Renal interstitial pressure and tubuloglomerular feedback control in rats during infusion of atrial natriuretic peptide (ANP).

Atrial natriuretic peptide (ANP), injected at physiological concentrations, is known to induce both natriuresis and diuresis. It has been suggested by some investigators that these changes result from an increasing glomerular filtration rate (GFR), but others have been unable to demonstrate an increased GFR. The tubuloglomerular feedback (TGF) mechanism is an important regulator of GFR, and the sensitivity of TGF is decreased during ANP administration. Furthermore, resetting of TGF is, in most instances, related to changes in renal interstitial hydrostatic and oncotic pressures. It is also known that ANP may increase capillary permeability which may change renal interstitial pressure. The present study was performed to examine renal interstitial pressures and the TGF mechanism during ANP infusion. In accordance with previous studies, TGF sensitivity was found to be decreased. The tubular flow rate which elicited half the maximal drop in stop-flow pressure (Psf) was increased from 18.5 to 25.7 nl min-1. In contrast, ANP infusion resulted in a decreased interstitial hydrostatic pressure and an increased interstitial oncotic pressure. From previous experiments, such changes in interstitial pressures would be expected to increase TGF sensitivity. The changes in interstitial pressure cannot, therefore, directly explain the resetting of the feedback mechanism. In conclusion, the present paper shows a decreased renal net interstitial pressure after intravenous administration of ANP.     

Effects of acute and chronic unilateral renal denervation on the tubuloglomerular feedback mechanism

We recently observed a time-dependent resetting of the tubuloglomerular feedback (TGF) sensitivity to a subnormal level after acute unilateral renal denervation (aDNX). The present investigation compares the effects of aDNX with those of chronic unilateral renal denervation (cDNX), i.e one week after aDNX. All experiments were performed in anaesthetized rats prepared for micropuncture. cDNX led to increases in urine, sodium and potassium excretion in denervated kidneys, while contralateral kidneys showed reduced excretion of these parameters. GFR was increased in denervated kidneys, but unchanged on the contralateral side. TGF activity was determined by measuring the maximal stop-flow pressure response (ΔP_sf) and the tubular flow rate at which 50% of the maximal response occurred (turning point; TP). cDNX decreased TGF sensitivity, as indicated by an increased TP from 19.1 nL/min in sham-DNX to 26.1 nL/min. Concomitantly, TP in contralateral kidneys was significantly decreased to 15.9 nL/min. aDNX led to a greater sensitivity reduction; TP increased from 19.8 to 34.0 nL/min and contralaterally TP decreased to 14.0 nL/min. ΔP_sf in cDNX increased by 63% compared to sham-DNX, while on the contralateral side this was unchanged. No difference in ΔP_sf was found between control, DNX and contralateral kidneys in the aDNX group. In summary, these experiments show that the previously reported decrease in TGF sensitivity in aDNX kidneys still persists after one week, although less pronounced. As a result of the decreased TGF sensitivity, GFR is kept on a high level in cDNX kidneys. Contralateral kidneys show reversed resetting.     

Origin and characterization of atrial natriuretic peptide in the rat parotid gland

Summary The heart atria represent the major site of synthesis for atrial natriuretic peptide (ANP) which exerts potent natriuretic, diuretic and vasoactive functions. Recently, ANP-immunoreactivity has been detected in extracardial organs involved in water and electrolyte homeostasis, such as the intestine and certain exocrine glands. The present study investigates ANP in the parotid gland. It was found by immunohistochemical techniques that the peptide is localized in ductal cells of the gland. An analysis of the immunoreactive material by high-pressure liquid chromatography and radioimmunoassay revealed the prohormone of ANP (ANP 1-126) and the biologically active fragment (ANP 99-126). Furthermore, Northern blot hybridization disclosed the presence of mRNA coding for ANP. It is suggested that ANP is synthesized and released from the parotid gland and functions in the control of saliva production.     

