PubMed HealthSearch

SEARCH · PubMed Health

Results for “Arterioles”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

[Tissue renin content in superficial, midcortical, and juxtamedullary afferent arterioles in rabbits].

Tissue renin content within the kidney decreases from outer to inner cortex. However, it is not known whether this gradient is due to a decrease in the number of afferent arterioles from the outer to inner cortex or the decrease in renin content per afferent arteriole. Furthermore, it is still controversial whether sodium depletion increases or decreases this gradient. According to Taugner et al., sodium depletion induces the extension of renin positive part of afferent arterioles from vascular pole toward interlobular artery. Since the length of extension may differ among superficial, midcortical, and juxtamedullary afferent arterioles, the observed gradient may vary depending on whether the entire afferent arteriole or only the vascular pole is examined. In the present study, we microdissected the entire afferent arterioles from superficial, middle, and juxtamedullary cortex of rabbit kidney, and examined tissue renin content. We studied: 1. whether tissue renin content per afferent arteriole decreases from the outer to inner cortex. 2. whether sodium depletion affects the gradient of tissue renin content within the cortex. In result, we reached the conclusions, as follows: 1. Tissue renin content per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles. 2. The absolute difference in renin content among the three types of afferent arterioles becomes greater during sodium depletion. The internephron heterogeneity of tissue renin content may contribute to functional heterogeneity.

Animals

Efferent arterioles in the cortex of the rat kidney.

Although a number of morphological studies have investigated the vascular system of the rat kidney, minimal data are available on the detailed anatomy of the efferent arterioles located throughout the cortex of the kidney. In the present study, the renal vascular system was filled with Microfil and the various efferent arteriole patterns were examined extensively. The efferent vessels of the entire cortex appear to form three major patterns which in turn divided the cortex into three separate regions: the outer, middle and inner cortex. The efferent arterioles of the outer cortex leave the glomerulus and run perpendicular to the kidney capsule. However, as the efferent arterioles ascend, they may show three variations in the way they branch: (1a) the efferent arteriole does not branch until directly beneath the capsule, (1b) the efferent vessel begins to divide into its major branches 100-200 mum below the surface of the kidney and (1c) the efferent vessel has only a short course before giving off many side branches. In the middle cortical area, the branches of the efferent arteriole run lateral to the glomerulus. However, the efferent arterioles of the inner cortex have a few branches which run lateral to the glomerulus while most of them descend into the medulla as vasa rectae. The unique morphological features of the efferent arterioles of the outer cortex are of particular interest in light of the functional data which suggests that the reabsorption of fluid by peritubular capillaries may indeed regulate the rate of net tubular sodium reabsorption.

Animals

[Renin release from microdissected superficial, midcortical, and juxtamedullary afferent arterioles in rabbits].

Though renin release from a single superficial afferent arteriole has been studied extensively, there is no report on renin release from a single midcortical or juxtamedullary afferent arteriole. In the present study, we microdissected the entire afferent arterioles from superficial, middle, and juxtamedullary cortex of rabbit kidney, and examined renin release from a single afferent arteriole. In result, we got the following conclusions. 1. Basal renin release per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles during both normal and low sodium intake. 2. Isoproterenol (1.6 x 10(-4)M) significantly stimulates renin release from all three types of arterioles on either diet; however, only in the superficial arterioles is the increase (delta) greater with dietary sodium restriction. These findings indicate substantial heterogeneity of basal and isoproterenol-stimulated renin release, and response to chronic sodium depletion.

Animals

Contributions of pressure and flow sensitivity to autoregulation in mesenteric arterioles.

The relative influence of presence and flow on dilation of arterioles with pressure reduction was examined in preparations of cat mesentery. Erythrocyte velocity and diameter were measured in individual arterioles during stepwise reduction in mesenteric arterial pressure. Volume flow was calculated from velocity and diameter data. Approximately half of the arterioles which dilated with pressure reduction also showed an increase in volume flow. In a second series of experiments, a graded reduction of flow in single arterioles was produced by local downstream occlusion. Graded occlusion caused dilation. In a third series, flow in single arterioles was completely stopped by downstream occlusion, and arterial pressure was then lowered. Most arterioles dilated with pressure reduction. In a fourth series, flow in the total preparation was completely stopped and static intravascular pressure set by a reservoir. Elevation of static pressure typically produced arteriolar constriction. We conclude from these studies that the mesenteric arteriole is sensitive both to intravascular pressure and flow, with the former probably more important than the latter in the phenomenon of autoregulation.

