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Biomedical subjects

P Gross

Publications and source records attributed to P Gross.

At least 73 records · Page 4Linked to original sources
PubMed1996

Lithium induced polyuria and renal vasopressin receptor density.

BACKGROUND: Lithium, a drug frequently used for treatment of affective disorders, is known to cause a vasopressin-resistant state, leading to polyuria and polydipsia. It has been suggested that lithium interacts with the renal V2-vasopressin receptor. Detailed studies on the influence of lithium on the AVP receptor, however, have so far been difficult due to the lack of a suitable radioligand with high specific activity and high affinity. METHODS: Using 125I-[8-(p-(OH)-phenylpropionyl)]- LVP, we studied the effects of lithium on V2-vasopressin receptors in male Sprague-Dawley rats and LLC-PK1 cells. Rats, having free access to water, were orally treated with 10 mg lithium/100 mg b.w./day or placebo for 10 days. Scatchard analysis was performed using membranes prepared from homogenized renal papillae. RESULTS: Lithium caused significant polyuria and an impaired renal concentration capacity after water deprivation. Binding studies showed no effect of lithium on binding affinity KD (0.98 +/- 0.21 nmol/l vs. 0.86 +/- 0.15 nmol/l (Li) (n.s.). Receptor density, however, significantly decreased from 130 +/- 12.3 nmol/kg protein in controls (n = 8) to 101.7 +/- 13.4 nmol/kg protein (n = 8), (P < 0.05). Plasma osmotically and AVP were not significantly altered by lithium treatment. Vasopressin receptor density on LLC-PK1-cells, a pig renal cell line, was not changed by preincubation with lithium (312 +/- 22 nmol/kg vs. 329 +/- 25 nmol/kg (Li) (n = 6, n.s.). CONCLUSIONS: The decrease of AVP-receptor density in vivo might be related to vasopressin resistance, either primary, or secondary to other factors, e.g. actual water transport.

Animals↗
PubMed1996

Paracrine renal endothelin system in rats with liver cirrhosis.

1. Liver cirrhosis was induced in rats by CCl4 administration. We analysed the expression of endothelin receptor subtypes in the renal cortex and medulla using Scatchard analysis and receptor autoradiography, and measured plasma as well as renal-tissue endothelin-1 concentrations using a specific radioimmunoassay. Furthermore, we analysed the effects of the non-selective (A/B) endothelin receptor antagonist, bosentan (6 and 100 mg kg-1 day-1) on mean arterial blood pressure, water and sodium excretion and glomerular filtration rate. 2. Our study revealed an overexpression of the endothelin B receptor (ETB) in the renal medulla of rats with liver cirrhosis (Cir: 2775 +/- 299 fmol mg-1; Con: 1695 +/- 255 fmol mg-1; n = 8; means +/- s.d., P < 0.01), whereas the density of ETB in the cortex and the endothelin A receptor (ETA) in the cortex and medulla were similar in both cirrhotic and control rats. Receptor autoradiography showed that the upregulation of medullary ETB in cirrhotic rats was due to an upregulation of ETB in the inner medullary collecting duct cells. 3. The tissue endothelin-1 concentrations were increased in the renal medulla of cirrhotic rats (Cir: 271 +/- 68 pg g-1wet wt.; Con: 153 +/- 36 pg g-1 wet wt., n = 8; means +/- s.d., P < 0.01). 4. The glomerular filtration rate was slightly decreased in cirrhotic rats but not altered after bosentan treatment in either cirrhotic or control rats. Bosentan decreased sodium excretion to a similar extent in both cirrhotic and control rats, whereas water excretion was significantly reduced by both dosages of bosentan in cirrhotic rats only (Cir + vehicle: 12.5 +/- 0.62 m day-1, Cir + 6 mg kg-1 day-1 bosentan: 8.6 +/- 1.0 ml day-1; Cir + 100 mg kg-1 day-1 bosentan: 7.4 +/- 0.6 ml day-1; n = 10; means +/- s.e.mean). 5. We therefore suggest that the upregulation of the medullary ETB in cirrhotic rats is involved in the regulation of water excretion in rats with CCl4-induced liver cirrhosis.

Animals↗
PubMed1996

Natural killer cell cytotoxicity in elderly humans after influenza immunization.

Previous studies have reported that human natural killer (NK) cytotoxicity can be augmented by either in vitro stimulation with influenza virus antigens or in vivo administration of killed influenza vaccine. The study demonstrating the latter conclusion reported an increase in NK cytotoxicity lasting for 4 weeks postvaccination in young subjects. We initiated our study to determine if a similar increase in NK activity was observed in an elderly population after immunization with the 1992-1993 influenza vaccine. NK activity of 34 elderly (mean age, 77.3 years) was determined at 3 time points: prevaccination, 4 to 6 weeks postvaccination, and 5 to 6 months after vaccination. In contrast to the results of the previous study, the NK cytotoxicity of our elderly subjects was not augmented by the influenza vaccine at any time tested. We also determined the number of CD56+ cells in whole-blood samples at each of the time points and found that there is no change in NK cell number after influenza vaccination.

