| 1. |
- Mulvany, M J, et al.
(author)
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Are isolated femoral resistance vessels or tail arteries good models for the hindquarter vasculature of spontaneously hypertensive rats?
- 1982
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In: Acta physiologica Scandinavica. - : Wiley. - 0001-6772 .- 1365-201X. ; 116:3, s. 275-83
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Journal article (peer-reviewed)abstract
- We have investigated the extent to which the properties of small arteries from the hindquarters of spontaneously hypertensive rats (SHRs) are consistent with the characteristics of perfused SHR hindquarter preparations (for which the relaxed vascular resistance, the reactivity and the sensitivity are reported to be increased). We have therefore compared the in vitro morphological and pharmacological properties of a femoral resistance vessel (i.d. ca 200 microns) and of the tail artery (i.d. ca 600 microns) from SHRs with those from control Wistar-Kyoto rats (WKYs). When relaxed, for any given wall tension, the internal circumference of the SHR resistance vessels was reduced, but that of the SHR tail artery was normal. When activated with 10 microM noradrenaline, the SHR resistance vessels had an increased calcium sensitivity, but the calcium sensitivity of the SHR tail arteries was normal. However, the maximum response of both types of SHR vessels was such that the vessels would have been able to contract against increased transmural pressure. The noradrenaline sensitivity of the SHR resistance vessels was normal but the SHR tail arteries had a decreased sensitivity. The results suggest that the femoral resistance vessel is in general a better model for the hindquarter vasculature than the tail artery.
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| 2. |
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| 3. |
- Mulvany, M J, et al.
(author)
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Effect of sodium-potassium-dependent ATPase inhibition on noradrenaline-activated calcium sensitivity of mesenteric resistance vessels in adult spontaneously hypertensive rats.
- 1980
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In: Clinical science (London, England : 1979). - 0143-5221. ; 59 Suppl 6
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Journal article (peer-reviewed)abstract
- 1. We have investigated the noradrenaline-activated calcium sensitivity of 150 micrometer mesenteric resistance blood vessels from spontaneously hypertensive and control Wistar-Kyoto rats. 2. Under control conditions the spontaneously hypertensive rat blood vessels had a greater calcium sensitivity than the Wistar-Kyoto rat vessels. 3. In the presence of 1 mmol of ouabain/l, a treatment known to inhibit the sodium-potassium-dependent ATPase, the responses of the spontaneously hypertensive rat blood vessels were reduced more than those of the Wistar-Kyoto rat blood vessels, so that the responses of spontaneously hypertensive rat and Wistar-Kyoto rat blood vessels were then similar. 4. Similar results were obtained by removing external potassium, a procedure which should also inhibit the sodium-potassium-ATPase. 5. The results suggest that the greater noradrenaline-activated calcium sensitivity of spontaneously hypertensive rat blood vessels may be associated with an increased sodium-potassium-ATPase activity.
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| 4. |
- Mulvany, M J, et al.
(author)
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Potentiating and depressive effects of ouabain and potassium-free solutions on rat mesenteric resistance vessels.
- 1982
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In: Circulation research. - 0009-7330. ; 51:4, s. 514-24
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Journal article (peer-reviewed)abstract
- We have investigated the in vitro effects of ouabain and K-free solutions on some pharmacological and electrophysiological properties of rat mesenteric resistance vessels (internal diameter approximately 190 micrometers). Vessels were mounted as ring preparations on a myograph capable of measuring their isometric wall tension. In normal saline solutions, vessels did not exhibit any tone and had a membrane potential of -54 mV. Both 1 mM ouabain and K-free solutions caused a transient depolarization of 5-8 mV; thereafter the membrane slowly depolarized to about -45 mV after 30 minutes. There was no mechanical response to ouabain, but K-free solutions caused a transient development of tension which could be inhibited by phentolamine (1 microM). In norepinephrine-activated vessels, exposure to ouabain or K-free solutions caused a small depolarization and an increase in tension. Long-term (30-minute) exposure to 1 mM ouabain or K-free solutions reduced the amplitude of norepinephrine responses and, for the lower (but not the higher) norepinephrine concentrations, the membranes were about 14 mV more depolarized than control. The mechanical responses to a cocktail of norepinephrine in a high potassium solution were, however, unaffected. Re-exposure to normal saline solution produced a transient hyperpolarization and transiently eliminated the norepinephrine response, but thereafter the membrane potential and response returned to normal. The results indicate that ouabain and K-free solutions can have both short-term potentiating and long-term depressive effects on the mechanical response of rat mesenteric resistance vessels to norepinephrine.
