Neurovascular function in the rat during pregnancy

1986 ◽  
Vol 251 (5) ◽  
pp. H1000-H1008 ◽  
Author(s):  
J. L. Hart ◽  
W. Freas ◽  
S. M. Muldoon
Keyword(s):  
Electrical Stimulation ◽  
Frequency Response ◽  
Mesenteric Artery ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Receptor Sensitivity ◽  
Maternal Circulation ◽  
Sympathetic Control ◽  
Caudal Artery ◽  
Neuroeffector Junction

Activity of the vascular neuroeffector junction was examined in pregnant (PG) and nonpregnant (NPG) rats to determine whether changes could account for the reported alterations in sympathetic control of the maternal circulation. Caudal and mesenteric arteries were removed from NPG and 19-21 day PG rats and prepared for isometric tension recording. Frequency-response measurements were obtained, followed by norepinephrine (NE) and tyramine concentration-response measurements. The caudal artery developed more tension in response to NE, tyramine, and electrical stimulation than did the mesenteric artery; however, there were no differences between vessels from NPG and PG rats. NE content, [3H]NE accumulation, and effects of plasma on [3H]NE accumulation of NPG and PG caudal arteries were also compared and found to be similar. Therefore, vascular neuroeffector functions of NE release, receptor sensitivity, and NE accumulation are not modified in the rat during pregnancy. Changes in sympathetic control of the maternal circulation are likely to be dependent on alterations at sites other than the neuroeffector junction.

scholarly journals Interaction of Perivascular Adipose Tissue and Sympathetic Nerves in Arteries From Normotensive and Hypertensive Rats

2016 ◽  
pp. S391-S399 ◽  
Author(s):  
J. TÖRÖK ◽  
A. ZEMANČÍKOVÁ ◽  
Z. KOCIANOVÁ
Keyword(s):  
Adipose Tissue ◽  
Electrical Stimulation ◽  
Mesenteric Artery ◽  
Sympathetic Nerves ◽  
Mesenteric Arteries ◽  
Inhibitory Influence ◽  
Hypertensive Rats ◽  
Response Curves ◽  
Perivascular Adipose Tissue ◽  
Endogenous Noradrenaline

The inhibitory action of perivascular adipose tissue (PVAT) in modulation of arterial contraction has been recently recognized and contrasted with the prohypertensive effect of obesity in humans. In this study we demonstrated that PVAT might have opposing effect on sympatho-adrenergic contractions in different rat conduit arteries. In superior mesenteric artery isolated from normotensive Wistar-Kyoto rats (WKY), PVAT exhibited inhibitory influence on the contractions to exogenous noradrenaline as well as to endogenous noradrenaline released from arterial sympathetic nerves during transmural electrical stimulation or after application of tyramine. In contrast, the abdominal aorta with intact PVAT responded with larger contractions to transmural electrical stimulation and tyramine when compared to the aorta after removing PVAT; the responses to noradrenaline were similar in both. This indicates that PVAT may contain additional sources of endogenous noradrenaline which could be responsible for the main difference in the modulatory effect of PVAT on adrenergic contractions between abdominal aortas and superior mesenteric arteries. In spontaneously hypertensive rats (SHR), the anticontractile effect of PVAT in mesenteric arteries was reduced, and the removal of PVAT completely eliminated the difference in the dose-response curves to exogenous noradrenaline between SHR and WKY. These results suggest that in mesenteric artery isolated from SHR, the impaired anticontractile influence of PVAT might significantly contribute to its increased sensitivity to adrenergic stimuli.

