Showing papers by "Ulf Ekelund published in 1997"
TL;DR: The present findings indicate that the vasconstrictor response to NPY in skeletal muscle is preferentially located in the small arterioles and mediated via the Y1 receptor and, further, that Y2 and Y3 receptors do not play a significant role in the vasoconstrictors response toNPY in cat skeletal muscle.
Abstract: 1 It has been suggested that the vasoconstrictor response to neuropeptide Y (NPY) is located in the microvessels and that it increases with reduced vessel diameter The aim of the present study was to analyse quantitatively, on the cat gastrocnemius muscle preparation in vivo, the effects of NPY on total regional vascular resistance (RT) and its distribution to large-bore arterial resistance vessels (> 25 microns; Ra,prox), small arterioles (< 25 microns; Ra,micro) and the veins (Rv) Associated effects on capillary pressure (Pc,v) and fluid exchange were also studied 2 Close-arterially infused NPY (1-32 micrograms kg-1 min-1) caused a dose-dependent, slowly developing vasoconstriction in all three vascular sections, yet with a preferential action in the small arterioles At 32 micrograms kg-1 min-1, NPY raised RT by 133 +/- 22%, Ra,prox by 94 +/- 15%, Ra,micro by 277 +/- 104% and Rv by 81 +/- 11% However, the veins (ED50 = 39 +/- 12 micrograms kg-1 min-1) were more sensitive to NPY than both large-bore arterial vessels (ED50 = 77 +/- 16) and small arterioles (ED50 = 70 +/- 14) NPY decreased Pc,v due to an increase in the pre-to post-capillary resistance ratio 3 Close-arterial infusions of Pro34NPY and peptide YY evoked vasoconstrictor responses which did not differ from the response to NPY In contrast, the Y2-preferring C-terminal fragments: Ac-[Leu28, Leu31]-NPY (24-36) and NPY(13-36) were without effect in the muscle vascular bed The selective NPY Y1 receptor antagonist BIBP3226 (100 micrograms kg-1 min-1, ia) abolished the vascular response to NPY 4 The present findings indicate that the vasoconstrictor response to NPY in skeletal muscle is preferentially located in the small arterioles and mediated via the Y1 receptor and, further, that Y2 and Y3 receptors do not play a significant role in the vasoconstrictor response to NPY in cat skeletal muscle BIBP3226 was found to be an effective NPY antagonist in vivo and to lack agonist activity
21 citations
TL;DR: Differences between the two groups of animals indicate that nitric oxide release, by its vasodilator action, to a significant extent helps to maintain an adequate nutritional blood supply to the tissues in acute haemorrhage.
Abstract: Our previous studies have indicated that endogenous nitric oxide serves as a physiologically important inhibitor of vascular tone during acute haemorrhage. This vasodilator action attenuates the concomitant reflex adrenergic constriction and thereby prevents critical reduction of tissue blood flow. The present study aimed to evaluate the overall importance of this nitric oxide regulation for survival after acute haemorrhage. This was done by comparative observations of survival time and circulatory, metabolic and histopathological changes after an acute standardized lethal blood loss (45%) in cats exposed to nitric oxide synthase (NOS) inhibition and in matched control animals with intact nitric oxide regulation. NOS inhibition was instituted by intravenously administered N omega-nitro-L-arginine methyl ester. The survival time averaged 2 h 49 min in the NOS-blocked animals and 10 h 14 min in the control animals (P < 0.001). NOS inhibition thus reduced the posthaemorrhagic survival time to < 30% of that in the control cats. Haemorrhage in the NOS-blocked animals led to rapidly developing arterial hypotension, increased anaerobic metabolism, metabolic lactacidosis, hyperkalaemia, and morphological tissue damage especially in heart and liver, in spite of maintained arterial normoxia, which signifies tissue hypoxia caused by seriously impaired nutritional blood supply. At the time of death of the NOS-blocked cats, the control animals still exhibited a virtually normal circulatory/metabolic state. A much later, and more slowly developing circulatory/metabolic deterioration was observed in the control animals. These differences between the two groups of animals indicate that nitric oxide release, by its vasodilator action, to a significant extent helps to maintain an adequate nutritional blood supply to the tissues in acute haemorrhage.
14 citations