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K Poulsen

Publications and source records attributed to K Poulsen.

At least 91 records · Page 5Linked to original sources
PubMed1991

Adrenalectomy causes a delayed increase of inactive plasma renin in rats.

Using a new assay for inactive renin in rat plasma, inactive renin was unchanged 24 h after bilateral adrenalectomy but increased about threefold, from 0.43 Goldblatt units (GU)/l (range 0.27-0.62 GU/l; n = 14) to 1.24 GU/l (0.74-1.94 GU/l; n = 14) after 48 h. The increase was abolished by substitution with the mineralocorticoid deoxycorticosterone acetate. The results are in accordance with the high plasma concentration of inactive renin, previously reported in humans with adrenal insufficiency, and do not support activation of inactive renin in the circulation.

Adrenalectomy↗
PubMed1991

Effect of gonadotropins and pregnancy on prorenin and renin in the rat.

1. Stimulation of adult female rats with pregnant mare serum gonadotropin (PMSG) and human chorion gonadotropin (hCG) increased active plasma renin about two-fold, but caused only a slight increase of plasma prorenin. The concentrations of active renin and prorenin in the ovaries, and active renin in the uterus all increased about two-fold 2 days after stimulation with PMSG. The prorenin in the uterus was below detection in unstimulated rats and did not change consistently after PMSG. 2. Active renin and prorenin in plasma were unchanged in relation to pregnancy, except for a slight decrease of prorenin in the third trimester. In the first and third trimester the concentration in the ovaries of active renin and prorenin was decreased to about one-third of that in normal female rats. In contrast active renin in the uterus was increased about two-fold in the first trimester, whereas prorenin did not change consistently. 3. Our results confirm that gonadotropins and pregnancy affect the renin-angiotensin system in rats. However, the changes in the plasma seem to be much smaller than those previously reported in humans. Accordingly, our results do not support a systemic role of prorenin for reproduction in the rat.

Amniotic Fluid↗
PubMed1991

Measurement of inactive renin in normal, nephrectomized, and adrenalectomized rats.

In a new method for measurement of inactive rat plasma renin, the trypsin generated angiotensin I immunoreactive material, which was HPLC characterized as similar to tetradecapeptide renin substrate, is removed by a cation exchange resin before the renin incubation step. The method also corrects for trypsin destruction of endogenous angiotensinogen by the addition of exogenous angiotensinogen. When measured with this method inactive renin in rat plasma decreased after nephrectomy and increased after adrenalectomy. This is in accordance with findings in humans. A sexual dimorphism of prorenin (inactive renin) in rat plasma, similar to that reported in humans and mice, was demonstrated. Thus, inactive renin in the rat is no exception among species, and the rat might be a suitable animal model for further studies dealing with the physiology of prorenin in plasma and tissues.

Adrenal Glands↗
PubMed1990

Retropseudogenes constitute the major part of the human elongation factor 1 alpha gene family.

The elongation factor 1 alpha (EF-1 alpha) is a protein which promotes the GTP-dependent binding of aminoacyl-tRNA to ribosomes in the protein synthesis process. A human gene coding for EF-1 alpha has previously been cloned and sequenced along with a pseudo-gene. Here, we have further analyzed the family of human EF-1 alpha genes. Using an EF-1 alpha cDNA as probe twelve genomic EF-1 alpha-like clones were isolated and analyzed. Four of these were sequenced and found to contain EF-1 alpha retropseudogenes. A Southern blot analysis indicated that the remaining eight clones also contained retropseudogenes. Genomic Southern blot analysis revealed at least twenty loci in the human genome with sequence homology to the EF-1 alpha cDNA. Besides the already described active gene only one potentially active locus was found. The others appeared to be retropseudogenes. EF-1 alpha retropseudogenes were also found to be abundant in the mammalian species mouse and pig, while the chicken contained only one presumably active EF-1 alpha gene.

Blotting, Southern↗
PubMed1990

Morphological and immunohistochemical characteristics of dimethylnitrosamine-induced malignant mesenchymal renal tumor in F-344 rats.

