Search PubMed⌕ Search

Biomedical subjects

P Hansell

Publications and source records attributed to P Hansell.

At least 73 records · Page 4Linked to original sources
PubMed1988

Renal effects of atriopeptin II and dopamine receptor blockade in acutely volume-expanded rats.

Studies were made of the effects of continuous intravenous infusion of a synthetic atrial natriuretic factor (ANF) or, pre-treatment with the dopamine receptor antagonist haloperidol, on the renal response in anaesthetized rats subjected to volume expansion with an isotonic solution at 2% kg-1 body weight (wt) h-1. A time-control group receiving vehicle alone was studied in parallel. Measurements were compared 75 and 145 min after initiation of the volume expansion. Seventy minutes of Atriopeptin II infusion at 10 micrograms h-1 kg-1 body wt did not significantly alter the glomerular filtration rate [control value 1.29 +/- 0.10 ml min-1 g-1 kidney wt (n = 7, mean +/- 1 SEM), experimental value 1.20 +/- 0.12], but increased sodium excretion by 49% (from 2.87 +/- 0.56 to 4.27 +/- 0.45 mumol min-1). The arterial blood pressure was reduced by 9%. In previous investigations we found that in the same dosage Atriopeptin II increased sodium excretion 10-fold in euvolaemic animals. In the time-control group (n = 7) the response was similar to that in the atrial natriuretic factor-treated animals with the exception that the blood pressure was unaltered. Thus, glomerular filtration rate showed no statistically significant change (1.28 +/- 0.06 vs. 1.27 +/- 0.09 ml min-1 g-1 kidney wt) while the sodium excretion increased by 96% (from 2.29 +/- 0.22 to 4.50 +/- 0.49 mumol min-1). In animals pretreated with haloperidol (n = 5), the natriuretic response to the volume expansion was attenuated and was about ten times below that in the time-control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

CNS-induced natriuresis during dopamine receptor blockade. Further support for the existence of, at least, two separate natriuretic hormonal systems.

Intracerebroventricular (ICV) stimulation with hypertonic sodium chloride solutions has previously shown indications to stimulate the release of a blood-borne natriuretic factor. Sodium excretion in this situation increases in the order of 10-20 times. Acute isotonic volume expansion has shown to be a potent stimulus for endogenous release of the atrial natriuretic factor (ANF). It has also been demonstrated that the natriuretic response to both volume expansion and exogenously applied ANF can be attenuated by the dopamine receptor blocker haloperidol. The present study was performed to investigate if the natriuretic response to ICV stimulation also could be attenuated with haloperidol, thus indicating similar effector mechanisms as for ANF. A first group of anaesthetized animals was, therefore, pre-treated with haloperidol (H) and then ICV stimulated (H-ICV). A second group of animals was subjected to acute isotonic volume expansion (VE, 2% b.w.h.-1) to evoke the documented ANF release. In a third group of animals pre-treatment with haloperidol was followed by volume expansion (H-VE). In the H-ICV group there was a more than 30-fold increase in sodium excretion, due to an increase both in urine flow rate (more than sixfold) and in the urinary concentration of sodium (more than fourfold). Potassium excretion increased more than eightfold, urine osmolality was unchanged, and blood pressure increased by 7%. In the VE group sodium excretion increased more than 18-fold, consequent to large increases in urine flow rate (more than 23-fold), while the urinary concentration of sodium tended to decrease. Potassium excretion increased more than threefold, urine osmolality decreased by 88%, and blood pressure was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The calcium entry blocker verapamil increases red cell flux in the vasa recta of the exposed renal papilla.

To investigate the vasoreactivity of the vessels of the juxtamedullary vasculature, measurements were made of the red blood cell flux (Qrbc) in the vasa recta of the exposed renal papilla of anaesthetized rats by means of fluorescently labelled erythrocytes. The flux was measured before and after intravenous administration of the calcium entry blocker verapamil, which was infused in two different doses. A control group receiving vehicle was studied in parallel. The lower dose of verapamil (0.6 mg h-1 kg-1 body wt) increased Qrbc by 30 +/- 6% (n = 9, P less than 0.05, mean +/- 1 SEM) and reduced the systemic blood pressure by 6% (P less than 0.05). The osmolality of urine samples from the papillary tip remained statistically unchanged (1199 +/- 60 vs. 1186 +/- 102 mosM kg-1 H2O). In the animals receiving the higher dose of verapamil (2.4 mg h-1 kg-1 body wt), Qrbc increased by 39 +/- 7% (n = 10, P less than 0.05) and the blood pressure was reduced by 9% (P less than 0.05), while urine osmolality was unchanged (1104 +/- 110 vs. 1264 +/- 123 mosM kg-1 H2O). In the time control group there was no statistically significant change in Qrbc (+6 +/- 8%, n = 10), blood pressure or urine osmolality (1006 +/- 61 vs. 1091 +/- 70 mosM kg-1 H2O). The verapamil-induced increase in Qrbc is probably mainly mediated by a relaxation of the afferent arteriole of the juxtamedullary nephrons. The results confirm our previous indication of a high vasoreactivity in the vessels of the juxtamedullary vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Atrial natriuretic factor, urinary catechol compounds and electrolyte excretion in rats during normal hydration and isotonic volume expansion. Influence of dopamine receptor blockade.

