PubMed Health⌕ Search

Biomedical subjects

A Modin

Publications and source records attributed to A Modin.

25 records · Page 2Linked to original sources
PubMed1993

Neuropeptide Y and differential sympathetic control of splenic blood flow and capacitance function in the pig and dog.

The roles of different mediators in the sympathetic regulation of the pig and dog spleens were investigated using a preparation with intact vascular perfusion in vivo. Sympathetic nerve stimulation caused overflow of neuropeptide Y-like immunoreactivity (NPY-LI) and noradrenaline (NA), arterial vasoconstriction, increase in venous blood flow and haematocrit. The dog spleen responded to single impulse stimulation, whereas more prolonged stimulation was required to elicit vascular responses in the pig spleen. Furthermore, the maximal splenic capacitance response was about 10 times larger in the dog than in the pig. After depletion of neuronal NA content by reserpine combined with preganglionic denervation, about 70% of the splenic arterial vasoconstrictor responses in the dog and pig still remained at 5 Hz stimulation. Fifty per cent of the capacitance response evoked by nerve stimulation still remained in the pig while in the dog spleen the capacitance response was virtually abolished after reserpine. The stimulation-evoked overflow of NPY-LI in pig spleen was increased several fold after reserpine treatment as compared to controls reaching levels in the venous effluent where exogenous NPY evokes vasoconstriction. In the dog spleen, overflow of NPY-LI was only observed after reserpine. Administration of NA caused arterial vasoconstriction with an initial increase in venous blood flow while NPY mainly reduced arterial blood flow. It is concluded that NA is involved in both the splenic arterial vasoconstriction and the capacitance responses while a non-adrenergic splenic vasoconstriction at least in the pig may be mediated by NPY.

Animals↗
PubMed1993

Sympathetic regulation of skeletal muscle blood flow in the pig: a non-adrenergic component likely to be mediated by neuropeptide Y.

The sympathetic regulation of blood flow in the skeletal muscle of the pig hind limb was investigated. Electrical stimulation of the lumbar sympathetic nerve with single impulses under control conditions decreased hind limb vascular conductance by 32%. After reserpine treatment combined with interruption of the sympathetic nerve activity in order to deplete the noradrenaline (NA) content, about 25% of the vasoconstrictor responses to single impulse stimulation still remained. In addition, an atropine sensitive dilatory component in the vascular response was also observed after reserpine treatment. Furthermore, intermittent stimulation with 20 Hz bursts (for 2 min) after reserpine caused a large vasoconstriction which was about 80% of the control response and lasted twice as long (about 15 min). This response was not affected by administration of the alpha-adrenoceptor antagonist phenoxybenzamine or the stable ATP-analogue alpha, beta-methylene-ATP. Furthermore, in the reserpine pretreated pigs 20 Hz burst stimulation caused detectable overflow of neuropeptide Y (NPY)-like immunoreactivity while NA release was reduced by 90%. Intra-arterial administration of the NPY analogues [Leu31Pro34]NPY (Y1-receptor agonist) and NPY(13-36) (Y2-receptor agonist) evoked dose dependent and long-lasting vasoconstriction, whereby the Y1 agonist was about 10-fold more potent than the Y2 agonist. In conclusion, the sympathetic regulation of the pig hind limb vasculature involves adrenergic, cholinergic and non-adrenergic mechanisms. Several indirect lines of evidence suggest that the non-adrenergic constrictor component, which is present even upon single impulse stimulation, is caused by NPY, possibly acting on Y1 receptors.

Animals↗
PubMed1993

Contractile effects of endothelin 1 and endothelin 3 on myometrium and small intramyometrial arteries of pregnant women at term.

This in vitro study was undertaken to investigate the effects of endothelin 1 (ET-1) and endothelin 3 (ET-3) on intramyometrial arteries and myometrial tissue of the uterus from pregnant women at term. Segments of small myometrial arteries (outer diameter 100-500 microns) obtained at cesarean section were isolated and mounted in tissue chambers. The effect of ET-1 and ET-3 on isometric tension was compared with the action of noradrenaline. In similar experiments on myometrial strips, the effect of ET-1 and ET-3 was studied in comparison with oxytocin. ET-1 and ET-3 both produced contractions of arteries and myometrial strips, ET-1 being the most potent. The response of ET-1 was more powerful than the effect of the reference compounds, i.e. noradrenaline with regard to myometrial arteries and oxytocin with regard to the myometrium. It is concluded that endothelins are powerful constrictors of myometrial arteries from pregnant women and possess strong oxytocic effects. In particular, ET-1 could be involved in the regulation of myometrial contractility and/or uteroplacental blood flow.

