Actions of adrenergic agonists on isolated excretory ducts of submandibular glands

1978 ◽  
Vol 235 (6) ◽  
pp. F548-F556 ◽  
Author(s):  
A. R. Denniss ◽  
L. H. Schneyer ◽  
C. Sucanthapree ◽  
J. A. Young
Keyword(s):  
Sympathetic Nerve Activity ◽  
Physiological Changes ◽  
Adrenergic Agonists ◽  
Nerve Activity ◽  
Bathing Medium ◽  
Submandibular Glands ◽  
Low Concentrations ◽  
K Secretion ◽  
Prior Administration

The effects of norepinephrine and isoproterenol on the transepithelial potential difference (PD) and the net transepithelial fluxes of Na, K, Cl, and HCO3 of the main ducts of the submandibular glands of rats and rabbits have been studied by microperfusion of ducts incubated in vitro in an artifical bathing medium. In the rabbit duct, both catecholamines caused depolarization and reduced transepithelial Na reabsorption at concentrations above 10(-29) M. In the rat duct, norepinephrine reduced PD and net Na reabsorption and, in addition, inhibited net K secretion at concentrations of 10(-7) M and above. Isoproterenol also depolarized the duct and reduced net K reabsorption, but at concentrations of 10(-9) M it stimulated net Na reabsorption, whereas at concentrations of 10(-4) M it inhibited Na reabsorption. The stimulation caused by isoproterenol at low concentrations could be blocked by prior administration of propranolol. The results suggest that electrolyte transport, by both rat and rabbit ducts, may be influenced not only by sympathetic nerve activity but also by physiological changes in the concentrations of circulating catecholamines. Inconsistencies in the literature regarding the sensitivity of the rabbit duct to catecholamines and the response of the rat duct to isoproterenol have now been resolved.

Sensitivity of lipolysis and lipogenesis to dibutyryl-cAMP and β-adrenergic agonists in swine adipocytes in vitro2

1990 ◽  
Vol 68 (4) ◽  
pp. 1017-1023 ◽  
Author(s):  
S. E. Mills ◽  
C. Y. Liu
Keyword(s):  
Adenosine Deaminase ◽  
Acid Synthesis ◽  
Adrenergic Agonists ◽  
Dibutyryl Camp ◽  
Adrenergic Stimulation ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Porcine Adipocytes ◽  
The Relationship

Abstract The sensitivities of lipolysis and fatty acid synthesis to dibutyryl-cAMP (dbcAMP), epinephrine, ractopamine and clenbuterol were quantified in vitro using porcine adipocytes. Insulin-stimulated lipogenesis showed a biphasic response to dbcAMP, with increased rates at low concentrations and decreased (55%) rates at higher concentrations of dbcAMP. In the absence of insulin, lipogenesis was inhibited 78% by dbcAMP. In the presence of adenosine deaminase or theophylline, all three β-adrenergic agonists inhibited basal lipogenesis, but only epinephrine and ractopamine inhibited insulin-stimulated lipogenesis. The relationship between suppressed lipogenesis and enhanced lipolysis in response to dbcAMP and the β-agonists revealed that 1) basal lipogenesis was more sensitive to inhibition than was the stimulation of lipolysis, 2) sensitivity differences were magnified if adenosine deaminase was present and 3) insulin decreased adipocyte sensitivity to the inhibitory effects of dbcAMP and the β-adrenergic agonists. These results indicate that the relative sensitivities of lipogenesis and lipolysis to β-adrenergic stimulation can be modified by adenosine and insulin. Furthermore, adenosine and insulin antagonize β-adrenergic responses, in part, by cAMP-independent mechanisms.

scholarly journals An in vitro experimental model for analysis of central control of sympathetic nerve activity

2017 ◽  
Vol 67 (5) ◽  
pp. 629-635 ◽  
Author(s):  
Yuji Oyama ◽  
Kamon Iigaya ◽  
Yoshino Minoura ◽  
Toshitaka Okabe ◽  
Masahiko Izumizaki ◽  
...  
Keyword(s):  
Experimental Model ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Central Control ◽  
Nerve Activity

scholarly journals Sympathetic nerve activity promotes cardiomyocyte cell-cycle arrest and binucleation

