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M Sjöquist

Publications and source records attributed to M Sjöquist.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effects of neurohypophyseal antagonists in postnephrectomy natriuresis in male rats.

Acute unilateral nephrectomy (AUN) in anesthetized male Lewis x DA rats induced rapid and consistent increases in electrolyte and fluid excretion by the remaining kidney during the first hours. Continuous infusion of a vasopressin (AVP) V1-receptor antagonist d(CH2)5Tyr(Me)AVP (V1-ant) reduced renal electrolyte and fluid excretion before and after AUN to a similar extent, whereas an oxytocin (OT)-receptor antagonist [Mpa1,D-Tyr(Et)2,Thr4,Orn8]-OT (CAP) at the same dose selectively attenuated the increase in sodium excretion after AUN. The plasma concentration of OT rose significantly after AUN (9.16 +/- 1.4 to 21.45 +/- 5.07 pg.ml-1). A similar OT level obtained by infusion of OT mimicked the renal responses to AUN without elevating blood pressure; however, only CAP but not V1-ant efficiently reversed OT-induced natriuresis. Also, the infusion of CAP at the same dose produced no effects on the rise of blood pressure caused by AVP while the infusion of the V1-ant prevented such a rise. Thus, CAP reduced the natriuresis after AUN by interfering with OT- and not V1-receptors. In conclusion, evidence is presented, for the first time, concerning the major role of OT receptors in the acute readjustment of the renal sodium excretion after AUN, and a synergistic role for AVP in terms of the general magnitude of renal excretion.

Animals↗
PubMed1994

Bikunin in rat plasma, lymph and bile.

Bikunin is a protease inhibitor consisting of a 16 kDa polypeptide and an 8 kDa chondroitin sulphate chain which has an apparent molecular mass of 60-70 kDa upon gel filtration. It is synthesized by hepatocytes and occurs in plasma, both in free form, and in complex with other polypeptides--mainly as the 180 kDa protein inter-alpha-inhibitor. Bikunin binds to proteases less avidly than other plasma inhibitors, making its role in the blood unclear. However, some observations indicate that bikunin has important functions outside the blood system. To assess its capacity to reach extravascular spaces, we have determined the total concentration of bikunin in plasma (0.17 mg/ml), lymph (31 micrograms/ml) and bile (0.2 microgram/ml). Quantitation after removal of complexed bikunin (inter-alpha-inhibitor) by acid precipitation showed that the concentration of free bikunin in those fluids was 3, 1.4 and 0.05 micrograms/ml, respectively. These values yield a lymph/plasma ratio of free bikunin of 0.5, which is higher than expected for a protein of the hydrodynamic size and charge of bikunin. The bile/plasma ratio (0.02), however, is similar to that of other proteins of comparable size. The corresponding values for inter-alpha-inhibitor, 0.16 and 0.001, respectively, indicate that its capacity to pass through the vascular endothelium is relatively high whereas transfer to bile is restricted. Furthermore, we have found that in a perfusate of an isolated rat liver, the ratio of free to complexed bikunin was 30-40 times higher than in plasma, consistent with previous observations showing that free bikunin is cleared from the blood stream much more rapidly than inter-alpha-inhibitor.

Animals↗
PubMed1992

Dopamine receptor blockade and synthesis inhibition during exaggerated natriuresis in spontaneously hypertensive rats.

The influence of dopamine receptor blockade and synthesis inhibition on natriuresis induced by isotonic saline volume expansion was investigated in anaesthetized spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. The aim of the study was to elucidate the mechanisms underlying the phenomenon of exaggerated natriuresis during volume expansion that has been observed in spontaneously hypertensive rats. Volume expansion, at 5% of body weight, resulted in a larger and faster natriuretic response in spontaneously hypertensive rats than in Wistar-Kyoto rats. Sixty minutes after commencement of volume expansion the natriuretic response (accumulated sodium excretion) in Wistar-Kyoto rats (n = 8) was only 24% of that in spontaneously hypertensive rats (n = 17). When spontaneously hypertensive rats were pretreated with the dopamine receptor blockers haloperidol (n = 14, 1 mg kg-1), SCH23390 (n = 8, 30 micrograms h-1 kg-1) or the dopamine synthesis inhibitor benserazide (n = 8, 50 mg kg-1; n = 5, 100 mg kg-1), the natriuretic response to volume expansion was only 16, 35, 59 and 42%, respectively, of that in untreated SHR. The corresponding proportion in the haloperidol-treated (n = 8) compared with untreated Wistar-Kyoto rats was 22%. In conclusion, isotonic volume loading results in more pronounced natriuresis in spontaneously hypertensive than in Wistar-Kyoto rats. Dopamine receptor blockade and synthesis inhibition attenuate the expansion of exaggerated natriuresis in spontaneously hypertensive rats and reduces the volume expansion natriuresis in Wistar-Kyoto rats, indicating that the dopamine system plays an important role.