Activation of the tubuloglomerular feedback mechanism in dehydrated rats

To study the influence of the tubuloglomerular feedback control (TGF) on the regulation of glomerular filtration rate (GFR) during dehydration, micropuncture experiments were performed on surface nephrons of dehydrated rats. Dehydration was achieved by withdrawal of food and water for 24 h. The urine flow rate decreased to 1.5 μl/min (controls 2.9 μl/min) and GFR decreased in these rats to 0.80 ml/min (controls 1.22). TGF was studied by two different micropuncture procedures. With the first technique the changes in proximal stop-flow pressure in response to changes of the late proximal microperfusion rate were measured. With this technique the perfusion rate necessary to induce a half maximal stop-flow pressure response, the turning point, was also determined. An increased TGF sensitivity was found in dehydrated rats, as indicated by increased stop-flow pressure responses (35 versus 26%) and decreased turning points (16 versus 21 nl/min). With the second micropuncture technique the single nephron GFR (SNGFR) was measured at distal and proximal tubular sites, in the same nephron. Distal SNGFR was decreased during dehydration to 32.2 nl/min, versus 42.7 nl/min in controls. A significant difference between paired SNGFR measurements in the same nephron was observed during dehydration, the proximal value being 5.3 nl/min higher than the distal, whereas this difference was not seen in control rats. This finding indicates that activation of the feedback mechanism takes place to reduce SNGFR. It is concluded that the decrease in whole kidney GFR is partly caused by the observed increase in feedback activity. The present results are also in agreement with our earlier hypothesis that the hydrostatic and oncotic pressure conditions within the interstitial space surrounding the macula densa cells modulate the sensitivity of the tubuloglomerular feedback mechanism.     

Atrial natriuretic peptide (ANP): response to NaCI is attenuated in rat atria in vitro after hypophysectomy

The present study documents the effects of hypophysectomy on the NaCl-stimulated release and on the basal secretion rates of ANP from rat atria in vitro. Three weeks before the experiments rats were subjected to hypophysectomy or to a corresponding sham operation. Atria were excised and superfused in an organ bath with a physiological buffer solution (PBS, 294 mosmol kg^-1). After a control period of 5 min, superfusion was made with hyperosmotic NaCI (330 mosmol kg^-1) for 10 min, and then again with PBS, but now for 15 min. Atria were paced with field stimulation (4 Hz, 20 V, 1 ms) and the resting tension was kept at 5 mN. The sham-operated animals responded with a significant increase (P < 0.05) in the secretion rate of ANP (from 137 ± 13 pg ml^-1 [n = 35] to 235 ± 24 [n = 34], means + SE) to the NaCI stimulus. The hypophysectomy blunted the ANP response to hyperosmotic NaCl. In addition, basal secretion rate was signficantly (P < 0.001) lower in the hypophysectomized than in the sham-operated animals during the whole experiment. Gel filtrations revealed that, during the hyperosmotic NaCI, both groups secreted exclusively ANP 1–28. We conclude that hypophysectomy blunts the basal as well as stimulus-induced in-vitro release of ANP from rat atria.     

Increased brain natriuretic peptide and atrial natriuretic peptide plasma concentrations in dialysis-dependent chronic renal failure and in patients with elevated left ventricular filling pressure

Brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) plasma concentrations were measured in patients with dialysis-dependent chronic renal failure and in patients with coronary artery disease exhibiting normal or elevated left ventricular end-diastolic pressure (LVEDP) (n = 30 each). Blood samples were obtained from the arterial line of the arteriovenous shunt before, 2 h after the beginning of, and at the end of hemodialysis in patients with chronic renal failure. In patients with coronary artery disease arterial blood samples were collected during cardiac catheterization. BNP and ANP concentrations were determined by radioimmunoassay after Sep Pak C₁₈ extraction. BNP and ANP concentrations decreased significantly (P < 0.001) during hemodialysis (BNP: 192.1 ± 24.9, 178.6 ± 23.0, 167.2 ± 21.8 pg/ml; ANP: 240.2 ± 28.7, 166.7 ± 21.3, 133.0 ± 15.5 pg/ml). The decrease in BNP plasma concentrations, however, was less marked than that in ANP plasma levels (BNP 13.5 ± 1.8%, ANP 40.2 ± 3.5%; P < 0.001). Plasma BNP and ANP concentrations were 10.7 ± 1.0 and 60.3 ± 4. 0 pg/ml in patients with normal LVEDP and 31.7 ± 3.6 and 118.3 ± 9.4 pg/ml in patients with elevated LVEDP. These data demonstrate that BNP and ANP levels are strongly elevated in patients with dialysis-dependent chronic renal failure compared to patients with normal LVEDP (BNP 15.6-fold, ANP 2.2-fold, after hemodialysis; P < 0.001 or elevated LVEDP (BNP 6.1-fold, ANP 2.0-fold, before hemodialysis; P < 0.001), and that the elevation in BNP concentrations was more pronounced than that in ANP plasma concentrations. The present results provide support that other factors than volume overload, for example, decreased renal clearance, are also involved in the elevationin BNP and ANP plasma levels in chronic renal failure. The stronger elevation in BNP concentrations in patients with chronic renal failure and in patients with elevated LVEDP and the less pronounced decrease during hemodialysis suggest a different regulation of BNP and ANP plasma concentrations.[/ p]Abbreviations ANP atrial natriuretic peptide - BNP brain natriuretic peptide - LVEDP left ventricular end-diastolic pressure Correspondence to: C. Haug     

人类心房利钠肽基因在自发性高血压大鼠体内表达及其对血压的影响

目的研究人类心房利钠肽（hANP）基因在自发性高血压大鼠（SHRs）体内表达、持续时间和对血压的影响。方法 12只8周龄雄性SHRs,随机分为两组,于左腿股四头肌注射pcDNA3.1-hANP质粒的为实验组,在同一部位注射pcDNA3.1空质粒的为对照组,每周测量大鼠尾动脉收缩压,及利用放射免疫方法监测血中hANP水平。结果转基因后第1周起与对照组比较,实验组血压开始下降,两组动物一直相差（13±3.1）mmHg（P〈0.05）,其作用可持续10周;且放射免疫方法监测实验组血中hANP水平较高;RT-PCR和Western印迹杂交技术检测显示实验组hANP基因在肌肉组织中高效表达,对照组则未见表达。结论肌肉注射法将hANP基因导入SHRs,hANP基因可在肌肉组织中高效表达,且hANP可释放入血,降低SHRs的血压,显示了hANP基因对高血压患者治疗的可能性。     

Diurnal rhythms of plasma renin activity,atrial natriuretic peptide and arterial pressure during head-down bed rest in humans

The effects of prolonged head-down bed rest on the rhythms of several parameters (blood pressure, heart rate, haematocrit, plasma renin activity (PRA), atrial natriuretic peptide (ANP) were assessed in six healthy men, aged 33 (SEM 2) years, who were submitted to bed rest for 28 days (D1-28). Systolic and diastolic blood pressure (BP_s and BP_d) and heart rate were measured at 0700 and 1900 hours; circulating PRA and ANP were determined from blood samples drawn at 0800, 1000, 1200, 1500, 1800 and 2200 hours before bed rest (D – 5), D1, 2, 7, 20, 27 during bed rest and post bed rest (D + 2). The BP_s was the lowest at 0700 hours and increased at 1900 hours. There was a significant difference between values during all the measurements. The BP_d and heart rate were lower at 0700 hours before and after bed rest and no significant difference appeared between these two values during the bed rest. The PRA and ANP concentrations were more stable during bed rest, and had not returned to original rhythmicity 2 days after bed rest. The mean daily concentration of ANP decreased during bed rest. It would seem from this study that changes occur in those rhythms during bed rest.     