To investigate the influence of acute isotonic volume expansion (VE) on the plasma concentration of atrial natriuretic factor (ANF), the excretion of catechol compounds and electrolytes and the whole kidney glomerular filtration rate (GFR), these variables were measured before and during 60 min of VE (2% of body weight per hour). Atrial natriuretic factor was measured at the end of the experiment. In a control group (n = 7) without volume expansion, plasma ANF was 58 +/- 4 pg ml-1. The excretion of sodium, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), noradrenaline (NA) and GFR did not change during the control study. In VE animals (n = 7) plasma ANF was 82 +/- 7 pg ml-1, significantly higher than in the control group. Sodium excretion increased more than 17-fold. The excretion of the DA increased by 38% and that of DOPAC by 30%. Noradrenaline excretion remained unchanged while GFR increased by 20%. In haloperidol-pretreated animals subjected to VE (n = 7), plasma ANF was 81 +/- 8 pg ml-1 during VE, significantly higher than in the control animals. Although the sodium excretion increased more than ninefold in this group during VE, this increase was only 55% of that in the VE group not given haloperidol. The DA and DOPAC excretion was increased by haloperidol, indicating a feedback effect of receptor blockade. DOPAC excretion was not increased further by VE, but the excretion of DA increased by 15% and GFR increased by 19%.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Effect of a converting-enzyme inhibitor on vasa recta blood flow in rat kidney.

In young anesthetized Munich-Wistar rats, red cell flux (Qrbc) was measured in the vasa recta of the exposed renal papilla by means of fluorescently labeled erythrocytes. To study the vasoreactivity of the juxtamedullary vasculature and its sensitivity to converting-enzyme inhibition, measurements of Qrbc were made before and after continuous intravenous infusion of the angiotensin I converting-enzyme inhibitor captopril (3 mg.h-1.kg body wt-1). A time control group that received vehicle alone was studied in parallel. Captopril acts as a vasodilator and reduces systemic arterial pressure. Captopril treatment increased Qrbc by 40 +/- 4% (n = 9, P less than 0.001) and decreased blood pressure by 9% (P less than 0.001). In the time control group no statistically significant change occurred in either Qrbc (+6 +/- 8%, n = 10) or blood pressure (-1%). Urine samples were taken from the papillary tip. In neither of the groups did the urine osmolality show a statistically significant change. In the time control group the values before and after intravenous infusion were 1,006 +/- 61 and 1,091 +/- 70 mosmol/kg H2O, respectively, and in the captopril-treated animals the corresponding values were 1,150 +/- 85 and 1,210 +/- 60 mosmol/kg H2O, respectively. These results confirm the suggestion that there is high vasoreactivity in the juxtamedullary vasculature and that this region is sensitive to inhibition of angiotensin I-converting enzyme, the latter sensitivity implying that angiotensin II plays a role in the regulation of juxtamedullary vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

CNS-induced natriuresis is not mediated by the atrial natriuretic factor.

Studies were performed on anaesthetized Wistar-Kyoto rats to investigate whether the natriuretic response to stimulation of the cerebroventricular system with a hypertonic sodium solution is in part caused by increased plasma concentrations of atrial natriuretic factor (ANF). Through a cannula inserted into a lateral cerebral ventricle a solution with a normal (CSF, 152 mmol l-1) or high (NaCSF, 1,000 mmol l-1) sodium ion content was infused. In the stimulated animals which received NaCSF, the sodium excretion increased more than 13-fold, from 0.07 +/- 0.02 (mean +/- SEM) to 0.97 +/- 0.22 mumol min-1 g-1 kidney wt (P less than 0.01). Potassium excretion rose more than eight-fold, from 0.37 +/- 0.05 to 3.01 +/- 0.13 mumol min-1 g-1 kidney wt (P less than 0.001), and the urine flow rate more than seven-fold, from 1.35 +/- 0.11 to 9.74 +/- 1.23 microliters min-1 g-1 kidney wt (P less than 0.001). The mean arterial blood pressure increased from 100 +/- 3 to 129 +/- 7 mmHg (P less than 0.001). In the control animals which received CSF throughout the experiment there was no significant change in the above variables. The concentrations of ANF in plasma taken at the end of the experiments were determined by a radioimmunoassay. The mean plasma concentration of ANF in animals receiving CSF throughout the experiment was 175 +/- 36 pg ml-1. This was not significantly different from the corresponding value in animals which were given NaCSF (118 +/- 34 pg ml-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The influence of Atriopeptins I and II on the relationship between glomerular filtration and natriuresis.

