of the telencephalon such as the nucleus olfactorius, the pallium mediale, and the striatum. In "space frogs," the intensity of labeling of the amygdala and nucleus olfactorius was similar to that seen in control animals. In contrast, the pallium and the striatum of "space frogs" were totally devoid of positive cell bodies. In the diencephalon, of all animals, numerous ANF-immunoreactive perikarya and fibers were seen in the hypothalamus, the anterior thalamus, the infundibulum, and the median eminence. ANF-positive cell bodies were also noted in the lateral forebrain bundle of control frogs but were absent in "space frogs." The major difference between control and "space frogs" was observed in the posterior nuclei of the thalamus. In "space frogs," the nucleus posterocentralis thalami and the nucleus posterolateralis thalami exhibited large ANF-immunoreactive perikarya, while, in control frogs, these nuclei only contained scarce positive nerve fibers. In the mesencephalon, ANF-positive cell bodies and nerve processes were seen in the nucleus tegmenti mesencephali, the interpeduncular nucleus, and the nucleus cerebelli of all animals. However, stained perikarya were only observed in the nucleus reticularis isthmi of control frogs. In the heart, atrial cardiocytes exhibited intense ANF-like immunoreactivity. ANF-positive myocytes were also detected in the subpericardial region of the ventricle. The density and distribution of the staining were identical in the heart of control and "space frogs." These data support the concept that prolonged exposure to microgravity affects biosynthesis and/or release of ANF-related peptides in discrete regions of the amphibian brain.
Animals↗
Effect of difluoromethylornithine on atrial natriuretic peptide in rat atria.
Polyamines are aliphatic cations known to have a role in cellular growth and differentiation. In this study, difluoromethylornithine (DFMO), an inhibitor of polyamine synthesis, was used to investigate its effect on atrial natriuretic peptide (ANP) in atria of rat. The rats were given DFMO (2%) in drinking water for 10 days and three intraperitoneal administrations (200 mg/kg), 24, 18 and 1 h prior to experiment. Radioimmunoassay of ANP in atrial extracts indicated that DFMO treatment increased ANP contents of atria. ANP from atrial extracts was immunoprecipitated using ANP antibody and the immunoprecipitate was resolved and detected by SDS-PAGE and Western blotting. The predominant ANP peptide in both control and DFMO group migrated at 17 kDa. The synthesis of ANP was studied following the intravenous administration of [35S]methionine. ANP in atrial extracts was immunoprecipitated by ANP antibody. The incorporation of ANP into control and DFMO group peaked at 30 min and returned to a basal level by 60 min. DFMO decreased the incorporation of [35S]methionine into ANP. At 30 min following the administration of [35S]methionine, putrescine restored the synthesis of tricholoroprecipitable atrial proteins, but had no effect on the synthesis of ANP. At 60 min following, the amount of labeled ANP in DFMO + putrescine-treated group was significantly lower than that in DFMO group. These results indicate that polyamines influence both the synthesis and secretion of ANP.
Animals↗
Atrial natriuretic factor: plasma concentration and specific binding to renal glomeruli during the development of genetic hypertension in rats of the Lyon strain.
1. The pathophysiologic role of atrial natriuretic factor (ANF) in genetic hypertension was investigated in 5- and 21-week-old genetically hypertensive (LH), normotensive (LN) and low blood pressure (LL) rats of the Lyon strain. 2. Plasma ANF was significantly higher in 5-week-old LH than in age-matched LN and LL animals. It tended to be lower in 21-week-old LH than in LN rats. 3. Left and right atrial ANF content was also significantly lower at 21 weeks in the LH group. 4. Glomerular ANF receptors showed a significant decrease in LH in comparison to LL and LN animals.
Animals↗
Brain atrial natriuretic peptide neurons play an essential role in volume expansion-induced release of atrial natriuretic peptide and natriuresis.
The brain atrial natriuretic peptide (ANP) neuronal system appears to be involved in the increase in plasma ANP which follows blood volume expansion in the rat. To determine if this neuronal system is essential to the natriuresis and increase in plasma ANP which follow volume expansion, highly specific antiserum against ANP (ANP-AB) and/or normal rabbit serum as a control was microinjected into the third cerebral ventricle (3V) of conscious rats, and the effect on the natriuresis and increase in plasma ANP induced by intravenous injection of 2 ml/100 g body weight of 0.3 M NaCl was examined. Although there was no effect of ANP-AB on initial levels of plasma ANP or natriuresis 3 h after 3V injection, the natriuresis in response to blood volume expansion was significantly inhibited. The increase in plasma ANP which followed volume expansion was also significantly reduced at 5 min but recovered at 15 min. The results indicate that the brain ANP neuronal system plays an essential role in the mediation of volume expansion-induced increase in plasma ANP and natriuresis. The failure to block these responses completely may be due to the use of an inadequate dose of antiserum or other brain mechanisms may be able to mediate these responses.
Animals↗