妊高征患者母血脐血中内皮素及心钠素的变化

应用放射免疫法测定１５例妊高征患者，１５例正常妊娠妇女母血和脐血中心钠素与内皮素含量。结果：妊高征组母血和脐血中心钠素均明显高于正常妊娠组（Ｐ＜０．０１），妊高征组母血中内皮素明显高于正常妊娠组（Ｐ＜０．０１），而两组脐血内皮素无明显差别（Ｐ＞０．０５），各组心钠素与内皮素之间均有明显正相关（Ｐ＜０．０１）。说明内皮素在妊高征发病中起重要作用。而心钠素在抑制妊高征发生中应起一定作用；心钠素与内皮素之间相互影响。     

人类心房利钠肽基因在自发性高血压大鼠体内表达及对血压和肾脏的组织学影响

目的研究人类心房利钠肽（hANP）基因在自发性高血压大鼠（SHR）体内表达、持续时间和对血压及肾脏的组织学影响。方法 12只8周龄雄性SHR,随机分为两组,于左腿股四头肌注射pc DNA3.1-h ANP质粒的为实验组,在同一部位注射pc DNA3.1空质粒的为对照组,每周测量大鼠尾动脉收缩压,及利用放射免疫方法监测血中h ANP水平;10周后处死动物,RT-PCR和Western印迹杂交技术检测h ANP基因表达情况;HE染色和Masson染色观察对肾脏的组织形态学的影响。结果转基因后第1周起与对照组比较,实验组血压开始下降,两组动物一直相差（12±3.1）mm Hg（P〈0.05）,其作用可持续10周;且放射免疫方法监测实验组血中hANP水平较高;RT-PCR和Western印迹杂交技术检测显示实验组hANP基因在肌肉组织中高效表达,对照组则未见表达;组织形态学分析结果显示实验组肾脏组织细胞形态基本正常,胶原沉积明显减少。结论肌肉注射法将hANP基因导入SHR,hANP基因可在肌肉组织中高效表达,且hANP可释放如血,降低SHR的血压并对高血压靶器官肾脏的损害起到了治疗及预防作用。显示了hANP基因对高血压患者治疗的可能性。     

人类心房利钠肽基因在自发性高血压大鼠体内表达及其对血压、心脏、血管的影响

目的研究人类心房利钠肽（hANP）基因在自发性高血压大鼠（SHR）体内表达、持续时间和对血压及心脏、血管的影响。方法12只8周龄雄性SHR,随机分为两组,于左腿股四头肌注射pcDNA3．1-hANP质粒的为实验组,在同一部位注射pcDNA3．1空质粒的为对照组,每周测量大鼠尾动脉收缩压,及利用放射免疫方法监测血中hANP水平;10周后处死动物。RT—PCR和Western印迹杂交技术检测hANP基因表达情况;分别称量体重、全心脏和左心室重量,大体评价对心肌重构的影响;苏木素-伊红（HE）染色和胶原组织学（VG）染色观察对心脏、血管组织形态学的影响。结果转基因后第1周起与对照组比较,实验组血压开始下降,两组动物一直相差（12±3．1）mmHg（P〈0．05）,其作用可持续10周;且放射免疫方法监测实验组血中hANP水平较高;RT—PCR和Western印迹杂交技术检测显示实验组hANP基因在肌肉组织中高效表达,对照组则未见表达;实验组心脏重量／体重比和左心室重量／心脏重量比明显低于对照组。组织形态学分析结果显示实验组心肌、血管组织细胞形态基本正常,胶原沉积明显减少。结论肌肉注射法将hANP基因导入SHR,hANP基因可在肌肉组织中高效表达,且hANP可释放如血,降低SHR的血压并对心脏、血管高血压靶器官的损害起到了预防作用。显示了hANP基因对高血压患者治疗的可能性。     

Plasma atrial natriuretic peptide (ANP) concentration and fluid balance during rapid intravenous saline infusions in camels

Human muscle samples were obtained with the percutaneous biopsy technique. The samples were membrane-hyperpermeabilized (skinned) using a chemical or freeze-drying technique. Short single fibre segments were dissected from the sample, transferred to an experimental chamber, connected to a force transducer and manipulator, and exposed to temperature-controlled solutions. The force generating-capacity, the sensitivity of the contractile apparatus to calcium and the caffeine threshold for calcium release from the sarcoplasmic reticulum could be studied in the short muscle fibre segments obtained from man with the percutaneous muscle biopsy technique. The average length of the fibre segments between the connectors was 0.44±0.21 mm. Thus, detailed studies of the contractile machinery can be made on human skinned muscle fibres with only minimal discomfort to the patient or subject during biopsy, which should be useful in studies of neuromuscular disease, muscle plasticity or in applied physiology.     