2017 ◽  
Author(s):  
Li Chen ◽  
Alexander Y. Payumo ◽  
Kentaro Hirose ◽  
Rachel B. Bigley ◽  
Jonathan Lovas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Sympathetic Nerve ◽  
Adrenergic Receptors ◽  
Sympathetic Nerve Activity ◽  
Cardiomyocyte Proliferation ◽  
Nerve Activity ◽  
Cycle Arrest ◽  
Β Adrenergic Receptors

ABSTRACTAdult mammalian hearts typically have little capacity to regenerate after injuries such as myocardial infarction. In contrast, neonatal mice during the first week of life possess an incredible ability to regenerate their hearts, though this capacity is lost shortly after birth. The physiological triggers mediating this transition remains poorly understood. In this study, we demonstrate that sympathetic nerve activity promotes cardiomyocyte cell-cycle arrest and binucleation. In mice hearts lacking sympathetic nerve inputs, we observe increased mononucleated cardiomyocyte numbers and elevated cardiomyocyte proliferation. Additionally, increased cardiomyocyte mononucleation and proliferation are observed in mice with genetic and pharmacological inhibition of β-adrenergic receptors (βARs), which mediate sympathetic nerve signaling. Using in vitro cultures of neonatal cardiomyocytes, we demonstrate that activation of β-adrenergic receptors results in decreased cardiomyocyte proliferation that is mediated through cyclic AMP-dependent protein kinase (PKA) signaling. Taken together, these results suggest that sympathetic nerve activity may play a role in limiting the ability of mammalian hearts to regenerate by restricting cardiomyocyte proliferation and promoting cytokinesis failure leading to multinucleation.

Osmolality: a physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure

1999 ◽  
Vol 276 (6) ◽  
pp. R1579-R1586 ◽  
Author(s):  
Karie E. Scrogin ◽  
Eugene T. Grygielko ◽  
Virginia L. Brooks
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Cumulative Effect ◽  
Physiological Changes ◽  
Progressive Reduction ◽  
Nerve Activity

Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P < 0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P < 0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P < 0.01). Two hours of 5DW infusion reduced osmolality (−15 ± 5 mosmol/kgH2O), LSNA (−23 ± 3% baseline), and MAP (−10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (−5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD ( P < 0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.

Neurogenic dilatation and constriction of rat superior mesenteric artery in vitro: mechanisms and mediators

1986 ◽  
Vol 64 (6) ◽  
pp. 729-736 ◽  
Author(s):  
M. S. Kannan ◽  
A. E. Seip
Keyword(s):  
Substance P ◽  
Sympathetic Nerve Activity ◽  
Mesenteric Arteries ◽  
Opioid Agonist ◽  
Nerve Activity ◽  
Mechanical Responses ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Voltage Dependent

In the rat superior mesenteric arteries, the mechanical responses to perivascular nerve stimulation were characterized. The predominant response was contraction mediated by the release of norepinephrine, acting postjunctionally on α1-adrenoceptors. These frequency-dependent contractions were unaffected by the α2-selective adrenoceptor antagonist yohimbine, but were markedly attenuated by clonidine, the α2-selective adrenoceptor agonist. In the presence of prazosin, the α1-selective antagonist, a significant component of the nerve-mediated contraction was still present. At the concentrations used, prazosin, yohimbine, as well as clonidine acted as competitive antagonists of response to exogenous norepinephrine. This differential inhibition of norepinephrine- and nerve-mediated responses suggested the presence of distinct postjunctional adrenoceptors. The effects of clonidine and yohimbine are interpreted to arise from prejunctional modulation of norepinephrine release. In 30 of the 100 vessels studied, there was spontaneous myogenic tone. In these arteries, field stimulation caused frequency- and voltage-dependent relaxations. These responses were neural in origin, dependent on sympathetic nerve activity, but were nonadrenergic and noncholinergic in nature. Naloxone, indomethacin, and substance P inhibited these relaxations with no significant effect on the tone. The opioid agonist, 1–13 dynorphin relaxed these vessels and only naloxone inhibited this response. The effects of these agents were selective against field-stimulated responses since they did not alter the relaxation to the nonspecific agent sodium nitroprusside. These results provide circumstantial evidence for opioid-mediated vascular relaxation that is presynaptically modulated by prostanoids and substance P.