Mesenchymal renal tumors in F-344 newborn rats were induced by a single dose of dimethylnitrosamine. The induced tumors were successfully transplanted into adult rats under the renal capsule. Neither the primary nor the transplanted neoplasms from various generations of grafts changed their morphological features during the tumor passage, having the same cellularity with high mitotic activity and the tendency to invade the host kidney rapidly. On the basis of lectin histochemistry and immunohistology, the tumor proved to be a mesenchymal neoplasm without any obvious capacity of the proliferating cells to differentiate into any well-known organoid element normally found in mature renal parenchyma. However, the proliferating neoplastic cells were found to have a strong vimentin positivity with desmin expression. Ultrastructurally, myofilaments with attachment bodies characteristic of smooth muscle cells were generally present in various amounts in many tumor cells. In addition, on the basis of the physiological data and on kidney/tumor renin activity obtained, it is interesting to note that the tumor-graft-invaded kidneys retained their enzyme activity, despite the obvious loss of renal tissue including glomeruli. However, the immunohistochemical findings with anti-renin antibody have clearly shown that this is not due to a renin-producing tumor but rather to the surviving (probably) non-neoplastic arterioles retaining the capacity to produce renin. Although these arterioles have mostly been found next to necrotic areas, commonly occurring in dimethylnitrosamine-induced transplantable renal tumors, the question of a possible physiological role of renin in tumor necrosis or in angiogenesis has remained open.

Animals↗
PubMed1990

Measurement of inactive renin in rat plasma: effect of nephrectomy and sialoadenectomy on the plasma concentration.

In this paper we describe a routine method of measuring inactive renin in rat plasma. The activation was performed by trypsin, at optimal concentration and incubation conditions. The trypsin treatment formed an interfering and high-performance liquid chromatography-verified tetradecapeptide-like material, which was removed before the assay by a simple batchwise use of a cation-exchange resin. The concentration of activated inactive renin was measured by an antibody-trapping method after the addition of exogenous angiotensinogen. Angiotensinogen was added in order to compensate for the trypsin destruction of angiotensinogen and in order to measure the parameter of renin concentration. The inactive renin concentration in plasma of conscious male rats was 0.48 +/- 0.13 Goldblatt units (GU) per litre (n = 38). This corresponds to 66% (range 42-92%) of the total renin concentration. Physiological experiments in conscious rats were initiated, demonstrating that nephrectomy decreased the inactive renin concentration from 0.45 +/- 0.14 to 0.27 +/- 0.05 GU/l after 24 h (n = 21; P less than 0.01). Submandibular sialoadenectomy decreased the plasma inactive renin concentration from 0.45 +/- 0.11 to 0.34 +/- 0.06 GU/l (n = 12; P less than 0.05) after 7 days. Combined sialoadenectomy and nephrectomy decreased the plasma inactive renin concentration from 0.45 +/- 0.11 to 0.24 +/- 0.06 (n = 12; P less than 0.01).

Angiotensinogen↗
PubMed1990

In vivo generation and elimination of angiotensin in the rat.

1. Combined high performance liquid chromatography (HPLC) and radio-immunoassays were used to study the in vivo kinetics of the renin-angiotensin system in the rat. The HPLC-verified plasma concentrations of angiotensin I (AI) were 1.0 nmol/L (0.52-1.6) in anaesthetized normal and 4.2 nmol/L (2.5-7.0) in salt-depleted rats. The plasma concentrations of angiotensin II (AII) were 0.07 nmol/L (0.04-0.13) in anaesthetized normal and 1.0 (0.60-1.6) nmol/L in salt-depleted rats. 2. The fate of injected AI and AII passing through the vascular bed of the lungs was determined. Two-thirds of the injected AI was converted to AII and one-third was unchanged after a single passage through the lungs. Only trace amounts of angiotensin III (AIII), the only other metabolite, were demonstrated. 3. This verifies that the majority of AI is metabolized through AII. Injected AII disappeared from the circulation with formation of only trace amounts of AIII, the half-life being about 10 s. This corresponds to a calculated in vivo generation rate of AII of about 12 nmol/L per h in normal rats. It is in agreement with the AI generation rate (plasma renin activity) measured as 9.5 nmol/L per h in vitro.

