ANG II modifies cardiomyocyte function via extracardiac and intracardiac neurons: in situ and in vitro studies

1997 ◽  
Vol 272 (3) ◽  
pp. R766-R775 ◽  
Author(s):  
M. Horackova ◽  
J. A. Armour
Keyword(s):  
Guinea Pig ◽  
Receptor Antagonist ◽  
Neuronal Activity ◽  
Ang Ii ◽  
Arterial Blood ◽  
Cardiac Ganglia ◽  
In Situ Experiments ◽  
Anesthetized Dogs

To determine whether angiotensin II (ANG II) affects cardiac performance via neurons in intrathoracic cardiac ganglia, studies were performed on anesthetized dogs. To exclude possible vascular regulatory effects of ANG II, experiments were also performed using long-term cultures of adult guinea pig ventricular cardiomyocytes with or without intrathoracic neurons. 1) In in situ experiments in 10 anesthetized dogs, cardiac augmentation occurred when ANG II (10 microl or 0.1 ml; 10-100 microM) was administered into limited loci within acutely decentralized stellate or middle cervical ganglia that were neurally connected to, but not those disconnected from, the heart. In another 18 dogs, ANG II increased intrinsic cardiac neuronal activity when administered adjacent to such neurons or into their local arterial blood supply. Ventricular ionotropic effects elicited by ANG II were eliminated by timolol, whereas increases in intrinsic cardiac neuronal activity were not affected. Effects elicited by ANG II were eliminated by administration of a selective AT1 receptor antagonist (losartan) but not by a selective AT2 receptor antagonist (PD-123319). 2) In in vitro experiments, ANG II (100 nM) induced positive chronotropic effects on cultured adult guinea pig cardiomyocytes innervated with adult extrinsic or intrinsic cardiac neurons, but not those cultured without neurons. The frequency of calcium inward current (Ca(i)) transients (recorded by fura 2 fluorescence) increased in innervated cocultures but not in the noninnervated cardiomyocyte cultures; however, the amplitude of Ca(i) transients was not affected by ANG II in cultures or in freshly isolated adult guinea pig cardiomyocytes. ANG II-induced effects in cocultures were blocked by losartan but not PD-123319 or timolol. Thus 1) ANG II-sensitive neurons exist in intrathoracic extracardiac and intrinsic cardiac ganglia; 2) these neurons possess AT1 receptors; and 3) these neurons appear to act directly and indirectly via adrenergic neurons to enhance cardiomyocyte function.

Decreased endothelium-dependent relaxation in subarachnoid hemorrhage-induced vasospasm: role of ET-1

1995 ◽  
Vol 269 (3) ◽  
pp. H1009-H1015 ◽  
Author(s):  
M. Zuccarello ◽  
A. Romano ◽  
M. Passalacqua ◽  
R. M. Rapoport
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Receptor Antagonist ◽  
Basilar Artery ◽  
Arterial Blood ◽  
Eta Receptor ◽  
Eta Receptor Antagonist ◽  
Endothelium Dependent Relaxation

The purpose of this study was to test whether endothelium-dependent relaxation is decreased during acute vasospasm following subarachnoid hemorrhage (SAH) and the mechanism underlying the decrease. Basilar artery in situ was 35% constricted 3 days following injection of autologous arterial blood into the rabbit cisterna magna compared with vessels from control rabbits. In situ suffusion with the endothelium-dependent relaxant, acetylcholine (ACh; 10 microM), relaxed resting and serotonin (5-HT)-contracted control vessels but not vasospastic and 5-HT-contracted vasospastic vessels. In contrast, the relaxant potency and efficacy of ACh was similar in control and vasospastic vessels contracted with 5-HT in vitro. In situ suffusion with the ETA-receptor antagonist, BQ-123 (1 microM), reversed the vasospasm by 51% and restored the magnitude of ACh relaxation of vasospastic and 5-HT-contracted vasospastic vessels to that of controls. ACh in situ and in vitro relaxed endothelin-1 (ET-1)-contracted control vessels to a smaller magnitude than 5-HT-contracted control vessels. These results suggest, in contrast to previous studies, that endothelium-dependent relaxation is decreased during acute vasospasm following SAH. The decreased endothelium-dependent relaxation is secondary to the underlying ET-1-mediated spasm. The inhibition of endothelium-dependent relaxation observed in situ following SAH cannot be demonstrated in vitro, presumably due to loss of the ET-1-mediated vasospasm.

