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Biomedical subjects

C Aalkjaer

Publications and source records attributed to C Aalkjaer.

At least 91 records · Page 5Linked to original sources
PubMed1987

Studies of isolated resistance vessels from offspring of essential hypertensive patients.

In order to investigate whether functional and morphological changes are present in the resistance vasculature before hypertension is established, isolated subcutaneous resistance vessels were studied from 21 young normotensive subjects with a family history of hypertension and 22 controls matched for age, sex, and weight. The vessels from the offspring of hypertensive patients displayed no morphological changes or differences in reactivity or sensitivity to the vasoconstrictor agonists norepinephrine, angiotensin II, serotonin, and vasopressin. In the presence of cocaine, however, vessels from offspring showed a significantly greater shift in sensitivity to norepinephrine, a phenomenon also observed in previous studies of vessels from hypertensive patients. The results suggest that in essential hypertension, while morphological and functional abnormalities of the resistance vasculature may develop as the blood pressure rises, a defect in neuroeffector activity is present before hypertension is established and may be a manifestation of abnormal sympathetic nervous system activity underlying the disease.

Adult↗
PubMed1987

Evidence for increased media thickness, increased neuronal amine uptake, and depressed excitation--contraction coupling in isolated resistance vessels from essential hypertensives.

The functional and morphologic characteristics of isolated subcutaneous resistance vessels (about 170 micron i.d.) from 15 untreated subjects with essential hypertension and 15 matched controls were examined. The vessels from the hypertensives had a 29% increase in the media-thickness-to-lumen-diameter ratio. The maximal force development to noradrenaline (NA) expressed as active pressure (an estimate of the pressure the vessels could have contracted against in vivo) was 30% higher in vessels from the hypertensives, while active media stress (force per square unit of smooth muscle) and sensitivity to NA was not significantly different. Increased active pressure, as well as unaltered active media stress and sensitivity, was seen for vasopressin, serotonin, angiotensin II, and K+. There was, however, an enhanced leftward shift of the NA sensitivity with cocaine (an inhibitor of the neuronal amine pump) in vessels from the hypertensives [pD2(+cocaine) and pD2(-cocaine) were 0.185 +/- 0.53) and 0.040 +/- 0.044, hypertensives and normotensives, respectively, p less than 0.05] suggesting an abnormality of presynaptic function in essential hypertension. Furthermore, the calcium sensitivity was depressed (pD2 was 4.197 +/- 0.050 and 4.381 +/- 0.068, hypertensives and normotensives, respectively, p less than 0.05), and the rate of relaxation was faster (p less than 0.05) in vessels from hypertensives, suggesting that excitation-contraction coupling might be depressed. The results suggest that the increased pressor response in essential hypertension can, to a large extent, be explained by altered vascular structure, while smooth muscle function is either unchanged or possibly depressed.

Arteries↗
PubMed1986

Cell membrane sodium transport: a correlation between human resistance vessels and leucocytes.

Sodium efflux was studied in leucocytes and resistance vessels from omental fat from 18 subjects undergoing laparotomy. The efflux of sodium was considerably faster from resistance vessels than from leucocytes, but there was a significant correlation between total efflux rate constants in the two tissues. This was attributable to a highly significant correlation between active sodium pumping as assessed by the ouabain-sensitive sodium efflux rate constants observed in both tissues. These results indicate that intrinsic characteristics of cell membrane electrolyte transport are shared by the leucocyte and vascular smooth muscle in human beings. Therefore, leucocytes can be used to provide information about altered vascular ion handling.

Aged↗
PubMed1986

Morphological and functional characteristics of isolated resistance vessels in advanced uraemia.

In order to obtain direct information on the properties of the resistance vasculature of patients with advanced uraemia, a technique was developed to dissect out small arteries (internal diameter about 165 microns) from biopsies of subcutaneous fat. Such arteries responded in a concentration-dependent manner to noradrenaline and angiotensin II, and the maximal force developed suggested that the vessels were fully viable. Although the biopsies were normally taken during operations under general anaesthesia, biopsies taken under local anaesthesia also appeared to be fully viable, suggesting that this technique may prove useful as a general method for studying the intrinsic vascular properties of humans. Biopsies were taken from 20 patients with uraemia, all of whom were treated with chronic intermittent dialysis, and 11 control subjects; up to three vessels were examined per biopsy. The uraemic state was not associated with changes in vascular morphology, or in vascular reactivity or sensitivity to noradrenaline, angiotensin II, potassium or calcium. However, for the uraemic patients and for the controls there was a positive correlation between mean blood pressure and the ratio of vessel media thickness to lumen diameter, as well as a negative correlation between mean blood pressure and vessel active media stress. The results suggest that uraemia treated with dialysis may not be associated with altered properties of the resistance vasculature. However, it appears that uraemic hypertension is associated with both morphological and functional abnormalities of the resistance vasculature.