Angiotensin I↗
PubMed1990

Exocrine and endocrine release of kallikrein after reflex-induced salivary secretion.

Exocrine and endocrine release of rat submandibular gland kallikrein has been shown to be low after parasympathetic and beta-adrenergic stimulation but greatly increased after alpha-adrenergic stimulation. In the present study, release of glandular kallikrein was investigated under conditions known to give a reflex-induced salivary gland response. Heat stress induced a rich flow of saliva originating in the submandibular glands. Salivary kallikrein secretory rate was higher than after parasympathetic stimulation but lower than after sympathetic stimulation (P less than 0.005). Only heat stress increased circulating glandular kallikrein (12.7 +/- 0.8 ng ml-1 before heat exposure and 53.3 +/- 14.1 ng ml-1 40 min afterwards, P less than 0.005). There were no indications that the endocrine release of kallikrein was due to non-specific leakage. Atropine abolished heat-induced salivation and endocrine kallikrein secretion, possibly through interference with central pathways (P less than 0.05). However, phentolamine did not, which may indicate as an yet unidentified mediator of endogenous kallikrein release. The salivary gland response to acid and ether was comparable to that observed after parasympathetic nerve stimulation and was abolished by atropine (P less than 0.005). Stimuli known to influence other salivary gland ductal cells, such as aggression and starvation followed by drinking, also did not increase the plasma concentration of glandular kallikrein. The fact that various conditions which induce salivation did not increase circulating glandular kallikrein, coupled with the fact that kallikrein concentration was the highest in animals that died from heat stress, may suggest that the increase in circulating glandular kallikrein seen after heat stress may be pathological and could contribute to the development of heat shock.

Animals↗
PubMed1990

Sexual dimorphism of inactive renin in rat plasma.

The plasma concentration of inactive renin was higher (p less than 0.002) in male (0.48 Goldblatt units (GU)/l, range 0.28-0.67 GU/l; n = 20) than in female rats (0.19 GU/l, range 0.09-0.30 GU/l; n = 20). This new finding indicates a sexual dimorphism of inactive plasma renin similar to that recently reported in mice and humans. Castration of male rats (n = 10) decreased (p less than 0.01) inactive plasma renin from 0.45 GU/l (range 0.22-0.65 GU/l) to 0.26 GU/l (range 0.15-0.37 GU/l) over a period of seven weeks. Similarly, inactive renin decreased (p less than 0.01) from 0.50 GU/l (range 0.28-0.67 GU/l) to 0.30 GU/l (range 0.19-0.47 GU/l) during treatment with the anti-androgen flutamide (n = 10). In castrated male rats (n = 10), inactive plasma renin was unaffected of substitution with testosterone. In intact female rats (n = 10), inactive renin increased (p less than 0.05) from 0.18 GU/l (range 0.12-0.30 GU/l) to 0.27 GU/l (range 0.15-0.40 GU/L) during testosterone treatment. Our findings indicate that androgens may be involved in the regulation of the plasma concentration of inactive renin in rats, but also suggest that other factors may be of importance.

Androgens↗
PubMed1990

The effect of a soluble dietary fibre supplement on 24-hour energy expenditure during a standardized physical activity programme.

Twenty-four hour energy expenditure during a standard physical activity programme was investigated in 19 healthy volunteers in a randomized, double-blind, cross-over design, after supplementation with a soluble dietary fibre amounting 7 g/day for 2 weeks. Energy intake and food fibre intake were kept constant during the treatment period. Twenty-four hour energy expenditure decreased insignificantly during fibre treatment (1.3 +/- 1.7 per cent). The dietary fibre supplement also had no significant effect on body weight, faecal energy loss or heart rate. Systolic blood pressure was insignificantly reduced during both placebo and fibre treatment (P = 0.09). There was, however, no difference between the groups after treatment.

Adolescent↗
PubMed1989

Inactive plasma renin exhibits sex difference in mice.

