Contraction and endothelium-dependent relaxation in mesenteric microvessels from pregnant rats
| Autor: | Marshall D. Lindheimer, I. F. Pascoal, C. Nalbantian-Brandt, J. G. Umans |
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| Rok vydání: | 1995 |
| Předmět: |
medicine.medical_specialty
Contraction (grammar) Physiology Vasodilation Arginine Nitroarginine Microcirculation Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Phenylephrine Pregnancy Physiology (medical) Internal medicine medicine Animals Vasoconstrictor Agents Splanchnic Circulation Mesenteric arteries reproductive and urinary physiology Acetylcholine Rats medicine.anatomical_structure Endocrinology chemistry Vasoconstriction Anesthesia Blood Vessels Pregnancy Animal Female Endothelium Vascular medicine.symptom Nitric Oxide Synthase Cardiology and Cardiovascular Medicine medicine.drug |
| Zdroj: | The American journal of physiology. 269(6 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | We assessed KCl- and phenylephrine (PE)-induced vasoconstriction as well as acetylcholine (ACh)-induced endothelium-dependent vasodilation in small, isometrically mounted mesenteric arteries from virgin and gravid rats, studied in the absence and presence of NG-nitro-L-arginine (L-NNA). Neither maximal vasoconstriction nor PE potency differed significantly between vessels from virgin and pregnant rats, either in the absence or presence of L-NNA. L-NNA resulted in similar twofold leftward shifts in the PE dose-response curves for both groups. ACh-induced relaxation was potentiated in vessels from gravid rats (half-maximum effective concentration = 0.25 vs. 0.04 microM, virgin and gravid rats, respectively). After L-NNA, maximal relaxation was inhibited significantly more in vessels from gravid rats (62 vs. 31%). Likewise, maximal slope of ACh dose-response curves and ACh potency were decreased in this group so that values no longer differed from those in virgins. We conclude that pregnancy does not alter basal nitric oxide (NO) synthesis in these isolated microvessels, but it does enhance ACh-induced NO release, while apparently inhibiting the action of a NO-independent, endothelium-derived vasodilator. |
| Databáze: | OpenAIRE |
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