Atrial natriuretic peptide and its mRNA in heart and brain of vasopressin-deficient Brattleboro rats

To understand the secretion and synthesis of atrial natriuretic peptide we measured immunoreactive atrial natriuretic peptide from plasma, heart tissues and brain areas, and ANP mRNA was determined from heart auricles and ventricles of vasopressin-deficient Brattleboro rats (DI) and from desmopressin treated Brattleboro rats (DI + DDAVP). Long-Evans rats (LE) served as controls. DI + DDAVP rats were given for 3 days sc. injections of 0.5/g l-desamino-8-D-arginine vasopressin in 1 ml. saline twice a day. The rats were housed in single metabolic cages and urinary output and water intake were measured daily. All the body and organ weight parameters were similar in the three groups when the rats were killed. No change was seen in the plasma ANP level between the groups. The right ventricle of DI + DDAVP rats had significantly (P < 0.05) higher concentration of ANP than LE rats (15.8 + 4.4 vs. 3.4 + 0.6 ng mg“¹ tissue). The left ventricle of DI and DI+DDAVP had significantly (P < 0.05) lower amounts of ANP mRNA than LE rats (0.5 ± 0.2 vs. 1.3 + 0.2 and 0.5 + 0.1 vs. 1.3 + 0.2 arbitrary units). In the hypothalamus, the ANP concentration was significantly (P < 0.05) lower both in DI and in DI + DDAVP rats than in LE rats (9.3 ±1.3 vs. 14.5 ±±1.6 and 6.1+0.6 vs. 14.5 ± 1.6 pg mg^-1 tissue). To conclude, although the water intake and urinary output of DI rats were changed towards normal with desmopressin treatment, the heart ventricular and hypothalamic ANP did not parallel the change. Desmopressin increased the ANP concentration in the right ventricle of DI rats. Thus the correction of the complete vasopressin deficiency-does not appear to associate with synthesis or release of atrial natriuretic peptide in heart or hypothalamus.     

Acute Effects of the Anti-Inflammatory Cyclooxygenase-2 Selective Inhibitor, Flosulide, on Renal Plasma Flow and Glomerular Filtration Rate in Rats

Nephrotoxicity of nonsteroidal anti-inflammatory drugs is associated with other risk factors (volume-depletion) and may be secondary to functional changes mediated by the inhibition of renal cyclooxygenases. Acute anti-inflammatory doses of flosulide and indomethacin were determined on carrageenan paw edema and its effects on renal plasma flow (RPF) and glomerular filtration rate (GFR) were studied in normovolemic and hypovolemic rats. In normovolemic rats, flosulide increased RPF and GFR (25 mg/kg) and indomethacin (5–10 mg/kg) was without effect. Volume-depleted rats were obtained by oral furosemide (32 mg/kg), urinary eicosanoids were determined. After furosemide, plasma volume, RPF and GFR and PGE₂ decreased. Treatment of hypovolemic rats with flosulide (5–25 mg/kg) or indomethacin 10 mg/kg reduced RPF and GFR. Flosulide at 5 mg/kg reduced 6-keto-PGF₁ whereas at 25 mg/kg and after indomethacin at 10 mg/kg a fall in 6-keto-PGF₁ and TXB₂ appeared. Our data suggest that acute COX-2 selective inhibition may alter renal function.     