1. The plasma concentration of inactive renin was two- to three-fold higher in male than in female mice independently of whether mice of strains with low (BALB/c) or high (Theiller) content of active renin in the submandibular salivary glands were studied. 2. Removal of the submandibular glands did not affect the high plasma concentration of inactive renin in male mice. 3. Inactive plasma renin decreased over several days after castration of normal and sialoadenectomized male mice to the same levels as those found in normal female mice. 4. Treatment of these castrated male mice with testosterone increased and normalized inactive plasma renin independently of whether the submandibular glands had been previously removed or not. 5. Testosterone treatment of sialoadenectomized female mice increased inactive renin to the same levels as those found in normal male mice. 6. Our findings suggest that the sex difference in inactive plasma renin in mice may be explained by an increased secretion of inactive renin in male mice stimulated by androgens. 7. Since we have recently found that inactive plasma renin in male mice is mainly of renal origin, this increased secretion is most likely located to the kidneys.

Androgen Antagonists↗
PubMed1989

Solution of methodological problems in measurement of inactive renin in rat plasma using trypsin activation, and the effect of nephrectomy and sialo-adenectomy on inactive plasma renin.

Trypsin activation of rat plasma destroys angiotensinogen and generates a tetradecapeptide-like material, verified by high performance liquid chromatography, which interferes with the measurement of inactive renin. Using an assay based on removal of the material by a cation-exchange resin and the addition of exogenous angiotensinogen, the plasma concentration of inactive renin in intact conscious male rat was 0.48 GU/l (range 0.28-0.67 GU/l, n = 20). Inactive renin comprised about 70% of the total plasma renin. The level of inactive renin was unchanged 24 h after bilateral nephrectomy and 7 days after submandibular sialo-adenectomy. Bilateral nephrectomy of previously sialo-adenectomized rats decreased the level of inactive renin significantly. Our findings are in contrast to the marked increase, reported by several other investigators, in inactive plasma renin in rats following bilateral nephrectomy, and do not support the previously suggested, mainly extrarenal, origin of inactive plasma renin.

Animals↗
PubMed1989

Evidence for the presence of angiotensins in normal, unstimulated alveolar macrophages and monocytes.

The presence of angiotensins was demonstrated in normal unstimulated alveolar macrophages and monocytes from both mice and rats. These peptides were partially purified from cell homogenates by ion exchange chromatography and identified as being [Ile5] angiotensin I (Ang I), [Ile5] angiotensin II (Ang II) and to a lesser extent [Ile4] angiotensin III (Ang III) using high performance liquid chromatography (HPLC). Based on the present data both alveolar macrophages and monocytes expressed Ang I as quantified by a specific and sensitive radio-immunoassay (RIA) from the HPLC eluates. In contrast to this, alveolar macrophages from both mice and rats exhibited a fairly low, if detectable Ang II content. It seems reasonable to suggest that, in contrast to monocytes, macrophages do not generate and/or incorporate Ang II appreciably, at least in their resting stage. Although it is still not obvious whether these mononuclear phagocytes generate or simply capture angiotensin(s) from the blood pool or from the tissues; they must serve as in vivo target cells for the angiotensin system, at least for the plasma or tissue clearance of these molecules.

Angiotensins↗
PubMed1989

On the measurement of inactive renin in rat plasma: activation by trypsin generates interfering tetradecapeptide-like material and destroys angiotensinogen.

Trypsin cleaved plasma angiotensinogen with apparent first-order kinetics and generated an angiotensin I (Ang I) immunoreactive material. Size exclusion high-performance liquid chromatography (HPLC) of rat plasma proteins demonstrated that the Ang I immunoreactive material was formed in those fractions which contained angiotensinogen. The Ang I immunoreactive material was higher in nephrectomized rat plasma than normal plasma, in accordance with the higher angiotensinogen concentration. These findings indicated that angiotensinogen could be the source of the Ang I immunoreactive material. Purification of the Ang I immunoreactive material by cation-exchange chromatography followed by reverse-phase HPLC demonstrated an elution pattern close to that of human tetradecapeptide. The purified Ang I immunoreactive material was cleaved by pure mouse submandibular renin to Ang I, exclusively. Incubation at 37 degrees C of the Ang I immunoreactive material with plasma partially destroyed the angiotensin immunoreactive material. These findings demonstrated that the angiotensin immunoreactive material was an Ang I containing tetradecapeptide (TDP)-like peptide, unstable during a renin incubation step, leading to erroneous values for plasma inactive renin if not removed. The Ang I immunoreactive material was removed by cation-exchange chromatography of trypsin-activated plasma allowing for a determination of inactive renin. The presence of inactive renin in plasma from normal and nephrectomized rats was confirmed, and identified by neutralization and immunoprecipitation with antirenins. These findings should enable us to develop a routine assay for plasma inactive renin in rat plasma.