Ion channel modifying agents influence the electrical activity generated by canine intrinsic cardiac neurons in situ

2000 ◽  
Vol 78 (4) ◽  
pp. 293-300 ◽  
Author(s):  
Gregory W Thompson ◽  
Magda Horackova ◽  
J Andrew Armour
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Neuronal Activity ◽  
Barium Chloride ◽  
Nickel Chloride ◽  
Blocking Agent ◽  
Right Atrial ◽  
Anesthetized Dogs

This study was designed to establish whether agents known to modify neuronal ion channels influence the behavior of mammalian intrinsic cardiac neurons in situ and, if so, in a manner consistent with that found previously in vitro. The activity generated by right atrial neurons was recorded extracellularly in varying numbers of anesthetized dogs before and during continuous local arterial infusion of several neuronal ion channel modifying agents. Veratridine (7.5 µM), the specific modifier of Na+-selective channels, increased neuronal activity (95% above control) in 80% of dogs tested (n = 25). The membrane depolarizing agent potassium chloride (40 mM) reduced neuronal activity (43% below control) in 84% of dogs tested (n = 19). The inhibitor of voltage-sensitive K+ channels, tetraethylammonium (10 mM), decreased neuronal activity (42% below control) in 73% of dogs tested (n = 11). The nonspecific potassium channel inhibitor barium chloride (5 mM) excited neurons (47% above control) in 13 of 19 animals tested. Cadmium chloride (200 µM), which inhibits Ca2+-selective channels and Ca2+-dependent K+ channels, increased neuronal activity (65% above control) in 79% of dogs tested (n = 14). The specific L-type Ca2+ channel blocking agent nifedipine (5 µM) reduced neuronal activity (52% blow control in 72% of 11 dogs tested), as did the nonspecific inhibitor of L-type Ca2+ channels, nickel chloride (5 mM) (36% below control in 69% of 13 dogs tested). Each agent induced either excitatory or inhibitory responses, depending on the agent tested. It is concluded that specific ion channels (INa, ICaL, IKv, and IKCa) that have been associated with intrinsic cardiac neurons in vitro are involved in their capacity to generate action potentials in situ.Key words: calcium channels, intrinsic cardiac neuron, potassium channels, sodium channels.

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II

1997 ◽  
Vol 273 (2) ◽  
pp. F307-F314 ◽  
Author(s):  
R. Loutzenhiser ◽  
L. Chilton ◽  
G. Trottier
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Membrane Potentials ◽  
Ang Ii ◽  
Ca Channels ◽  
Renal Perfusion Pressure

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

Salt-sensitive hypertension in ANP knockout mice is prevented by AT1 receptor antagonist losartan

1999 ◽  
Vol 277 (3) ◽  
pp. R624-R630 ◽  
Author(s):  
Luis G. Melo ◽  
Anthony T. Veress ◽  
Chee K. Chong ◽  
Uwe Ackermann ◽  
Harald Sonnenberg
Keyword(s):  
Receptor Antagonist ◽  
Knockout Mice ◽  
Plasma Renin ◽  
Plasma Catecholamine ◽  
Ang Ii ◽  
Dietary Salt ◽  
Water Control ◽  
Dietary Regimen ◽  
Arterial Blood ◽  
Salt Sensitive Hypertension

