0000000000115537
AUTHOR
Steffen-sebastian Bolz
Nitric Oxide Opposes Myogenic Pressure Responses Predominantly in Large Arterioles In Vivo
Abstract —A myogenic vasoconstriction may amplify the effects of circulating vasoconstrictors. In cremaster arterioles, the contribution of a myogenic component to the constriction on intravenous infusion of norepinephrine (NE) or angiotensin II (Ang II) was studied. Second, the role of endothelium-derived nitric oxide (NO) in the control of these myogenic constrictions and its site of action in the resistance vascular bed was investigated. In 30 anesthetized (pentobarbital) hamsters, the cremaster was prepared for intravital microscopy, and a pneumatic vessel occluder was placed around the aorta to vary blood pressure in the hindquarter of the animal. Intravenous infusion of NE (0.5 nmol/…
Pentobarbital-sensitive EDHF comediates ACh-induced arteriolar dilation in the hamster microcirculation
It is unclear to what extent the endothelium-derived hyperpolarizing factor (EDHF) contributes to the control of microcirculatory blood flow in vivo. We analyzed, by intravital microscopy in hamster muscles, the potential role of EDHF along the vascular tree under stimulated (ACh) or basal conditions. Experiments were performed in conscious as well as anesthetized (pentobarbital, urethan) animals. Additionally, cellular effects of the potential EDHF were studied in isolated small arteries. In pentobarbital-anesthetized animals, treatment with N ω-nitro-l-arginine (l-NNA; 30 μmol/l) and indomethacin (3 μmol/l) reduced the dilation in response to 10 μmol/l ACh from 60 ± 6 to 20 ± 4%. This ni…
Elevation of plasma viscosity induces sustained NO-mediated dilation in the hamster cremaster microcirculation in vivo
We studied whether a flow-independent increase of luminal wall shear stress (WSS) could dilate hamster arterioles in vivo and which endothelial mediators are potentially involved. To this end the plasma viscosity was elevated by exchanging blood for dextran-erythrocyte solution thereby augmenting WSS. Diameters of small and large arterioles as well as red blood cell velocities were measured before and after exchange of blood for solutions of identical haematocrit containing either high- (HMWD) or low-molecular weight dextran (LMWD). The potential role of endothelial autacoids was investigated by local application of the NO-synthase inhibitor NG-nitro-L-arginine (L-NNA), the inhibitor of cyc…
Indomethacin enhances endothelial NO release — evidence for a role of PGI2 in the autocrine control of calcium-dependent autacoid production
Objective: We studied whether NO or prostacyclin (PGI2), which are continuously released by endothelial cells, have autocrine/paracrine effects on the calcium-dependent autacoid production by modulating the intracellular Ca2+ concentration ([Ca2+]i). Methods: Histamine(His)-induced [Ca2+]i increases (Fura 2-method) and NO-dependent cGMP increase were measured in human umbilical vein endothelial cells (HUVECs) before and after cyclooxygenase inhibition or application of cAMP- and cGMP-elevating drugs. Results: 0.3 μM His increased endothelial [Ca2+]i from 77±2 nM to 418±59 nM. The His-induced [Ca2+]i increases were significantly attenuated following treatment with PGI2 (by 23%) and forskolin…
Myogenic effects enhance norepinephrine constriction: Inhibition by nitric oxide and felodipine
Myogenic effects enhance norepinephrine constriction: Inhibition by nitric oxide and felodipine. Myogenic, pressure-induced vasoconstriction may amplify the effects of circulating vasoconstrictors. Through intravital microscopy in cremaster arterioles (31 to 115 μm diameter), the relative contribution of myogenic responses (MR) to norepinephrine (NE)-induced constriction and the inhibitor potency of nitric oxide (NO) or a Ca2+ entry blocker (CEB), felodipine (F), were examined. In 24 anesthetized hamsters, a vessel occluder was placed around the aorta to control cremaster vessel inflow pressure (IP). NE infusion increased blood pressure (by 50 ± 2mm Hg) and induced significant constriction …