Adipose Tissue↗
PubMed1985

Abnormal vascular function and morphology in pre-eclampsia: a study of isolated resistance vessels.

In order to obtain direct information about vascular changes associated with pre-eclampsia, the morphological and functional characteristics of isolated omental resistance vessels from 11 women with pre-eclampsia, 10 normotensive pregnant women and eight normotensive non-pregnant women were determined. In vessels from the women with pre-eclampsia, the ratio of media thickness to lumen diameter was increased, compared with that in vessels from the other two groups. The vessels from the women with pre-eclampsia had an increased responsiveness to angiotensin II and a decreased rate of relaxation, but only when compared with the vessels from the normotensive pregnant women. However, no difference in responsiveness to noradrenaline was found between any of the groups. The angiotensin II responsiveness of the vessels from the women with pre-eclampsia and from the non-pregnant women were similar, suggesting that pre-eclampsia is associated with an absence of the change in vascular function which normally occurs during pregnancy. The study provides direct evidence for an involvement of vascular abnormalities in the pathogenesis of pre-eclampsia.

Adult↗
PubMed1985

Atrial natriuretic factor causes specific relaxation of rat renal arcuate arteries.

We have investigated the effect of a synthetic 'atrial natriuretic factor' (ANF) on induced tone in rat isolated renal arcuate arteries (lumen diameter ca. 250 microns), and compared this with the effects of synthetic ANF on resistance vessels of similar size taken from the mesenteric, femoral, cerebral and coronary vasculature. Synthetic ANF was found to cause relaxation of the renal vessels when these were sub-maximally activated with K+, noradrenaline or 5-hydroxytryptamine, but had no effect on the responses of the other vessels to these agonists. Synthetic ANF had a near maximal effect (65% relaxation) at 100 nM, with an IC50 of 7.9 nM. The relaxant effect of synthetic ANF on the renal vessels was fully maintained for at least 15 min. Hydralazine (100 microM) caused relaxation of renal vessels (47%) and coronary vessels (42%), but had no effect on the other vessel types. By contrast, sodium nitroprusside (1 microM) relaxed all vessel types. The relaxant action of synthetic ANF on the renal vessels was seen in the presence of ouabain (1 mM), propranolol (1 microM), phentolamine (1 microM), atropine (1 microM) and felodipine (1 nM). In t renal vessels, synthetic ANF had no effect on membrane potential, measured with intracellular electrodes, despite the simultaneously measured relaxation. Synthetic ANF had no effect on the efflux of 22Na+ in either renal or mesenteric vessels. The results demonstrate that synthetic ANF has a specific and prolonged relaxant effect on renal small arteries, and are consistent with this effect being mediated through specific receptors.

Animals↗
PubMed1985

Effect of ouabain on tone, membrane potential and sodium efflux compared with [3H]ouabain binding in rat resistance vessels.

To investigate the mechanism by which ouabain causes acute increase in peripheral resistance, the effect of ouabain on vessel tone, 22Na efflux and membrane potential has been compared with the binding of [3H]ouabain in rat isolated mesenteric resistance vessels (lumen diameter approximately 200 microns). Ouabain at concentrations between 1 X 10(-8) and 1 X 10(-3) M had no effect on the tone of resting vessels but caused potentiation of the tone of vessels which were submaximally contracted with noradrenaline. In the entire concentration range, these acute potentiating effects of ouabain on vessel tone correlated well with an acute inhibitory effect on 22Na efflux and with acute [3H]ouabain binding, consistent with the vasoconstrictor effect of ouabain being associated with inhibition of the Na-K pump. At all concentrations, in both resting and activated vessels, ouabain exposure caused an acute concentration-dependent depolarization of the membrane. At low ouabain concentrations (1 X 10(-6) and 1 X 10(-5) M) the potentiating effect on vessel tone and the inhibitory effect on 22Na efflux were transient, so that after 10 min no effect of ouabain was seen. This was consistent with these ouabain concentrations failing to cause a measurable increase in the intracellular Na concentration ([Na]i) after longer term (up to 2 h) exposure. The recovery of 22Na efflux was due to a recovery of the ouabain-sensitive part of the 22Na efflux, suggesting that the transitory nature of these effects is due to stimulation of uninhibited Na-K pumps. The transient effects of low ouabain concentrations contrasted with binding experiments where, with 1 X 10(-6) M-ouabain, the binding first peaked after 30 min with only a small decline thereafter. With higher concentrations of ouabain (1 X 10(-4) and 1 X 10(-3) M), the potentiating effect was also transitory, but 22Na efflux was permanently inhibited and the [Na]i rose. The possibility of there being two populations of ouabain binding sites having different affinities, was supported by the observation of shoulders in the ouabain concentration-effect characteristics obtained with respect to the mechanical potentiation of noradrenaline responses, the 22Na efflux and the acute ouabain binding. In all cases a shoulder was seen between 1 X 10(-6) and 1 X 10(-5) M-ouabain. The results are consistent with the vasoconstrictor effect of ouabain being due to depolarization of the membrane as a consequence of inhibition of the Na-K pump.