Mice harboring a functional deletion of the pro-atrial natriuretic peptide (ANP) gene (−/−) develop salt-sensitive hypertension relative to their wild-type (+/+) counterparts after prolonged (>1 wk) maintenance on high-salt (HS, 8% NaCl) diet. We reported recently that the sensitization of arterial blood pressure (ABP) to dietary salt in the −/− mice is associated with failure to downregulate plasma renin activity. To further characterize the role and mechanism of ANG II in the sensitization of ABP to salt in the ANP “knockout” mice, we measured ABP, heart rate (HR), and plasma catecholamine and aldosterone concentrations in −/− and +/+ mice maintained on HS for 4 wk and treated with daily injections of AT1 receptor antagonist DuP-753 (losartan) or distilled water (control). Daily food and water intake and fluid and electrolyte excretion were also measured during the first and last weeks of the dietary regimen. Cumulative urinary excretion of fluid and electrolytes did not differ significantly between genotypes and was not altered by chronic treatment with losartan. Basal ABP and HR were significantly elevated in control −/− mice compared with control +/+ mice. Losartan did not affect ABP or HR in +/+ mice, but reduced ABP and HR in the −/− mice to the levels in the +/+ mice. Total plasma catecholamine was elevated by approximately ten-fold in control −/− mice compared with control +/+ mice. Losartan reduced plasma catecholamine concentration significantly in −/− mice and abrogated the difference in plasma catecholamine between −/− and +/+ mice on HS diet. Plasma aldosterone did not differ significantly between genotypes and was not altered by losartan. We conclude that salt sensitivity of ABP in ANP knockout mice is mediated, at least in part, by a synergistic interaction between ANG II and sympathetic nerve activity.

1812 Optical imaging of neuronal activity with a voltage-sensitive dye in guinea pig piriform cortex in vitro

1993 ◽  
Vol 18 ◽  
pp. S199
Author(s):  
Michio Sugitani ◽  
Tokio Sugai ◽  
Manabu Tanifuji ◽  
Kazuyuki Murase ◽  
Norihiko Onoda
Keyword(s):  
Guinea Pig ◽  
Optical Imaging ◽  
Neuronal Activity ◽  
Piriform Cortex ◽  
Voltage Sensitive Dye

scholarly journals Electrical impedance measurement system to assess in-situ experiments on epithelia under ELF magnetic fields exposure

2021 ◽  
Vol 19 (3) ◽  
pp. 217-226
Author(s):  
G. Domínguez ◽  
E. Cardiel ◽  
J.L Reyes ◽  
E. Sánchez ◽  
P.R. Hernández
Keyword(s):  
Impedance Spectroscopy ◽  
Magnetic Fields ◽  
Cell Cultures ◽  
Electrical Impedance ◽  
Controlled Environment ◽  
Spectroscopy Technique ◽  
In Situ Experiments ◽  
Impedance Spectroscopy Technique

Purpose: The development of an electric impedance meter based on the impedance spectroscopy technique, for in vitro and in situ experimentation, with cellular epithelia submitted to extremely low frequency magnetic fields in a controlled environment. Unlike other reported systems, a strength of the one presented here is that it avoids the influence of external factors on the experiment. Materials and methods: The designed system employs the electrical impedance values obtained by the impedance spectroscopy technique to determine the parameters of the simple equivalent electrical model of a cellular monolayer. The Madin-Darby Canine Kidney (MDCK) cell cultures were used as subjects of study in the experimental protocol. Results: The validation was carried out by comparing the transepithelial electrical impedance data of the cell cultures obtained with the developed system and those of the Cellzscope® commercial system used as the standard. Non-significant differences were obtained. Conclusion: It was confirmed that the developed system provides reliable values of transepithelial electrical impedance to experiment with cell cultures and take advantage of the controlled environment to reduce the effects of experimental management.

In vivo characterization of vasocontractile activities in erythrocytes

1983 ◽  
Vol 58 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Michael P. McIlhany ◽  
Lydia M. Johns ◽  
Thomas Leipzig ◽  
Nicholas J. Patronas ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Content Type ◽  
Control Value ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Chronic Cerebral Vasospasm ◽  
In Vivo Characterization

✓ Partially purified protein from washed and artificially hemolyzed erythrocytes, known to cause significant contractions of isolated canine cerebral vessels in vitro, was injected into the cisterna magna of intact anesthetized dogs. Cerebral blood flow, measured by the xenon-133 washout technique, decreased from a control value of 49.5 ± 1.17 ml/100 gm/min to an experimental value of 34.1 ± 1.65 ml/100 gm/min at 2 hours. Cerebral vascular resistance rose from a control value of 2.05 ± 0.17 PRU (peripheral resistance units) to an experimental value of 2.91 ± 0.25 PRU at 2 hours. Mean arterial blood pressure, heart rate, intracranial pressure, and cerebral perfusion pressure remained stable. Cardiac output also fell significantly (in 2-hour control animals it was 2.89 ± 0.37 liter/min, and in 2-hour experimental animals 1.43 ± 0.13 liter/min) and peripheral vascular resistance rose. These changes were evident by 10 minutes after the cisternal injection of the hemolysate protein, and remained for the duration of the 2-hour monitoring period. Serial vertebrobasilar angiograms demonstrated marked narrowing of the intracranial basilar artery when compared to control values. The narrowing persisted for several days in most animals, and tended to increase with time. Relaxation occurred by the 10th through the 14th day. The authors conclude that this experimental preparation may be a useful model for both in vitro and in vivo investigation of chronic cerebral vasospasm.

