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Digitale Medien

Substance P and calcitonin gene-related peptide: immunohistochemical localisation and microvascular effects in rabbit skeletal muscle (1987)

Öhlen, A. ; Liudbom, L. ; Staines, W. ; [weitere]

Springer

Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 87-93

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ISSN: 1432-1912

Schlagwort(e): Substance P ; CGRP ; Immunohistochemistry ; Microcirculation ; Vasodilation

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: Summary 1. The distribution and microvascular effects of substance P (SP) and calcitonin gene-related peptide (CGRP) were studied in the rabbit tenuissimus muscle using immunohistochemistry and intravital microscopy. 2. Individual fibers within nerve bundles and along blood vessels in the muscle were found to be immunoreactive (IR) for both SP and CGRP, thus showing an apparently complete coexistence for these peptides. In dorsal root ganglia most SP-positive cells were also CGRP-IR, but the latter cells were somewhat more numerous than SP-IR cells. 3. When applied topically to the muscle, both SP and CGRP increased blood flow in a dose-dependent manner, but CGRP was more potent and caused responses of longer duration. Both SP and CGRP dilated transverse arterioles, but they had little or no effect on the smaller terminal arterioles. This resulted in a redistribution of blood flow to the connective tissue adjacent to the muscle. 4. SP, but not CGRP, elicited vigorous vasomotion in larger arterioles and caused the formation of aggregates of platelets and leukocytes in the venules. Neither flow increase, nor vasomotion or aggregate formation were influenced by pretreatment of the animals with mepyramine, cimetidine or indomethacin. Capsaicin (1 μM) had a powerful effect on transverse arterioles resembling that of both SP and CGRP. 5. It is concluded that some of the vascular effects hitherto ascribed to SP on the basis of nerve stimulation and application of capsaicin might, at least in part, be due to release of CGRP.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00177756

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Digitale Medien

Role of adenosine in functional hyperemia in skeletal muscle as indicated by pharmacological tools (1991)

Persson, M. G. ; Öhlén, A. ; Lindbom, L. ; [weitere]

Springer

Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 52-57

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ISSN: 1432-1912

Schlagwort(e): Adenosine ; Microcirculation ; Post-exercise hyperemia ; Skeletal muscle ; Theophylline derivatives

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: Summary The hypothesis that adenosine mediates blood flow increments in contracting skeletal muscle was evaluated by intravital microscopy of the microcirculation in the tenuissimus muscle of anesthetized rabbits. Motor nerve stimulation elicited muscle contractions and frequency-dependent arteriolar dilatation, particularly in terminal arterioles. The pulse duration (0.05 ms) and voltage (1.5–5 V) precluded activation of vasoconstrictor fibers, as also indicated by the lack of effect of phentolamine on resting vascular tone and on the hyperemic response to nerve stimulation. The specific adenosine receptor antagonist, 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX; 10−5 M), attenuated the hyperemic response to muscle contractions. The adenosine uptake inhibitor dipyridamole (10−8−10−6 M) dose-dependently dilated microvessels, an effect prevented by DPSPX (10−5 M). Moreover, dipyridamole (10−7 M) augmented contraction-induced hyperemia. The enhancement by dipyridamole was reversed by DPSPX (10−5 M). The effects of adenosine uptake inhibitor and antagonist were invariably more marked in terminal than in transverse arterioles, and also more pronounced at higher stimulation frequencies. Motor nerve stimulation failed to induce alterations in vascular diameters when the neuromuscular junction was blocked by pancuronium. Thus, our observations indicate that functional hyperemia after motor nerve-induced contractions of the skeletal muscle was of postjunctional origin. Apparently, activation of adenosine receptors was responsible for a part of the evoked vasodilation.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00180676

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