Effects of 5-hydroxytryptamine on neuroeffector junction in human pulmonary artery

1981 ◽  
Vol 51 (3) ◽  
pp. 693-698 ◽  
Author(s):  
W. K. Freeman ◽  
D. K. Rorie ◽  
G. M. Tyce
Keyword(s):  
Smooth Muscle ◽  
Electrical Stimulation ◽  
Pulmonary Artery ◽  
Total Radioactivity ◽  
Isometric Tension ◽  
Hydroxytryptamine Receptors ◽  
Human Pulmonary Artery ◽  
Neuroeffector Junction

The effects of 5-hydroxytryptamine on release of norepinephrine and on contraction of smooth muscle in human pulmonary artery were studied. Helical strips were prepared from intra-parenchymal arteries removed 3–18 h after death. The strips were labeled with L-[7–3H]norepinephrine and mounted for superfusion and isometric tension recording. Electrical stimulation (10 V, 2 ms, 2 Hz) of the strips increased the release of total radioactivity; this release was blocked by tetrodotoxin. 5-Hydroxytryptamine (10(-5) M) exerted a cocaine-sensitive, indirect sympathomimetic effect on the overflow of norepinephrine from resting strips. This action was not blocked by methysergide. No effect of 5-hydroxytryptamine on release of norepinephrine from electrically stimulated tissue could be demonstrated. 5-Hydroxytryptamine (10(-5) M) also caused contractions of pulmonary smooth muscle, not blocked by phentolamine (10(-5) M) but mediated in part through methysergide-sensitive 5-hydroxytryptamine receptors.

Increased Ca2+ sensitivity of alpha 1-adrenoceptor-stimulated contraction in SHR caudal artery

1986 ◽  
Vol 250 (2) ◽  
pp. C275-C282 ◽  
Author(s):  
M. B. Aqel ◽  
R. V. Sharma ◽  
R. C. Bhalla
Keyword(s):  
Adrenergic Receptor ◽  
Isometric Tension ◽  
Effective Concentration ◽  
Nerve Terminals ◽  
Receptor Sensitivity ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Caudal Artery ◽  
Wistar Kyoto ◽  
Smooth Muscle Contractions

Potassium and alpha-receptor-stimulated contractile responses of caudal artery rings of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were measured under conditions in which norepinephrine (NE) uptake and K+-induced NE release by nerve terminals were eliminated. The maximum isometric tension developed by SHR arterial rings was significantly more compared with WKY arterial rings when arteries were stimulated with NE but not when stimulated with K+. The Ca2+ sensitivity of NE-stimulated arterial rings was about twofold higher compared with WKY arterial rings. However, the Ca2+ sensitivity of K+-depolarized arterial rings was comparable between WKY and SHR. This increase in Ca2+ sensitivity was specifically due to changes in the alpha 1-receptor-mediated mechanisms in SHR. The 50% effective concentration (EC50) values for both NE and alpha 1-specific agonist, methoxamine hydrochloride, were comparable between WKY and SHR, suggesting that alpha 1-receptor sensitivity is not altered in SHR. The relative contributions of postsynaptic alpha 1- and alpha 2-receptors in caudal artery contractions as calculated from the experiments with alpha 1- and alpha 2-receptor agonist and antagonists were 80 and 20% in WKY and 95 and 5% in SHR, respectively. Nifedipine inhibition of caudal artery contractions was significantly greater (P less than 0.05) in SHR when stimulated with NE but not when stimulated with potassium. Our results indicate that the mechanisms involved in K+ depolarization-dependent contractions are not altered in SHR. However, the mechanisms involved in the coupling of alpha 1-adrenergic receptor and smooth muscle contractions may be altered in SHR caudal artery rings.

scholarly journals Mechanism of the Enhanced Vasoconstrictor Responses to Endothelin-1 in Canine Cerebral Arteries

1991 ◽  
Vol 11 (3) ◽  
pp. 371-379 ◽  
Author(s):  
Chiharu Tanoi ◽  
Yoshio Suzuki ◽  
Masato Shibuya ◽  
Kenichiro Sugita ◽  
Kaoru Masuzawa ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Resting State ◽  
Mesenteric Artery ◽  
Cerebral Arteries ◽  
Mesenteric Arteries ◽  
Free Solution ◽  
Contractile Responses ◽  
Endothelin 1 ◽  
Voltage Dependent ◽  
Small Contraction