A Mathematical Model of Renal Blood Distribution Coupling TGF, MR and Tubular System

Objective：To investigate the relationship between renal blood distribution and the physiological activities of the kidney. Methods：A mathematical model is developed based on response （MR） Hagan-Poiseuille law and mass transport, coupling mechanics of myogenic tubuloglomerular feedback （TGF） and the tubular system in the renal medulla. The model parameters, including the permeability coefficients, the vascular lumen radius and the solute concentration at the inlet of the tubes, are derived from the experimental results. Simulations of the blood and water flow in the loop of Henel, the collecting duct and vas rectum, are carried out by the model of the tubular system in the renal medulla, based on conservations of water and solutes for transmural transport. Then the tubular model is coupled with MR and TGF mechanics. Results：The results predict the dynamics of renal autoregulation on its blood pressure and flow, and the distributions are 88.5% in the cortex, 10.3% in the medulla, and 1.2% at papilla,respectively. The fluid flow and solute concentrations along the tubules and vasa recta are obtained. Conclusion ：The present model could assess renal functions qualitatively and quantitatively and provide a methodological approach for clinical research.     

Development of immunoreactive atrial natriuretic peptide in fetal hearts of spontaneously hypertensive and Wistar-Kyoto rats

Summary The development of immunoreactive atrial natriuretic peptide (ANP) was studied in fetal hearts of spontaneously hypertensive (SHR) and compared to normotensive Wistar-Kyoto (WKY) rats. While SHR fetal hearts were noticeably less developed than those of WKY at 10 and 11 days gestation, both strains showed ANP immunoreactive cells in some but not all primitive heart tubes. At 12 days additional ANP immunoreactive cells appeared in formative trabeculae of the ventricle and atrium. ANP cells were also observed in the myogenic layer of the truncus and bulbus arteriosus and their derivatives from 11 through 16 days, but not at 18 days. In both strains, there were more ANP cells in the left ventricle than in right beginning at day 13. There were no obvious strain differences in the developmental pattern and timing of ANP producing cells. However, on the day of birth, staining was reduced in hearts from some WKY newborn pups compared with hearts from SHR newborns and ventricular staining was reduced in both strains when compared to fetal hearts. These observations indicate that ANP is one of the earliest peptide hormones produced and that the predisposition to genetic hypertension does not appear to influence the development of ANP.     

Demonstration of atrial natriuretic peptide/cardiodilatin (ANP/CDD)-immunoreactivity in the salt gland of the pekin duck

Summary A novel peptide hormone, atrial natriuretic factor/cardiodilatin (ANP/CDD), was recently isolated and characterized from mammalian heart. Its presence has been demonstrated in several organs that contribute to water and sodium homeostasis, such as salivary glands. This study demonstrates the presence of ANP/CDD immunoreactivity in the salt gland of Pekin ducks by high performance liquid chromatography, radioimmunoassay and immunocytochemistry, using a specific antibody against atriopeptide I. A small number of distinct, ovoid or cuboid shaped ANP/CDD-immunoreactive cells were localized in the connective tissue surrounding and separating the central secretory tubules, whereas no immunostaining was observed in the peripheral tubules. Salt glands of ducks that were adapted to salt water revealed a significant hypertrophy of their secretory lobules. However, no differences were found between the number or localization of immunoreactive cells in the salt gland of salt water-acclimatized ducks and non-stimulated glands of ducks that were housed with ad libitum access to fresh water. Our results indicate that ANP/CDD may play a role in the regulation of sodium secretion in the salt gland of aquatic birds.Supported by the Walter-Schulz-Stiftung and Deutsche Forschungsgemeinschaft DFG, We 608/8-2Dedicated to Prof. Dr. med. Dr. phil. h.c. D. Starck on the occasion of his 80th birthday     

Isolation and structural analysis of the circulating human cardiodilatin (alpha ANP)