Animals

Structural alterations in proliferating, remodeling, and regressing tooth pulp arterioles.

In the continuously growing upper incisor of 100 g rats about 25 arterioles arise from an artery outside the tooth and pass through the apical foramen to run parallel to one another in the central part of the pulp, each supplying a well-defined sector of the migrating odontoblast layer. The arterioles pass through a cycle of proliferation, growth, remodeling, regression and decay, phase displaced in relation to each other. Proliferative and degenerative processes occur in the arteriole wall throughout the cycle, but vary considerably in intensity at different phases. Proliferation takes place by mitosis in the endothelium and the innermost smooth muscle cells. The degenerative process consists of reduction in size of smooth muscle cells by partial autodigestion and by cell death. When the odontoblasts reach the incisal extremity of the tooth, they die, and the associated regressed arteriole disappears. The system of pulpal arterioles has remarkable spatio-temporal features and each of its vessels appears to be in a state of sensitive structural equilibrium.

Animals

An analysis of excitatory junctional potentials recorded from arterioles.

1. Arterioles were impaled with two independent micro-electrodes, one to pass current and the other to record membrane potential. 2. When current was injected into one branch of an arteriole, a membrane potential change could be detected either in the same branch or in an adjoining branch indicating that the arteriolar smooth muscle cells were electrically connected. 3. Fine dissection of the arteriolar tree gave short segments of arteriole which appeared to behave electrically as short cables with sealed ends. 4. Analysis of the electrotonic potentials recorded from isolated segments of arterioles allowed a determination of the arteriole cable properties. 5. Using the data from the cable analyses it was concluded that the junctional current underlying an excitatory junction potential has a duration that is brief when compared with that of the potential.

Animals

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2.

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

Animals

Ultrastructure of arterioles in the cat brain.

A total of 110 arterioles were examined in the brains of cats; different sites were studied including the cortex, putamen, pons and crus cerebri. No internal elastic laminae were seen in the subendothelial space, although occasional fragments of elastic material were present in the larger arterioles. The media was composed of one, two or three layers of smooth muscle cells which interlocked in such a way that the vessel wall thickness was constant. Numerous tight junctions were seen between adjacent smooth muscle cells and between the endothelium and smooth muscle cells. Apart from the usual cell organelles, the smooth muscle cells of arterioles had numerous dense patches on the cell surface. The structure of the adventitia varied according to the diameter of the vessel and the site in the brain; it contained adventitial cells, bundles of collagen fibres and nerve fibres. Innervation of arterioles was more constant in the brain stem than in the cortex. Metarterioles had less specialised, atypical smooth muscle cells, a discontinuous media and numerous, extensive myoendothelial tight junctions; they were not innervated by nerve fibres. The diameter of metarterioles was less than 10 micronm whereas that of arterioles was 10-45 micronm. The possible functional aspects of arteriolar innervation are discussed.

Animals

Reactivity of gomerular afferent and efferent arterioles in renal hypertension.

Renal tissue from neonatal hamsters was grafted into the cheek pouch of adult hamsters. Renal hypertension was induced in 28 hamsters, and sham operation was performed in 27. When blood pressure became elevated in hypertensive hamsters (10 to 12 days), the renal microcirculation of both groups was evaluated by direct microscopy. Wall and luminal diameter and vascular responses to norepinephrine (NE) and angiotensin II (AII) were determined on glomerular afferent and efferent arterioles and on the corresponding cheek pouch arterioles. In the hypertensive hamsters, the luminal diameter of the afferent arteriole increased, as did the wall/lumen ratio of the efferent arteriole. Although all vessels responded to direct application of NE and AII in both groups, the response of the afferent to AII and the response of the efferent to both NE and AII was greater in the hypertensive hamsters as compared to the sham-operated hamsters. These results indicate that during the development of renal hypertension structural alterations of glomerular vessels and the selective vascular responses to vasoactive agents would lead to an increased glomerular capillary pressure.

Angiotensin II

Diameter of afferent arterioles during autoregulation estimated from microsphere data in the dog kidney.