Nitric oxide-independent effects of tempol on sympathetic nerve activity and blood pressure in DOCA-salt rats

2002 ◽  
Vol 283 (3) ◽  
pp. H885-H892 ◽  
Author(s):  
Hui Xu ◽  
Gregory D. Fink ◽  
James J. Galligan
Keyword(s):  
Nitric Oxide ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Sympathetic Nerves ◽  
Nerve Activity ◽  
Independent Effects ◽  
Arteries And Veins

The role of sympathetic nerves and nitric oxide (NO) in tempol-induced cardiovascular responses was evaluated in urethane-anesthetized sham and deoxycorticosterone acetate (DOCA)-salt-treated (DOCA-salt) rats. Tempol (30–300 μmol/kg iv), a superoxide (O[Formula: see text]) scavenger, decreased renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), and heart rate (HR) in DOCA-salt and sham rats. The antioxidants tiron and ascorbate did not alter MAP, HR, or RSNA in any rat. Tempol responses were unaffected after sham rats were treated with N G-nitro-l-arginine (l-NNA, 13 mg/kg). In DOCA-salt rats, l-NNA reduced tempol-induced depressor responses but not the inhibition of HR or RSNA. Tempol did not significantly decrease MAP, HR, or RSNA after hexamethonium (30 mg/kg iv) treatment in any rat. Dihydroethidine histochemistry revealed increased O[Formula: see text] levels in arteries and veins from DOCA-salt rats. Tempol treatment in vitro reduced O[Formula: see text] levels in arteries and veins from DOCA-salt rats. In conclusion, tempol-induced depressor responses are mediated largely by NO-independent sympathoinhibition in sham and DOCA-salt rats. There is an additional interaction between NO and tempol that contributes to depressor responses in DOCA-salt rats.

Isoproterenol increases Ca, Mg, and NaCl reabsorption in mouse thick ascending limb

1990 ◽  
Vol 258 (5) ◽  
pp. F1224-F1231 ◽  
Author(s):  
C. Bailly ◽  
M. Imbert-Teboul ◽  
N. Roinel ◽  
C. Amiel
Keyword(s):  
Adenylate Cyclase ◽  
Distal Tubule ◽  
Mouse Kidney ◽  
Thick Ascending Limb ◽  
Adrenergic Agonists ◽  
Beta Adrenergic Agonists ◽  
Tubular Transport ◽  
K Secretion ◽  
Transepithelial Voltage

The effect of isoproterenol (Iso) on tubular transport in the thick ascending limb of Henle's loop (TAL) was investigated by in vitro microperfusion of MTAL (medullary) and CTAL (cortical) from White Swiss mouse kidney. The pattern of activation of adenylate cyclase along the distal tubule was investigated in this strain: results indicated that Iso stimulated adenylate cyclase fivefold in MTAL and ninefold in CTAL. Data from microperfusion experiments showed that Iso (10(-7) M in the bath) significantly and reversibly increased Ca and Mg reabsorption in CTAL. No net transport of Ca and Mg was observed in MTAL whether Iso was present or not. With regard to Na and Cl, Iso significantly stimulated their reabsorption in both segments and increased the transepithelial voltage in MTAL. Iso abolished K reabsorption in MTAL and induced a net K secretion in CTAL, the latter effect being also observed with 10(-9) M of Iso. When applied on CTAL, propranolol (10(-6) M in the bath) inhibited all these effects. These data indicate that beta-adrenergic agonists are involved in the multihormonal modulation of the TAL function.

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