Animals↗
PubMed1992

Tubuglomerular feedback control in long-looped nephrons. Topical minireview.

The tubuloglomerular feedback mechanism is highly activated in juxtamedullary nephrons and considered to play a major role in intrarenal regulation of glomerular filtration rate. The vasculature of juxtamedullary nephrons is highly vasoreactive with a high ability for vasodilation. This vasoreactivity is a prerequisite for an important influence of the tubuloglomerular feedback mechanism on the medullary blood flow and its regulation.

Animals↗
PubMed1991

Sodium and potassium load in the loop of Henle, measured with intact and blocked tubuloglomerular feedback mechanism in juxtamedullary nephrons.

For the juxtamedullary nephrons only the loop of Henle is easily accessible for micropuncture. We have shown that the tubuloglomerular feedback (TGF) mechanism is highly activated in these nephrons. Techniques have been developed for measurements on these nephrons without disrupting the normal flow to the macula densa. The tubular flow rate was measured by a real-time videodensitometric method in juxtamedullary nephrons in Lewis x DA rats. For the determination of tubular fluid composition a small fraction (less than 10%) of the fluid was sampled. Measurements were also performed according to the conventional technique, where all the tubular fluid was sampled. Despite a more than twofold increase in tubular flow rate when the flow to the macula densa region was interrupted, sodium concentration was only reduced by 25%, whereas potassium concentration was reduced by 40%. The results demonstrate that interruption of the urine flow to the macula densa results in a 52% increase in the tubular load of Na in the loop of Henle of juxtamedullary nephrons, and a corresponding increase of 24% for K. Thus, TGF exerts a strong influence on these nephrons which is why previous data on water and electrolyte loads, based on stop-flow measurements, greatly overestimate these loads.

Animals↗
PubMed1990

Effect of papillary exposure on intrarenal distribution of glomerular filtration rate and of plasma flow.

Removal of the renal pelvis in order to expose the renal papilla has been shown to cause impairment of the renal concentrating ability by an unknown mechanism. To study this phenomenon, urine osmolality (Uosm), single-nephron glomerular filtration rate (SNGFR) in outer and inner cortical nephrons and the inner and outer medullary plasma flow were determined. Measurements were performed on groups of rats before (control) and 15, 45 and 90 min after exposure of the left renal papilla. Rats with an intact ureter were studied in parallel to see whether the variables varied within the 90-min period of the study. In all groups of animals with an exposed papilla, Uosm was lower than in non-exposed animals. Outer cortical SNGFR in rats with exposed papillae, regardless of time, was not different from that in control rats. Inner cortical SNGFR after 45 and 90 min of exposure did not differ from that in controls, but after 15 min of exposure it was lower than in control animals. Outer and inner medullary plasma flow did not differ between rats with exposed papillae and controls, irrespective of exposure time. In conclusion, papillary exposure results in a permanent decrease in urine osmolality. This impairment of the concentrating ability cannot be attributed to prolonged changes in renal haemodynamics.

Animals↗
PubMed1990

Hemodynamic responses in rabbit tenuissimus muscle arterioles during local reduction in perfusion pressure.

Transverse (TR) and terminal (TE) arteriolar diameters and TR pressure were measured in the rabbit tenuissimus muscle during steady state reductions in perfusion pressure. An inflatable occluder was positioned on the abdominal aorta proximal to the bifurcation to alter perfusion pressure. In the control conditions, TEs exhibited highly regular cyclic activity (20 +/- 4 cpm). In contrast, TRs seldom exhibited regular vasomotor activity. Pressure reductions from 76 +/- 1 to 40-50 mm Hg caused no significant change in the observed hemodynamic variables. Reductions below this level caused proportional dilations of TRs and a change in vasomotion pattern of TEs; i.e. the fundamental frequency was unaltered, but periods without vasomotion increased in duration. At an arterial pressure of 30-40 mm Hg, vasomotion in the TEs completely disappeared. Pressure in the distal TR was autoregulated at 40 +/- 4 mm Hg until a threshold (40-50 mm Hg) was reached; thereafter TR pressure decreased in proportion to the arterial pressure decrements. These results suggest that the TRs are the last generation of arterioles involved in the autoregulation of microvascular pressure. Furthermore, the basic frequency and maximal amplitude of vasomotion in TEs are not affected by pressure reductions.

Animals↗
PubMed1989

Biochemical evidence for the GABA regulation of vasopressin levels in microdissected brain structures after servo-controlled hypotension.

Discrete brain structures were analysed for gamma-aminobutyric acid (GABA) and vasopressin content in normo- and hypotensive rats treated with the glutamic acid decarboxylase inhibitor, 3-mercaptopropionic acid (MPA) and the GABAA agonist muscimol. In the normotensive group treated with MPA only, the concentration of vasopressin increased in the supraoptic nucleus, indicating an inhibitory role for GABA. In the hypotensive group a rise in the vasopressin level in the nucleus of the solitary tract was detected and the GABA level decreased in the supraoptic nucleus. Muscimol decreased the concentration of vasopressin in the nucleus of the solitary tract. The changes in the concentration of vasopressin may be a result of increased or decreased activation of the GABAergic system. The results show that the GABA- and vasopressinergic systems somehow interact although the more precise way of action remains to be clarified.