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| 5. |
- Mulvany, M J, et al.
(author)
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Role of membrane potential in the response of rat small mesenteric arteries to exogenous noradrenaline stimulation.
- 1982
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In: The Journal of physiology. - 0022-3751. ; 332, s. 363-73
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Journal article (peer-reviewed)abstract
- 1. We have made simultaneous measurements of membrane potential and wall tension in rat 200 microns mesenteric arteries. 2. The resting membrane potential was -59.2 +/- 0.4 mV and stable (218 measurements, fifty-two vessels). 3. With maximal exogenous noradrenaline stimulation (10 microM) the membrane depolarized to about -34 mV. During the onset of tension development oscillations (period about 6 sec) in both tension and membrane potential were often seen; the membrane potential changes led the tension changes by about 1.2 sec. 4. In the presence of increased K+ (e.g. 40 mM), vessels had an increased noradrenaline sensitivity, and here noradrenaline stimulation produced little change in membrane potential. 5. With maximal K+ stimulation (85 mM), in the presence of phentolamine (1 microM), the membrane depolarized to about -17 mV, the tension being about 70% of the maximal noradrenaline response. 6. In the presence of phentolamine (1 microM), noradrenaline caused hyperpolarization without tension development. The hyperpolarization was inhibited by propranolol and mimicked by isoprenaline. 7. The results suggest that in these small vessels membrane potential variations are not essential to, but have an important modulating influence on, the tension response to exogenous noradrenaline.
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| 6. |
- Nilsson, Holger, 1956, et al.
(author)
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Extent of structurally reduced venous distensibility in rats.
- 1981
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In: Clinical science (London, England : 1979). - 0143-5221. ; 61 Suppl 7
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Journal article (peer-reviewed)abstract
- 1. Venous pressure--volume relations were studied in maximally vasodilated whole-body preparations after cardiac arrest, as well as in fully vasodilated, perfused hindquarter preparations of spontaneously hypertensive rats (SHR) and normotensive controls. Central venous pressures were measured also in the anaesthetized animals before cardiac arrest. 2. Central venous pressure in intact, anaesthetized SHR was 1.9 +/- 0.20 mmHg compared with 0.75 +/- 0.25 in controls (P less than 0.001). 3. In both preparations SHR showed a nearly 20% reduction in venous compliance, whereas calculated 'unstressed' volumes (volumes at zero transmural pressure) were largely equal in SHR and controls. 4. SHR capacitance vessels thus appear to have a structurally reduced wall distensibility of about 10% with no change in overall size. It probably reflects a structural adaptation to a modest increase of average transmural pressure that also affects the low-pressure side.
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| 7. |
- Nilsson, Holger, 1956, et al.
(author)
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Prolonged exposure to ouabain eliminates the greater norepinephrine-dependent calcium sensitivity of resistance vessels in spontaneously hypertensive rats.
- 1981
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In: Hypertension (Dallas, Tex. : 1979). - 0194-911X. ; 3:6, s. 691-7
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Journal article (peer-reviewed)abstract
- The effects of 30 minutes of exposure to ouabain on calcium sensitivity have been investigated in two types of resistance vessels from 12 pairs of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Branches of the superior mesenteric and femoral arteries, with internal diameters of about 200 micrometer, were mounted as ring preparations in a myograph capable of measuring their isometric wall tension. Dose-response curves for calcium upon norepinephrine stimulation were determined under conditions where neuronal uptake was eliminated. Initially, when stimulated with norepinephrine, the SHR vessels from both locations were more sensitive to calcium and had stronger contractions than their controls. The addition of ouabain (1 mM) to the relaxed vessels immediately elicited a moderate, transient contraction in the branches of the femoral artery, whereas no response was observed in the mesenteric vessels. Although the addition of ouabain to activated vessels produced an immediate potentiation of the response, prolonged (30-minute) exposure to ouabain reduced active tension development upon norepinephrine stimulation in all vessels. The reduction was greatest in the SHR vessels, so that, under these conditions, the norepinephrine-activated calcium sensitivity of corresponding SHR and WKY vessels was similar. By contrast, responses to norepinephrine in high potassium solution were unaffected. The results suggest that under normal conditions, SHR vessels may have a specific increase in the permeability of the norepinephrine-activated calcium channels. Prolonged exposure to ouabain appears to reduce the permeability of these channels, providing an explanation for why this treatment eliminates the difference in calcium sensitivity of the SHR and WKY vessels.
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