Vasoconstrictor effects of endothelin-1 (ET) were investigated in endothelium-denuded strips of cerebral (basilar and posterior cerebral) and mesenteric arteries of the dog. ET produced a concentration-dependent contraction in these arteries. Contractile responses to lower concentrations (below 3 × 10−10 M) of ET were significantly greater in the cerebral arteries than in the mesenteric artery. Inhibition by nifedipine of the contractile responses to ET was greater in the basilar artery than in the mesenteric artery. After the inhibition by 10−7 M nifedipine, the remaining responses to ET were similar in the two arteries. Cerebral arteries, but not the mesenteric artery, relaxed significantly from the resting level when placed in a Ca2+ -free solution containing 0.1 m M EGTA (0-Ca solution). Readdition of Ca2+ to the cerebral arteries placed in the 0-Ca solution caused a biphasic contraction that was sensitive to nifedipine. When 10−9 M ET was introduced before the Ca2+-induced contraction, this peptide produced only a very small contraction, but enhanced the Ca2+-induced contraction. The extent of the enhancement induced by ET was much greater in the cerebral arteries than in the mesenteric artery. These results indicate that the enhanced responses to ET in the cerebral arteries were dependent to a large extent on Ca2+ influx through voltage-dependent Ca2+ channels (VDCs). It is likely that the VDCs in these arteries are more activated in the resting state than those in the mesenteric artery.

Functional changes in adenylyl cyclases and associated decreases in relaxation responses in mesenteric arteries from diabetic rats

2005 ◽  
Vol 289 (5) ◽  
pp. H2234-H2243 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Kentaro Wakabayashi ◽  
Tsuneo Kobayashi ◽  
Katsuo Kamata
Keyword(s):  
Mesenteric Artery ◽  
Diabetic Rats ◽  
Functional Change ◽  
Water Soluble ◽  
Mesenteric Arteries ◽  
Diabetic Rat ◽  
Adenylyl Cyclases ◽  
Camp Production ◽  
Functional Changes ◽  
Rat Mesenteric Artery

To assess the functional change in adenylyl cyclases (AC) associated with the diabetic state, we investigated AC-mediated relaxations and cAMP production in mesenteric arteries from rats with streptozotocin (STZ)-induced diabetes. The relaxations induced by the water-soluble forskolin (FSK) analog NKH477, which is a putative AC5 activator, but not by the β-adrenoceptor agonist isoproterenol (Iso) and the AC activator FSK, were reduced in intact diabetic mesenteric artery. In diabetic rats, however, Iso-, FSK-, and NKH477-induced relaxations were attenuated in the presence of inhibitors of nitric oxide synthase and cyclooxygenase. To exclude the influence of phosphodiesterase (PDE), we also examined the relaxations induced by several AC activators in the presence of 3-isobutyl-1-methylxanthine (IBMX; a PDE inhibitor). Under these conditions, the relaxation induced by Iso was greatly impaired in STZ-diabetic rats. This Iso-induced relaxation was significantly attenuated by pretreatment with SQ-22536, an AC inhibitor, in mesenteric rings from age-matched controls but not in those from STZ-diabetic rats. Under the same conditions, the relaxations induced by FSK or NKH477 were impaired in STZ-diabetic rats. Neither FSK- nor A-23187 (a Ca2+ ionophore)-induced cAMP production was significantly different between diabetics and controls. However, cAMP production induced by Iso or NKH477 was significantly impaired in diabetic mesenteric arteries. Expression of mRNAs and proteins for AC5/6 was lower in diabetic mesenteric arteries than in controls. These results suggest that AC-mediated relaxation is impaired in the STZ-diabetic rat mesenteric artery, perhaps reflecting a reduction in AC5/6 activity.

scholarly journals in vitro Effects of Calcium Antagonists PN 200-110, Nifedipine, and Nimodipine on Human and Canine Cerebral Arteries

1983 ◽  
Vol 3 (3) ◽  
pp. 354-361 ◽  
Author(s):  
E. Müller-Schweinitzer ◽  
P. Neumann
Keyword(s):  
Rank Order ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Organ Bath ◽  
Vasoconstrictor Response ◽  
Dihydropyridine Derivative ◽  
Basilar Arteries ◽  
In Vitro Effects