Aged↗
PubMed1996

Hyponatremia: pathophysiology, differential diagnosis and new aspects of treatment.

Hyponatremia is the most frequent electrolyte disorder in clinical medicine. It is usually attributable to primary vasopressin excess, causing the syndrome of inappropriate antidiuresis (SIAD), or to secondary vasopressin stimulation, involving a baroreceptor mechanism. The latter is regularly found in the hyponatremia of liver cirrhosis, cardiac failure and volume contraction. In the first kind of setting the concentrations of creatinine, urea and urate in plasma will be low because of the associated volume expanded state. In the second type of setting they will be elevated because of the circulatory compromise of these patients. The hyponatremia of SIAD may be treated by water restriction, furosemide and substitution of the inadvertent sodium losses by giving 3% NaCl. Baroreceptor hyponatremia is best treated by fluid restriction together with judiciously administered saline. In correcting severe chronic hyponatremia, the rate of correction should not exceed 1 mM/l/h and the corrected serum sodium concentration should not be higher than 130 mM/l. In the foreseeable future oral non-peptide oral vasopressin antagonists will become available. They are expected to become new tools for the treatment of hyponatremia.

Humans↗
PubMed1995

Isolation and characterization of the EF-1 alpha gene of the filamentous fungus Puccinia graminis f. sp. tritici.

A gene of Puccinia graminis f. sp. tritici, coding for the translation elongation factor 1 alpha (EF-1 alpha), was isolated from a P. graminis genomic library using the EF-1 alpha gene sequence of Absidia glauca. The coding region of 1389 nucleotides encodes a polypeptide of 463 amino acids and is interrupted by eight introns. An additional intron is located in the 5' untranslated region. A single transcription start point (tsp) was mapped by primer extension. A cDNA fragment corresponding to P. graminis EF-1 alpha mRNA hybridized with a 1.9-kb-long poly(A+)RNA, sufficient to encode the EF-1 alpha protein. Southern hybridization of digested genomic DNA revealed that two copies of the EF-1 alpha gene exist in the genome of P. graminis.

Amino Acid Sequence↗
PubMed1995

Plasma endothelin-1 in patients with left-to-right shunt.

Endothelin-1 (ET-1) has been implicated in the pathogenesis of pulmonary vascular disease in patients with congenital heart disease. We studied the effect of pulmonary blood flow on plasma ET-1 concentrations. Systemic venous, pulmonary arterial, and pulmonary venous blood samples were obtained from 40 patients with atrial septal defect II (n = 21), ventricular septal defect (n = 10), persistent ductus arteriosus (n = 6), and complete (n = 2) and partial (n = 1) atrioventricular canal at cardiac catheterization and analyzed by radioimmunoassay. Median age (range) was 5.2 years (8 months to 66 years), and the resistance ratio (Rp/Rs) was 0.08 (0.03 to 0.67). Pulmonary vein to pulmonary artery ET-1 ratio in patients with "high flow" (n = 26, Qp/Qs > or = 1.5; ET-1 ratio = 0.8) did not differ from those with "low flow" (n = 14, Qp/Qs < 1.5; ET-1 ratio = 1.0). We conclude that an increase in pulmonary blood flow alone does not result in an increase in plasma ET-1.

Adolescent↗
PubMed1995

Water retention after oral chlorpropamide is associated with an increase in renal papillary arginine vasopressin receptors.

Chlorpropamide (CP), a sulfonylurea used for treatment of non-insulin dependent diabetes mellitus, is known to potentiate the antidiuretic action of arginine vasopressin (AVP), predisposing to hyponatremia. It has been suggested that CP acts directly on the antidiuretic vasopressin receptor. Detailed studies on the influence of CP on the AVP receptor, however, have been hampered by lack of a suitable radioligand. Using a newly developed radioiodinated derivative of AVP with high specific activity and high affinity for the AVP V2-receptor (125I-[8-(p-(OH)-phenylpropionyl)]-LVP), we studied the role of AVP V2-receptors in CP-induced water retention. Male-Sprague-Dawley rats were treated orally with 40 mg CP/day or placebo for 7 days, after which Scatchard analysis was performed using membranes prepared from homogenized renal papilla. After oral water load, CP-treated rats but not control rats showed a significant decrease in plasma osmolality (289 +/- 2.2 to 284 +/- 0.8 mosmol/kg, p < 0.05). The Kd was 0.69 +/- 0.16 nmol/l in controls and 0.70 +/- 0.12 nmol/l after CP treatment (NS); Bmax was 129 +/- 5.3 nmol/kg protein in controls (N = 8). Chlorpropamide significantly increased receptor density (Bmax) to 167 +/- 8.4 nmol/kg protein (N = 8) (p < 0.05). Plasma AVP did not change significantly during CP treatment. These data show for the first time that CP in vivo increases the density of AVP V2 receptors without altering plasma AVP. This is associated with an impairment in water excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Disseminated histoplasmosis in a patient with acquired immunodeficiency syndrome.