Adult↗
PubMed1992

No effect of D-myo-inositol-1,2,6-triphosphate on vasoconstriction evoked by neuropeptide Y and non-adrenergic sympathetic nerve stimulation.

The effects of the proposed neuropeptide Y (NPY) antagonist, D-myo-inositol-1,2,6-triphosphate (PP56), on vasoconstrictor responses evoked by NPY and non-adrenergic sympathetic nerve stimulation were investigated in the pig in vivo. Under control conditions, exogenous NPY evoked a dose-dependent increase in arterial blood pressure and vasoconstriction in spleen, kidney and skeletal muscle. After administration of PP56 (50 mg/kg), which transiently reduced systemic blood pressure by 18 +/- 5 mm Hg, the vascular responses evoked by NPY did not differ from those observed under control conditions. Stimulation of the splenic nerve and the lumbar sympathetic chain with 20-Hz burst activity in reserpine-pretreated pigs, which are devoid of their noradrenaline content, decreased splenic and hindlimb vascular conductance by 67 +/- 7 and 57 +/- 7%, respectively, under control conditions. In the presence of PP56 the nerve stimulation-evoked reductions in splenic and hindlimb vascular conductance were slightly but not significantly reduced to 59 +/- 9 and 48 +/- 7%, respectively. It is concluded that PP56 in the presently used high dose, which causes non-selective inhibition of vasoconstriction in the rat, cannot be used as an antagonist of vasoconstrictor responses evoked by NPY or non-adrenergic sympathetic nerve stimulation in the pig.

Animals↗
PubMed1991

Evidence for two neuropeptide Y receptors mediating vasoconstriction.

The presence of receptor subtypes mediating the vascular and prejunctional effects of neuropeptide Y (NPY) was investigated using the Y2 receptor agonist, NPY-(13-36), and the Y1 agonist, [Leu31,Pro34]NPY. NPY-(1-36) and [Leu31,Pro34]NPY administered i.v. to anesthetized pigs evoked dose-dependent increases in mean arterial blood pressure and splenic and renal vascular resistance, and a decrease in heart rate. The potency of [Leu31,Pro34]NPY was 10-30% that of NPY-(1-36). In the spleen, NPY-(13-36) evoked vasoconstriction similar to that evoked by [Leu31,Pro34]NPY, but did not significantly increase renal vascular resistance or mean arterial blood pressure. Local intra-arterial administration of [Leu31,Pro34]NPY caused an increase in nasal mucosal vascular resistance with a potency similar to that of NPY-(13-36) evoked only a minor (17%) increase in nasal mucosal vascular resistance. The NPY analogues were further characterized in receptor binding studies on pig spleen membranes. Compared to NPY-(1-36), 800 times higher concentrations of [Leu31,Pro34]NPY, and 7 times higher concentrations of NPY-(13-36) were required to achieve the same 50% displacement of [125I]NPY-(1-36). Electrically evoked contractions in rat vas deferens were inhibited by 50% by 0.05 microM NPY-(1-36) and 0.3 microM NPY-(13-36), while [Leu31,Pro34]NPY only slightly attenuated the contractions (by 24% at 1 microM). The present data suggest the existence of subtypes of NPY receptors mediating vasoconstriction. Thus, the splenic vascular bed of the pig contains both Y1 and Y2 receptors while the Y1 subtype predominates in the kidney, nasal mucosa and for blood pressure control. The prejunctional receptor in rat vas deferens seems to be of the Y2 subtype.

Animals↗
PubMed1991

Phosphoramidon inhibits the vasoconstrictor effects evoked by big endothelin-1 but not the elevation of plasma endothelin-1 in vivo.

Intravenous injections of big endothelin (ET)-1 (700 pmol/kg) in the pig increased arterial plasma levels of ET-1-like immunoreactivity (ET-1-LI) from 11.1 +/- 0.7 pM to 46.3 +/- 6.7 pM in the control situation and from 11.5 +/- 0.4 pM to 58.2 +/- 17 pM in the presence of the neutral endopeptidase inhibitor phosphoramidon (3 mg/kg). Big ET-1 increased splenic vascular resistance by 29% in the control situation. The vasoconstriction evoked by big ET-1 in the spleen was reduced after phosphoramidon treatment whereas the elevation of arterial ET-1-LI was not influenced. Furthermore the splenic vasoconstriction evoked by ET-1 was reduced after phosphoramidon without influencing plasma ET-1-LI. Also in rats the pressor effect of big ET-1 (1 nmol/kg) was inhibited by phosphoramidon (5 mg/kg) whereas the elevation of plasma ET-1 was not influenced. It is concluded that the vasoconstrictor effects of both big ET-1 and ET-1 are inhibited, but the increase in plasma ET-1 is unaffected by phosphoramidon.

Animals↗