Afferent arteiolar diameters, relative flow distribution, and flow conductance factors are estimated by nonlinear regression analysis of the sieving effect on microspheres in different vascular structures of the dog renal cortex. The data presented are from experiments in which microspheres of 10-30 microgram were injected into the abdominal aorta during normotension and after lowering the blood pressure to the lower limit of autoregulation. Microscopic examination of the spheres trapped in the glomeruli and the renal arteries showed an increasing exclusion of microspheres greater than 15 micrometer from the afferent arterioles during normotension. This effect was most pronounced for the deeper cortical layers and can be explained mainly as geometrical exclusion of spheres from afferent arterioles. During hypotension, progressively larger microspheres entered glomeruli and afferent arterioles, presumably due to vasodilation of the vessels. There was a significant redistribution of microspheres larger than 15 micrometer from the outer to the inner cortex during hypotension without a corresponding redistribution of smaller spheres or the estimated blood flow. Approximately the same degree of dilation of afferent arterioles was observed during autoregulatory hypotension in three cortical layers.

Animals

Effects of trigeminal neurotransmitters on piglet pial arterioles.

We investigated effects of calcitonin gene-related peptide (CGRP), substance P (SP), and neurokinin A (NKA) on pial arterioles in newborn pigs. Pial arteriolar diameter was determined using a closed cranial window and intravital microscopy. Initial diameters were approximately 100 microns. Calcitonin-gene related peptide dilated pial arterioles by 22 +/- 8% at 10(-9)M and by 34 +/- 6% at 10(-8)M (n = 8), and this response was not significantly altered by prior administration of indomethacin (5mg/kg, iv) (n = 6) or administration of NG-methyl-L-arginine (5mg/kg, iv, and 10(-3)M in CSF) (n = 10). Substance P dilated arterioles at 10(-10)M through 10(-5)M (maximal response = 23 +/- 3%) (n = 6), and this response was unaffected by indomethacin administration (n = 6). In contrast, NG-methyl-L-arginine blocked much of the pial arteriolar dilation to SP. Unlike the other two peptides, NKA did not change pial arteriolar diameter. Radioimmunoassay determinations indicated that cerebrospinal fluid levels of 6-keto-prostaglandin F1 and prostaglandin E2 did not change appreciably during application of CGRP or SP. We conclude that CGRP and SP but not NKA are dilator stimuli in the piglet pial circulation. Dilation by CGRP probably involves direct activation of receptors on vascular smooth muscle, while SP probably partially dilates pial arterioles via release of an endothelium-dependent relaxing factor.

6-Ketoprostaglandin F1 alpha

Occlusive retinal arteriolitis with neovascularization.

A 34-year-old white woman who had used oral contraceptives for six years showed an occlusive bilateral retinal arteriolitis that resulted in a branch arteriolar occlusion in the right eye and retinal neovascularization. Three years later, we observed active arteriolitis in the left eye with successive occlusion of several branch arterioles. The disease has shown spontaneous remissions and exacerbations. An extensive medical evaluation revealed only old pulmonary granulomatous disease and an elevated sedimentation rate in association with exacerbations of the arteriolitis.

Adult

Fine structure of precapillary arterioles of skeletal muscle in the rat.

The submicroscopic structure of the precapillary arterioles with a diameter of 25-6 mum was followed in m. spinotrapezius of the rat. The walls of the precapillary arterioles of the diameter of 25-20 mum consist of the endothelium, one layer of smooth muscle cells, 3-4 bundles of nerve fibres and a one-layer coat of fibrocytes. Arterioles of the diameter of 20-10 mum have an incomplete fibrocytar coat. Arterioles of the diameter of 10-6 mum also have an incomplete, disseminated muscular layer. The side-branching of true capillaries was not detected. Hence the described arteriolar portion cannot be considered as a metarteriole, but as a regulation device of a segmentary type, regulating the blood flow through the corresponding part of the capillary network as a whole.

Animals

Double afferent arterioles of the rat renal glomerulus as studied by the injection replica scanning electron microscopic method.

One thousand eight hundred and fifty-six specimens of replicated rat renal glomerulus were examined under the scanning electron microscope, and an extremely rare anomaly of the glomerulus with double afferent arterioles was described. The double afferent arterioles arose separately from a terminal twig of the interlobular artery and reached the vascular pole of a subcapsular glomerulus which possessed a single efferent arteriole. Microdissection revealed that this glomerulus was composed of three fairly independent lobules of anastomosing capillaries. Microdissection also revealed that the double afferent arterioles were isolated from each other even in the glomerulus: the one supplied two lobules, while the other the third one only.