No matter how typical a cutaneous eruption may be in a patient with the acquired immunodeficiency syndrome, early histologic evaluation is necessary if a delay in diagnosis and treatment is to be avoided. We report the case of a 33-year-old man with acquired immunodeficiency syndrome who was clinically misdiagnosed as having a drug-induced eruption. Three weeks later he died with disseminated histoplasmosis.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Failure of arginine-vasopressin and other pressor hormones to increase in severe recurrent dialysis hypotension.

BACKGROUND: Recurrent dialysis hypotension is common in long-term dialysis patients. Arginine-vasopressin (AVP) is a potent vasoconstrictor hormone, release of which is stimulated in hypotension. STUDY DESIGN: We measured AVP as well as adrenaline and noradrenaline in 23 patients with recurrent dialysis hypotension during severe symptomatic episodes of dialysis hypotension (BP syst. < 70 mmHg). We also tested autonomic function (amyl nitrate inhalation, cold pressor test) during the interdialytic interval. RESULTS: We observed that systolic blood pressure decreased from 127 +/- 8 (at the end of the first hour of dialysis; taken as control state) to 64 +/- 1 mmHg (symptomatic hypotension) in 23 patients. In six of the 23 patients hypotension was accompanied by nausea, which is a known direct stimulus of AVP. In these six patients, plasma AVP showed a large increase: control state, 6.2 +/- 0.9; hypotension, 130.4 +/- 51.1 pg/ml; P < 0.5). Of the remaining 17 patients without nausea, AVP fell moderately in nine and increased in eight. Taken together, this group of 17 hypotensive patients failed to show significant AVP stimulation: control state, 9.0 +/- 1.4; hypotension, 13.8 +/- 3.8 pg/ml, NS). Adrenaline and noradrenaline did not change during hypotension. During autonomic testing the patients with recurrent dialysis hypotension (compared to healthy controls) showed blunted baroreflex response (assessed by amyl nitrate inhalation) but intact sympathetic outflow (assessed by cold pressor test). CONCLUSION: The observations of AVP are taken as further evidence of defects in the afferent rather than the efferent limb of autonomic reflexes in dialysis patients with recurrent dialysis hypotension.

Acute Disease↗
PubMed1995

Chronic hypokalaemia of adults: Gitelman's syndrome is frequent but classical Bartter's syndrome is rare.

We evaluated 27 adult patients with chronic hypokalaemia (K+ = 2.9 +/- 0.2 mmol/l), documented over at least 5 years, in whom the cause of the hypokalaemia had not been clarified in spite of previous testing. In 15 patients it was possible to establish a diagnosis by a thorough outpatient workup (diuretic abuse (n = 5), surreptitious vomiting (n = 8), laxative abuse (n = 1), renal tubular acidosis (n = 1)). Commonly utilized tests such as measurements of plasma renin activity, plasma aldosterone, and urinary potassium concentration proved not to be useful in the differential diagnosis of these patients. In contrast the following were diagnostically important: in surreptitious vomiting the hypochloraemia, the mild renal insufficiency, and the extremely low urinary chloride concentration; in diuretic abuse the high urinary concentration of chloride together with repeatedly positive toxicology screens for diuretics; in laxative abuse the high stool weight and extremely low urinary sodium concentration. In the remaining 12 patients none of these diagnoses applied and further tests for suspected Bartter's syndrome were done in the hospital.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Renal endothelin system in rats with liver cirrhosis.

Rats with experimental liver cirrhosis have increased endothelin-1 (ET-1) plasma concentrations and show a tendency toward sodium and water retention. We therefore analyzed the renal ET system in cirrhotic rats and control rats, as the renal ET system is involved in the regulation of water and sodium excretion. Cirrhosis was induced by carbon tetrachloride (CCl4) administration. We analyzed the expression of ET receptor subtypes in the renal cortex and medulla using Scatchard analysis and receptor autoradiography, and measured plasma and renal tissue ET-1 concentrations using a specific radioimmunoassay. Furthermore, we analyzed the effects of the nonselective (A/B) ET receptor antagonist bosentan on water and sodium excretion and glomerular filtration rate. Our study revealed an overexpression of the ETB receptor in the renal medulla of rats with liver cirrhosis, whereas the density of ETB receptor in the cortex and the ETA receptor in the cortex and medulla were similar in both cirrhotic and control rats. Receptor autoradiography showed that the upregulation of medullary ETB in cirrhotic rats was due to an upregulation of ETB in the inner medullary collecting duct cells. The highest ET-1 concentrations were observed in the renal medulla of cirrhotic rats. Glomerular filtration rate decreased in cirrhotic rats but was not altered after bosentan treatment in cirrhotic and control rats. Bosentan decreased sodium excretion in both cirrhotic and control rats to a similar extent, whereas water excretion was reduced by bosentan only in cirrhotic rats. We therefore suggest that the upregulation of medullary ETB in cirrhotic rats is involved int he regulation of water excretion in rats with CCl4-induced cirrhosis.

Animals↗