The effects of two pure synthetic atrial natriuretic factors, Atriopeptin (AP) I and AP II, on the whole kidney glomerular filtration rate (GFR), sodium and potassium excretion (UNaV, UKV), urine flow rate (V) and arterial blood pressure (BP) were studied in adult male Sprague-Dawley rats. The variables were measured during a control period and during 70 min of continuous intravenous infusion of AP I or AP II at a rate of 10 micrograms h-1 kg-1 body wt. A time control group was studied in parallel to see whether the variables under study changed with time. The AP I infusion did not affect GFR (change from 1.34 +/- 0.10 to 1.24 +/- 0.04 ml min-1 g-1 kidney wt), but was clearly natriuretic (UNaV changed from 0.071 +/- 0.011 to 0.229 +/- 0.038 mumol min-1 g-1 kidney wt, P less than 0.01). The UKV increased from 0.504 +/- 0.073 to 1.138 +/- 0.121 mumol min-1 g-1 kidney wt, (P less than 0.001) and V from 1.88 +/- 0.10 to 2.94 +/- 0.15 microliter min-1 g-1 kidney wt, (P less than 0.001). Urine osmolality (Uosm) and BP were unaffected. During AP II infusion GFR remained unchanged but was slightly below the pre-infusion level during the last infusion period (1.05 +/- 0.07 as against 1.37 +/- 0.09 ml min-1 g-1 kidney wt, P less than 0.05). Despite this fact, UNaV was significantly elevated throughout the infusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effects of atrial natriuretic peptide (ANP) during converting enzyme inhibition.

Studies were performed on anesthetized adult Münich-Wistar rats to investigate the role of angiotensin II in the natriuretic response to synthetic atrial natriuretic peptide (ANP, 28 amino acids). For this purpose the whole kidney glomerular filtration rate (GFR) and urinary excretion of electrolytes were measured in groups of animals pretreated with the converting enzyme inhibitor captopril (3 mg h-1 kg-1 body wt) or vehicle and then given a continuous intravenous infusion of ANP at 10 micrograms h-1 kg-1 body wt. In the vehicle-pretreated animals, 45 min of ANP infusion did not change GFR (control value 1.17 +/- 0.11, experimental value 1.17 +/- 0.06 ml min-1 g-1 kidney wt). Sodium excretion (UNaV) increased more than three-fold from 0.036 +/- 0.010 to 0.134 +/- 0.058 mumol min-1 g-1 kidney wt (p less than 0.05) and potassium excretion (UKV) increased from 0.481 +/- 0.055 to 0.946 +/- 0.068 mumol min-1 g-1 kidney wt (P less than 0.05). Urine osmolality (UOsm) remained unchanged, while the blood pressure (BP) decreased by 15%. In animals pretreated with captopril, ANP infusion led to a decrease in GFR from 1.27 +/- 0.11 to 1.05 +/- 0.09 ml min-1 g-1 kidney wt (P less than 0.05). Despite this effect, UNaV increased more than two-fold from 0.076 +/- 0.020 to 0.193 +/- 0.087 mumol min-1 g-1 kidney wt (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1987

The dopamine receptor antagonist haloperidol blocks natriuretic but not hypotensive effects of the atrial natriuretic factor.