3-Mercaptopropionic Acid↗
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

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

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↗
PubMed1987

Functional characteristics of peritubular capillary membrane in rat kidney.

The permeability characteristics of the peritubular capillary membrane in the rat kidney were investigated on the basis of the transport of hippuran, inulin, myoglobin, horseradish peroxidase, albumin, and gamma-globulin from peritubular capillary blood to renal hilar lymph. Data obtained in a previous investigation on single-nephron plasma flow, filtration fraction, net driving force, and fluid reabsorption along the peritubular capillary were also used. The data were analyzed in a computer-based model taking into account the transport both by diffusion and by convection. The results show that the membrane contains a few large pores through which the plasma proteins leak out into the renal interstitium and a system of several smaller pores responsible for the fluid reabsorption. The mean equivalent radius of the large pores was estimated from the larger molecular probes to be approximately 180 A (range 150-225 A), and the corresponding total pore area over pore length was estimated at 3 X 10(-4) cm (range 6 X 10(-4) to 1 X 10(-4) cm). The small-pore system was analyzed from the transport of hippuran, inulin, and myoglobin and from fluid reabsorption and showed a pore radius of somewhat below 20 A and pore areas over pore length of 50 cm. Here, the fluid reabsorption and the transport of hippuran turned out to be a sensitive marker of the pore area and the transport of inulin and myoglobin of the pore radius.

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↗
PubMed1986

Superficial and juxtamedullary nephron function during converting enzyme inhibition.

The influence of the renin-angiotensin system on whole-kidney and regional single-nephron function was studied in anesthetized Munich-Wistar rats by use of a converting enzyme inhibitor (CEI), captopril (3 mg . h-1 . kg-1 body wt-1). Single-nephron glomerular filtration rate (SNGFR) was measured in superficial (S) and juxtamedullary (JM) nephrons by a micropuncture technique that blocked tubuloglomerular feedback (TGF) activity. Hydrostatic free-flow pressure (FFP) measurements were conducted in S proximal tubules, in JM loops of Henle, and in papillary vasa recta. Glomerular filtration rate (GFR) and urinary electrolyte excretion were measured in the contralateral kidney. In the control situation SNGFR of S nephrons was 35.4 +/- 2.24 nl . min-1 . g kidney wt-1 and of JM nephrons was 75.0 +/- 9.41 nl . min-1 . g-1 kidney wt-1. Thus it was more than twice as high in JM as in S nephrons when the TGF activity was blocked. In this situation administration of CEI had no additional effect on either S or JM nephrons. However, administration of CEI resulted in a significant increase in whole-kidney GFR by 25% (P less than 0.05) and in urine flow rate by 60% (P less than 0.001) under free-flow conditions. Further, intratubular FFP increased significantly in JM nephrons by an average of 2.9 +/- 0.52 mmHg (P less than 0.001), indicating an increase in tubular urine flow in JM nephrons, whereas S nephrons were unaffected. These results suggest an active preglomerular vasoconstriction in JM nephrons under normal free-flow conditions. This seems to be mediated by TGF and modulated by angiotensin II.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Whole kidney response to reduced arterial pressure during converting enzyme inhibition in the rat.

Autoregulatory efficiency of renal blood flow (RBF) and glomerular filtration rate (GFR) was evaluated in male Sprague-Dawley rats during interference with the renin-angiotensin system by a converting enzyme inhibitor (CEI), captopril (3 mg X h-1 X kg-1 BW). RBF and GFR were approximately 25 (p less than 0.01) and 20% (p less than 0.02) higher, respectively, in rats infused with CEI than in control rats at spontaneous renal arterial pressure (RAP). A reduction of RAP to 100 mm Hg (within the autoregulatory range) resulted in effective autoregulation of GFR and RBF in control rats. In rats given CEI, however, the autoregulation of GFR was markedly impaired. GFR decreased by 35% (p less than 0.001), while RBF remained relatively unchanged. This caused the filtration fraction to decrease from 0.33 +/- 0.01 to 0.29 +/- 0.01 (p less than 0.001). RAP had a consistent effect on the urine flow rate, even though both GFR and RBF were well autoregulated in control rats. No significant decrease in electrolyte excretion was detected within the autoregulatory range in control rats, but during converting enzyme blockade this excretion decreased progressively as RAP was reduced, and the decrease correlated well to the reduction in GFR. In summary, these results suggest that the renin-angiotensin system plays an important intrarenal role in the autoregulation of GFR, probably through an efferent arteriolar mechanism. Furthermore, it is demonstrated that the contralateral kidney efficiently compensates in urinary electrolyte excretion for an acute unilateral reduction of RAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