Animals↗
PubMed1985

Synthetic atrial natriuretic factor is a specific dilator of noradrenaline and serotonin activated renal resistance vessels.

The action of a synthetic 'atrial natriuretic factor' (sANF) on induced tone in isolated rat renal resistance vessels (lumen diameter about 200 microns) was examined and compared with the effects of sANF on resistance vessels of similar size taken from the cerebral, mesenteric and femoral vasculature. Synthetic ANF caused a relaxation of the renal vessels when these were submaximally activated with noradrenaline or serotonin, but had no effect on the responses of the other vessels to these agonists. In contrast to previous reports concerning rabbit aortic vessels, methylene blue (which is thought to cause inhibition of guanyl cyclase) did not reduce the dilator response to sANF in the renal vessels. The results demonstrate that sANF has a specific relaxing effect on renal resistance vessels, and are consistent with its effect being mediated through specific receptors. The mechanism of this relaxant effect remains unknown.

Animals↗
PubMed1984

Intracellular sodium, membrane potential, and contractility of rat mesenteric small arteries.

We have investigated effects of altered extracellular sodium, intracellular sodium concentration, and membrane potential on the contractile responses of rat isolated mesenteric small arteries (internal diameter ca. 200 microns), when mounted as ring preparations on an isometric myograph. To avoid possible neural effects, all vessels were denervated in vitro using 6-hydroxydopamine. In unstimulated vessels, exposure to low-Na+ solutions (25 mM sodium, sucrose, or choline-substituted) did not cause any response nor did exposure to ouabain (1 mM) for 1 hour [when intracellular sodium concentration increased to 64 mmol/(liter-cell)]. However, a response was obtained if ouabain-exposed vessels were subjected to low-sodium solutions (ca. 15% of maximal response). The magnitude of the response was dependent on the ratio of intracellular to extracellular sodium and was not inhibitable by the calcium blockers, felodipine (1 nM) or D600 (10 microM). This response could therefore be explained in terms of Na-Ca exchange mechanism. The responses of activated vessels to ouabain and to low-sodium solutions were also investigated. The responses of vessels to submaximal doses of noradrenaline or potassium were potentiated acutely by ouabain (by 10-30% of the maximal response), even if the extracellular sodium was reduced to 25 mM. In all cases, the potentiation by ouabain was accompanied by a depolarization (3-12 mV). However, only in the case of noradrenaline-activated vessels with normal extracellular sodium was the potentiation accompanied by an increase in intracellular sodium [by ca. 7 mmol/(liter-cell)]. Moreover, the latter response was inhibited by felodipine and D600. The results suggest that Na-Ca exchange mechanisms may be present in these vessels but that they only play a role under extreme conditions; under normal conditions the effect of ouabain on activated vessels seems to be primarily due to its depolarizing effect, and not to its effect on intracellular sodium.

Animals↗
PubMed1984

Characteristics of resistance vessels in pre-eclampsia and normotensive pregnancy.

Isolated omental resistance vessels from women with pre-eclampsia had an increased media thickness/lumen diameter ratio compared to similar vessels from normotensive pregnant women. The active and passive tension length curves for the two groups of vessels were similar and like the classical tension length curve for skeletal muscles. The maximal media stress (force per media cross-section) was also similar; however, calculating in terms of equivalent pressure (on basis of Laplaces law) indicated that the vessels in vivo would have been able to contract against an increased blood pressure. The results indicate that pre-eclampsia is associated with structural alterations of the resistance vessels which might be of importance for the haemodynamics of pre-eclampsia.

Arteries↗
PubMed1983

Human and rat resistance vessels: a comparison of their morphological and pharmacological characteristics.

The morphology and pharmacology of isolated human omental and rat mesenterial resistance vessels of about 200 micron i.d. have been compared. The results show a similarity in the gross morphology, the maximal responses and the sensitivity of the smooth muscle cells to noradrenaline and Ca2+. There were differences in the vascular smooth cell size and minor qualitative differences in the pharmacological responses. More importantly, we found that there was a very sparse adrenergic innervation of the human vessels as compared to the rat vessels, suggesting that these human vessels may not be under sympathetic control. The results suggest that, with the exception of the differences noted, the rat vessels are a reasonable model for the human vessels.

Animals↗