Studies were performed on anesthetized male Münich-Wistar rats to investigate the influence of the dopamine (DA) receptor antagonist haloperidol on the natriuretic response to infusion of a synthetic atrial natriuretic factor. The whole kidney glomerular filtration rate (GFR), urinary excretion of electrolytes, and arterial blood pressure (BP) were therefore measured in groups of animals pretreated with haloperidol or vehicle and given a continuous intravenous infusion of atrial natriuretic peptide (ANP; 28 amino acids). Forty-five minutes of ANP infusion at 10 micrograms h-1 kg-1 body wt did not increase GFR (change from 1.14 +/- 0.08 to 1.15 +/- 0.05 ml min-1 g-1 kidney wt). Sodium excretion (UNaV) increased more than four-fold from 0.037 +/- 0.008 to 0.165 +/- 0.070 mumol min-1 g-1 kidney wt (P less than 0.01). Potassium excretion (UKV) increased by 86% (P less than 0.001) and the urine flow rate (V) increased transiently by 63% (P less than 0.05) and did not differ from the control value during the last 15 min of ANP infusion. The urinary sodium concentration (UNa) increased almost three-fold, while BP decreased by 14%. There was no change in urine osmolality. In animals pretreated with haloperidol (1 mg kg-1 body wt), 45 min of ANP infusion did not significantly alter GFR (from 1.10 +/- 0.08 to 0.98 +/- 0.09 ml min-1 g-1 kidney wt). The UNaV did not increase significantly (change from 0.026 +/- 0.006 to 0.030 +/- 0.009 mumol min-1 g-1 kidney wt). The UKV was not elevated by ANP infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Atriopeptins and renal cortical and papillary blood flow.

Studies were made of the effect of two pure synthetic atrial natriuretic factors (ANF) on renal cortical and papillary blood flow and on the excretion of sodium, potassium and water in young Munich Wistar rats by means of laser-Doppler flowmetry. The effects of Atriopeptin I (AP I), which selectively relaxes intestinal smooth muscle, were compared with those of Atriopeptin II (AP II), which relaxes both vascular and intestinal smooth muscle. Both peptides were administered by continuous intravenous infusion at 10 micrograms h-1 kg-1 body wt after a control period. A time control group was studied in parallel to see whether the variables investigated varied with time. In rats receiving vehicle alone (time control) and in those receiving AP I, there was no significant change either in the cortical or papillary blood flow, or in blood pressure (BP). The AP II infusion resulted in an increase in blood flow which was only transient despite the continuous infusion. Cortical blood flow increased by 22% (peak value) and papillary blood flow increased by 95% (peak value). The blood pressure (BP) decreased by 12% to a steady state level (103 +/- 2 vs. 91 +/- 2 mm Hg). The AP I caused a steady two-fold increase in sodium excretion (UNaV), a 35% increase in potassium excretion (UKV) and and 85% transient increase in urine flow rate (V). Infusion of AP II resulted in a more than 60-fold increase in UNaV during the period of increased blood flow, and then reached a steady state level 10 times higher than the control value.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Redistribution of glomerular filtration and renal plasma flow in CNS-induced natriuresis.

Infusion of hypertonic sodium chloride solution into the third cerebral ventricle results in a marked increase in renal sodium output, indicating an important regulator of extracellular volume homeostasis. The intrarenal events governing the enhanced excretion have not been thoroughly studied previously. In 12 anaesthetized male rats a stainless steel cannula was introduced stereotaxically into the right lateral cerebral ventricle. Urine volume and excretion rates, Na, K, and osmotically active particles were measured during control infusion of artificial cerebrospinal fluid and during stimulation of central mechanisms with I M NaCl (520 nl min-1). At the end of the stimulation period, regional renal plasma flow (86RbCl) and glomerular filtration rate (51Cr-EDTA) were measured with single injection techniques. A second group of 12 non-stimulated rats served as controls. During ICV stimulation, the urine flow rate increased from 1.8 +/- 0.19 to 6.4 +/- 1.01 microliter min-1 (P less than 0.001). The urinary concentrations of Na and K increased, leading to a rise in the excretion rates of these ions from 0.12 +/- 0.025 to 0.96 +/- 0.352 mumol min-1 (P less than 0.001) and 0.40 +/- 0.083 to 1.70 +/- 0.196 (P less than 0.001), respectively. The osmolar excretion rate was 2.9 +/- 0.35 mu Osm min-1 before stimulation and 9.6 +/- 1.09 higher (P less than 0.001) during stimulation. Simultaneously the inner medullary plasma flow rose two-fold from 0.7 +/- 0.06 to 1.4 +/- 0.12 microliter min-1 tissue (P less than 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

A method for in situ measurement of ionic concentration in picoliter samples of renal tubular fluid.

A method permitting rapid and frequent determination of the total ionic concentration in renal tubular fluid samples, by measuring sample electrical impedance, is described. No special electrodes or sophisticated equipment are required. Since picoliter volumes are sufficient for measurement, tubular fluid dynamics are not significantly disturbed by the sampling procedure. The sample is aspirated into the tip of the standard glass micropipette and its ionic concentration, in the range of 100-1000 mmol/l, can be determined by any sensitive impedance-measuring device. In the present studies the Wheatstone bridge of the Wiederhielm apparatus for pressure measurement in micropuncture studies was used for the purpose. The obvious limitation of the method is that the measurements do not include non-electrolytes and cannot differentiate between individual ion species.

Animals↗