Angiotensin I↗
PubMed1989

Cloning and sequencing of the immunoglobulin A1 protease gene (iga) of Haemophilus influenzae serotype b.

Secretion of immunoglobulin A1 (IgA1) proteases is a characteristic of Haemophilus influenzae and several other bacterial pathogens causing infectious diseases, including meningitis. Indirect evidence suggests that the proteases are important virulence factors. In this study, we cloned the iga gene encoding immunoglobulin A1 (IgA1) protease from H. influenzae serotype b into Escherichia coli, in which the recombinant H. influenzae iga gene was expressed and the resulting protease was secreted. Sequencing a part of a 7.5-kilobase DNA fragment containing the iga gene revealed a large open reading frame with a strongly biased codon usage and having the potential of encoding a protein of 1,541 amino acids and a molecular mass of 169 kilodaltons. Putative promoter and terminator elements flanking the open reading frame were identified. Comparison of the deduced amino acid sequence of this H. influenzae IgA1 protease with that of a similar protease from Neisseria gonorrhoeae revealed several domains with a high degree of homology. Analogous to mechanisms known from the N. gonorrhoeae IgA protease secretion, we propose a scheme of posttranslational modifications of the H. influenzae IgA1 protease precursor, leading to a secreted protease with a molecular mass of 108 kilodaltons, which is close to the 100 kilodaltons reported for the mature IgA1 protease.

Amino Acid Sequence↗
PubMed1989

Urinary excretion of inactive renin during blockade of the renal tubular protein reabsorption with lysine.

The purpose was to study whether the kidneys eliminate inactive renin from the circulation of mice. The urinary concentration, excretion rate and clearance of inactive renin were very low during basal conditions. After blockade of the reabsorption of proteins in the renal tubules with the basic amino acid lysine, the urinary concentration, excretion rate and clearance of inactive renin increased very markedly. This finding indicates that inactive plasma renin is subjected to glomerular ultrafiltration followed by reabsorption in the renal tubules by mechanisms which are most likely the same as for active renin and other filtered proteins. The urinary clearance of inactive renin after blockade of the renal tubular protein reabsorption was 13% of that of active renin. Our findings demonstrate that glomerular ultrafiltration is a route of elimination from the circulation for inactive renin.

Animals↗
PubMed1988

Ultrafiltration of renin in the mouse kidney studied by inhibition of tubular protein reabsorption with lysine.

1. In order to study the role of the kidney in the elimination of endogenous plasma renin, renin was measured in the plasma and urine of female mice. 2. The renin concentration was two orders of magnitude lower in urine than in plasma, but it increased after intraperitoneal injection of submandibular mouse renin. No correlation between the plasma renin concentration and the urinary renin concentration and renin excretion rate could be demonstrated. 3. Blockade of the tubular reabsorption of proteins by intraperitoneal injection of the basic amino acid lysine increased the urinary renin concentration, renin excretion rate and renin clearance two to three orders of magnitude, without affecting the plasma renin concentration. 4. This finding demonstrates that ultrafiltered renin is reabsorbed almost completely in the renal tubules and that the mechanism most likely is the same as for other filtered proteins. 5. The large renal renin clearance obtained after intraperitoneal lysine is in accordance with a major role of the kidneys in the elimination of renin from the circulation, by a glomerular ultrafiltration and tubular reabsorption and metabolization of renin.

Absorption↗