Sensitivity of canine intrinsic cardiac neurons to H2O2and hydroxyl radical

1998 ◽  
Vol 275 (4) ◽  
pp. H1434-H1440 ◽  
Author(s):  
Gregory W. Thompson ◽  
Magda Horackova ◽  
J. Andrew Armour
Keyword(s):  
Free Radicals ◽  
Blood Supply ◽  
Neuronal Activity ◽  
Chelating Agent ◽  
Right Atrial ◽  
Arterial Blood Supply ◽  
Arterial Blood ◽  
Oxygen Derived Free Radicals ◽  
Oxidative Challenge

To determine whether intrinsic cardiac neurons are sensitive to oxygen-derived free radicals in situ, studies were performed in 44 open-chest anesthetized dogs. 1) When H2O2(600 μM) was administered to right atrial neurons of 36 dogs via their local arterial blood supply, neuronal activity either increased (+92% in 16 dogs) or decreased (−61% in 20 dogs), depending on the population of neurons studied. H2O2(600 μM) administered into the systemic circulation did not affect neuronal activity, measured cardiac indexes, or aortic pressure. 2) The iron-chelating agent deferoxamine (20 mg/kg iv), a chemical that prevents the formation of oxygen-derived free radicals, reduced the activity generated by neurons (−57%) in 8 of 10 dogs. 3) H2O2did not affect neuronal activity when administered in the presence of deferoxamine in these 10 dogs. 4) When the ATP-sensitive potassium (KATP) channel opener cromakalim (20 μM) was administered to intrinsic cardiac neurons in another 21 animals via their regional arterial blood supply, ongoing neuronal activity in 15 of these dogs decreased by 54%. 5) Neuronal activity was not affected by H2O2when administered in the presence of cromakalim in 16 dogs. These data indicate that 1) some intrinsic cardiac neurons are sensitive to exogenous H2O2, 2) such neurons are tonically influenced by locally produced oxygen-derived free radicals in situ, and 3) intrinsic cardiac neurons possess KATPchannels that are functionally important during oxidative challenge.

scholarly journals Agrobiological Interactions of Essential Oils of Two Menthol Mints: Mentha piperita and Mentha arvensis

Molecules ◽  
2019 ◽  
Vol 25 (1) ◽  
pp. 59 ◽  
Author(s):  
Danuta Kalemba ◽  
Agnieszka Synowiec
Keyword(s):  
Biological Activities ◽  
Review Article ◽  
Mentha Piperita ◽  
Agricultural Pest ◽  
Mentha Arvensis ◽  
Botanical Pesticides ◽  
New Methods ◽  
In Situ Experiments

This review article discusses the active constituents and potential of two menthol mint oils, Mentha piperita (MPEO) and Mentha arvensis (MAEO), as natural sources for botanical pesticides. The biological activities of these menthol mint oils, which can be useful in agriculture, have been broadly researched, especially toward phytotoxic microorganisms. To a lesser extent, the insecticidal and herbicidal activities of mint EOs have also been studied. It is apparent that the prospect of using menthol mint oils in agriculture is increasing in popularity. A number of investigations showed that the in vitro efficacy of MPEO and MAEO, as well as that of their main constituent, menthol, is pronounced. The results of in vitro research are useful for choosing EOs for further investigations. However, it is clear that in situ experiments are crucial and should be more extensively developed. At the same time, known techniques are to be applied to this area and new methods should be worked out, aiming at the improvement of EOs’ pesticidal efficacy and cost-effectiveness, for future implementation in agricultural pest control.

Sign in / Sign up

Export Citation Format

Share Document