PN 200–110 [4-(2, 1, 3-benzoxadiazol - 4 -) - 1,4-dihydro - 2,6 - dimethyl - pyridine - 3,5 - dicarboxylic acid methyl 1-methylethyl ester], a new dihydropyridine derivative, was investigated by recording isometric tension on spiral strips from human and canine arteries in tissue baths at 37°C. Responses to increasing concentrations of CaCl2 were investigated in calcium-free depolarizing solution (60 mmol/L KCl in equimolar replacement for NaCl, 50 mmol/L TRIZMA buffer, pH 7.4). Comparison of those concentrations that reduced the vasoconstrictor response to 1.6 mmol/L CaCl2 by 50% revealed the following order of potencies on both human and canine arteries: PN 200–110 > nimodipine > nifedipine. Responses to 5-hydroxytryptamine (5-HT) and blood were investigated in Krebs–Henseleit solution (NaHCO3 buffer). On canine arteries, PN 200–110 antagonized responses to 5-HT when used at 10–30 pmol/L; it was ∼70 times more potent on basilar than on mesenteric arteries, whereas both nifedipine and nimodipine were, respectively, ∼10 and 6 times more potent on basilar than on mesenteric arteries. When canine basilar arteries were constricted by the addition of blood to the organ bath, each of the investigated dihydropyridine derivatives elicited concentration-dependent relaxation, producing the following order of potencies: PN 200–110 > nifedipine = nimodipine. On human anterior cerebral arteries, the blood-induced contractions were counteracted in the following rank order: PN 200–110 = nimodipine > nifedipine. The results suggest that due to its potent calcium-blocking activity on cerebral arteries, PN 200–110 might be of value for the prevention and treatment of cerebrovascular spasms following subarachnoid hemorrhage.

scholarly journals Role of NO in arterial vascular function of intertidal fish (Girella laevifrons) and marine fish (Isacia conceptionis)

2016 ◽  
Vol 76 (2) ◽  
pp. 500-505
Author(s):  
F. A. Moraga ◽  
N. Urriola-Urriola
Keyword(s):  
Nitric Oxide ◽  
Sodium Nitroprusside ◽  
Marine Fish ◽  
Vascular Function ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Response Curves ◽  
Intertidal Fish ◽  
Branchial Arteries

Abstract Previous studies performed in intertidal fish (Girella laevifrons),as well as marine fish (Isacia conceptionis), showed that acetylcholine (ACh) produced contractions mediated by cyclooxygenases that were dependent on the area and potency of contraction in several arterial vessels. Given that the role of nitric oxide is poorly understood in fish, the objective of our study was to evaluate the role of nitric oxide in branchial afferent (ABA), branchial efferent (ABE), dorsal (DA) and mesenteric (MA) arterial vessels from both Girella laevifrons and Isacia conceptionis. We studied afferent and efferent branchial, dorsal and mesenteric arteries that were dissected from 6 juvenile specimens. Isometric tension studies were done using dose response curves (DRC) for Ach (10–13 to 10–3 M) and blockade with L-NAME (10–5 M), and DRC for sodium nitroprusside (SNP, a donor of NO). L-NAME produced an attenuation of the contractile response in the dorsal, afferent and efferent branchial arteries and a potentiation of the contraction in the MA. SNP caused 70% dilation in the mesenteric artery and 40% in the dorsal artery. Our results suggest that Ach promotes precarious dilatation in MA mediated by NO; data that is supported by the use of sodium nitroprusside. In contrast, in the vessels DA, ABA and EBA our results support that the pathway Ach-NO-relaxation is absent in both species.

Sex Differences in the Relation Between Frailty and Endothelial Dysfunction in Old Mice

2021 ◽  
Author(s):  
Jazmin A Cole ◽  
Mackenzie N Kehmeier ◽  
Bradley R Bedell ◽  
Sahana Krishna Kumaran ◽  
Grant D Henson ◽  
...  
Keyword(s):  
Sex Differences ◽  
Endothelial Function ◽  
Vascular Function ◽  
Mesenteric Artery ◽  
Frailty Index ◽  
Mesenteric Arteries ◽  
Male Mice ◽  
Male And Female ◽  
Female Mice ◽  
Age Related