Animals

Role of prostaglandins and histamine in reactive hyperemia: in-vivo studies on single mesenteric arterioles.

Direct, in vivo microcirculatory experiments were undertaken with anesthetized rats to determine whether prostaglandin (PG)-like compounds and histamine may mediate post-occlusion hyperemia in single mesenteric arterioles. Superfusion of the mesenteric vasculature with two structurally different PG synthetase inhibitors, indomethacin and 5,8,11,14-eicosatetraynoic acid (ETA), was found to markedly inhibit postocclusion vasodilator responses in arterioles 20-22 micrometer i.d. Superfusion of mesentery with an H2-histamine receptor antagonist, metiamide, resulted in a 40% inhibition of the postocclusion vasodilator responses in arterioles. Superfusion of the mesenteric vasculature with a combination of indomethacin and metiamide resulted in a 95% suppression of the postocclusion dilator responses. Administration of either the PG synthetase inhibitors, metiamide, or a combination of both types of drugs did not, however, influence resting arteriolar tone or responsiveness to PGE1 or epinephrine. Although the results of these experiments implicate a role for PG-like substances and histamine in reactive or postocclusion hypermia, they do not provide evidence for a role of these humoral substances in the normal moment-to-moment regulation of arteriolar tone.

5,8,11,14-Eicosatetraynoic Acid

Responses of pial arterioles after prolonged hypercapnia and hypoxia in the awake rabbit.

The changes in the responsiveness of pial arterioles to CO2 and in the composition of cortical cerebrospinal fluid bathing these vessels were studied in the awake rabbit before and after 6 days exposure to hypercapnia (7% CO2) or hypoxia (10% O2). The vasodilator response of pial arterioles to inhalation of 3--10% CO2 was diminished after prolonged hypercapnia and enhanced after prolonged hypoxia. After both hypoxia and hypercapnia, pial arteriolar responsiveness to CO2 was immediately returned toward control levels by washing the brain surface with normal artificial cerebrospinal fluid. The bicarbonate concentration of cerebrospinal fluid bathing the pial vasculature showed a significant decrease after hypoxia and a significant increase after hypercapnia, whereas CSF pH remained unaltered. We conclude that the alteration in responsiveness of pial arterioles to CO2 is due to a change in the chemical composition of the CSF bathing these vessels, involving an adjustment in the concentration of bicarbonate ions.

Animals

Effects of combined parenchymal and vascular injury on platelet aggregation in pial arterioles of living mice: evidence for release of aggregate-inhibiting materials.

Platelet aggregation was produced in pial arterioles by exposing them to appropriately filtered light from a mercury lamp, following intravascular injection of sodium fluorescein. The dye acted as a target for the radiant energy and initiated a sequence of events resulting in the platelet aggregation. The aggregates adhered to the vessel in which they first appeared. When a microneedle punctured the brain adjacent to a subsequently irradiated arteriole, platelet aggregation was inhibited, even though the arteriole was not touched by the microneedle. Inhibition was manifested by prolongation of the exposure time required for the light-dye stimulus to initiate an adherent aggregate and by lengthening the time required for the aggregate to grow and totally block erythrocyte flow in the affected vessel. It is suggested that a material(s) diffuses from the zone of brain puncture, to and through the arteriolar wall, with a resultant inhibition of aggregation. It is noted that the inhibiting effect is reduced as the distance between puncture and wall increases.

Animals

[The reactivity of the skeletal muscle arterioles of rats to noradrenaline after whole-body gamma irradiation at a dose of 1 Gy].

Male Wistar rats were exposed by total gamma-irradiation at 1 Gy, Reactions of skeletal muscle arterioles and mean arterial pressure on intravenous doses of noradrenaline (0.1, 0.3, 1.0 and 3.0 micrograms/kg) was studied by intravital microscopy in acute experiments 1, 3 and 5-6 days after irradiation. The exposure causes arterial hypotension on day 1 after that as well as marked reduction of spontaneous arteriole vasomotions and decrease of arteriole constrictions at any doses and dates under study. There are no differences of arterial pressure reaction amplitudes in per cent between control and exposed animals at any doses and dates under investigation.

Animals