Summary A new method was applied to isolate a polypeptide hormone from human blood. The polypeptides from 1,000 1 of hemofiltrate with a molecular weight lower than 20 kDaltons were adsorbed to 2.5 kg alginic acid, then eluted, precipitated, and desalted on a G-25 Sephadex column, thus obtaining a crude lyophilised plasma polypeptide extract. These polypeptides were further submitted to ion-exchange chromatography. Thereafter, two steps of HPLC were carried out to purify a distinct polypeptide which was the circulating form of cardiodilatin (CDD) in this case. The amino acid analysis, C-terminal enzymatic cleavage by carboxypeptidase A, and sequence analysis showed that the only form of circulating cardiodilatin is the 28 amino acid residue containing molecule, cardiodilatin-99-126 cleaved from the C-terminus of cardiodilatin-126 and identical with alpha-ANP (alpha atrial natriuretic polypeptide). Other bioactive molecular forms of the polypeptide hormones of the cardiodilatin family were not detected in the hemofiltrate. The isolation procedure was followed up by a bioassay using in vitro vascular smooth muscle relaxation.Abkürzungsverzeichnis ANP atrial natriuretic polypeptide - CDD Cardiodilatin - HPLC high performance liquid chromatography - NA noradrenaline - OD optical density - RIA radioimmunoassay - RP reverse phase     

Expression and glucocorticoid regulation of natriuretic peptide clearance receptor (NPR-C) mRNA in rat brain and choroid plexus

The natriuretic peptide clearance receptor (NPR-C) binds atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide with high affinity. This receptor lacks an intracellular guanylate cyclase domain, and is believed to exert biological actions by sequestration of released natriuretic peptides and/or inhibition of adenylate cyclase. The present report summarizes the first detailed mapping of NPR-C mRNA in rat brain. In situ hybridization analysis revealed high levels of NPR-C mRNA expression in frontal and retrosplenial granular cortices, medial preoptic nucleus, ventral cochlear nucleus and choroid plexus. NPR-C mRNA expression was also observed in deep layers of neocortex and limbic cortex, posterior cortical amygdala, ventral subiculum, amygdalohippocampal area, and dentate gyrus. Positive hybridization signal was observed in both anterior and intermediate lobes of the pituitary gland. Regulatory studies indicated that expression of NPR-C mRNA was increased in the medial preoptic nucleus of adrenalectomized rats, suggesting negative glucocorticoid regulation. No changes in NPR-C mRNA expression were observed in frontal cortex or choroid plexus. These results suggest a role for the NPR-C in modulation of natriuretic peptide availability and/or adenylate cyclase activity in a subset of central natriuretic peptide circuits concerned with cortical, olfactory and neuroendocrine functions. Response of the NPR-C gene to changes in circulating hormones suggests the capacity for glucocorticoid modulation of natriuretic peptide action at the receptor level.     

Fluid balance and arterial blood pressure during intracarotid infusions of atrial natriuretic peptide (ANP) in water-deprived goats

The aim of this study was to investigate if atrial natriuretic peptide (ANP) plays a role in the control of water balance in goats and whether ANP affects the increase in mean arterial blood pressure (MAP) which accompanies drinking in water-deprived animals. Bilateral intracarotid infusions were made in female adult goats deprived of water for 48 h. ANP (1.5 micrograms min-1, n = 5, or 4.75 micrograms min-1, n = 5) was infused for 40 min. In control experiments isotonic saline (n = 7) was infused. The goats got access to water 35 min after the start of the infusions. During saline infusions they drank 2.9 +/- 0.4 litres, during the low dose of ANP 1.9 +/- 0.6 litres (n.s. vs saline), and during the high dose of ANP 0.6 +/- 0.2 litres (P less than 0.01 vs saline). Plasma vasopressin concentration did not change during saline infusions until after drinking, when it decreased. The vasopressin concentration increased in one goat after infusion of the low dose of ANP and in two goats after the high dose of ANP. The low dose of ANP caused no change in MAP in four goats, but MAP dropped in the one in which vasopressin concentration increased. MAP fell in all goats infused with the high dose (P less than 0.01), with the largest changes occurring in animals showing increased vasopressin concentration. During the act of drinking a temporary increase of MAP was observed when saline or the low dose of ANP was infused, but this response was attenuated during infusions of the high dose.(ABSTRACT TRUNCATED AT 250 WORDS)