Abstract Vascular endothelial function declines with age on average, but there is high variability in the magnitude of this decline within populations. Measurements of frailty, known as frailty index (FI), can be used as surrogates for biological age, but it is unknown if frailty relates to the age-related decline in vascular function. To examine this relation, we studied young (4-9 months) and old (23-32 months) C57BL6 mice of both sexes. We found that FI was greater in old compared with young mice, but did not differ between old male and female mice. Middle cerebral artery (MCA) and mesenteric artery endothelium-dependent dilation (EDD) also did not differ between old male and female mice; however, there were sex differences in the relations between FI and EDD. For the MCA, FI was inversely related to EDD among old female mice, but not old male mice. In contrast, for the mesenteric artery, FI was inversely related to EDD among old male mice, but not old female mice. A higher FI was related to a greater improvement in EDD with the superoxide scavenger TEMPOL in the MCAs for old female mice and in the mesenteric arteries for old male mice. FI related to mesenteric artery gene expression negatively for extracellular superoxide dismutase (Sod3) and positively for interleukin-1β (Il1b). In summary, we found that the relation between frailty and endothelial function is dependent on sex and the artery examined. Arterial oxidative stress and pro-inflammatory signaling are potential mediators of the relations of frailty and endothelial function.

Abstract P093: Cytochrome B5 Reductase 3 And Xanthine Oxidase Coordinately Regulate Soluble Guanylyl Cyclase Physiological Redox State

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Brittany G Durgin ◽  
Heidi M Schmidt ◽  
Scott A Hahn ◽  
Adam C Straub
Keyword(s):  
Xanthine Oxidase ◽  
Guanylyl Cyclase ◽  
Mesenteric Artery ◽  
Cytochrome B5 ◽  
Pulmonary Arteries ◽  
Soluble Guanylyl Cyclase ◽  
Mesenteric Arteries ◽  
Cytochrome B5 Reductase ◽  
Cgmp Production ◽  
Sgc Activators

In cardiovascular disease, oxidative stress can drive soluble guanylyl cyclase (sGC) heme oxidation resulting in the loss of the sGC heme (apo-sGC), the impairment of nitric oxide (NO) binding and cGMP production, and vasoconstriction. Consequently, a new class of therapeutic compounds sGC activators have been developed which target oxidized and apo-sGC to cause irreversible, NO-independent reactivation of cGMP production and vasodilation. While sGC activators have had varied clinical success, surprisingly few studies have defined the impact of NO-independent sGC activation on vascular physiology in healthy conditions. We found mesenteric and pulmonary arteries are two log orders more sensitive to NO-independent sGC activator BAY 58-2667 induced vasodilation than aorta; no difference in NO-dependent sGC vasodilation between vessels was observed. These data indicate the presence of an activatable physiological pool of oxidized and/or apo-sGC in pulmonary and mesenteric arteries. We recently published that smooth muscle cell cytochrome b5 reductase 3 (CYB5R3) acts to reduce oxidized heme sGC back to its NO-sensitive reduced heme state during vascular disease. We found transgenic CYB5R3 overexpression (CYB5R3 OE) mice were more resistant to BAY 58-2667 mesenteric artery vasodilation and blood pressure lowering compared to wild-type controls (n=5-9) under physiologic conditions. Also, healthy CYB5R3 OE pulmonary arteries had a near complete loss of BAY 58-2667 vasodilation suggesting both mesenteric and pulmonary arteries contain a pool of oxidized sGC. We next asked if physiological H 2 O 2 production accounts for changes in BAY 58-2667 responsiveness. We found using mitochondrial-specific catalase overexpression mice, that BAY 58-2667 vasodilation did not differ from controls in any vascular bed (n=4-6). We next tested whether xanthine oxidase (XO), which can produce H 2 O 2 at the endothelial cell surface of vessels, can impact physiological BAY 58-2667 vasodilation. We found that Febuxostat, a XO inhibitor, led to a significant decrease in mesenteric artery BAY 58-2667 induced vasodilation from ~70% to ~30% (n=6). Combined, these data provide evidence for CYB5R3 and XO as regulators of physiological sGC resistance artery vasodilation.

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