Muscarinic and alpha-adrenergic stimulation of Na and Ca uptake by dispersed lacrimal cells

1980 ◽  
Vol 239 (2) ◽  
pp. G99-G105 ◽  
Author(s):  
R. J. Parod ◽  
B. A. Leslie ◽  
J. W. Putney
Keyword(s):  
Lacrimal Gland ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Alpha Adrenergic Receptor ◽  
Ca Uptake ◽  
Isotope Technique ◽  
Ca Ions ◽  
Double Isotope

Rat lacrimal gland acinar cells were isolated and observed to be physiologically stable for several hours of incubation in vitro. With a double-isotope technique, it was found that carbachol and epinephrine stimulated the uptake of 22Na and 45Ca by lacrimal cells. These respnses were maximal at agonist concentrations of 10(-5) M and were blocked by atropine and phentolamine, respectively. It is concluded that muscarinic and alpha-adrenergic receptor activation increase the membrane permeability of the lacrimal gland acinar cell to Na and Ca, ions that may be important in the secretion of water by the lacrimal gland.

Ca2+-dependent facilitated shortening in isotonic contraction of trachealis muscle

1989 ◽  
Vol 66 (2) ◽  
pp. 632-637 ◽  
Author(s):  
R. W. Mitchell ◽  
S. M. Koenig ◽  
E. Kelly ◽  
N. L. Stephens ◽  
A. R. Leff
Keyword(s):  
Adrenergic Receptor ◽  
Isometric Force ◽  
Receptor Activation ◽  
Isometric Tension ◽  
Force Generation ◽  
Response Curves ◽  
Beta Adrenoceptor ◽  
Alpha Adrenergic Receptor ◽  
Isotonic Shortening

We compared isotonic shortening with isometric force generation as a function of external Ca2+ in 166 tracheal smooth muscle (TSM) strips from 27 mongrel dogs in vitro. Concentration-response curves were generated with muscarinic stimulation (acetylcholine, ACh), alpha-adrenergic receptor activation (norepinephrine after beta-adrenoceptor blockade, NE), serotonin (5-HT), and KCl-substituted Krebs-Henseleit solution. The concentrations of 5-HT causing half-maximal shortening (ECS50, 1.54 +/- 0.14 X 10(-7) M) and half-maximal active isometric tension (ECT50, 1.72 +/- 0.30 X 10(-7) M) were similar (P = NS). Likewise, ECS50 (21.9 +/- 0.7 mM) and ECT50, (22.0 +/- 0.9 mM) were similar for KCl. In contrast, facilitated isotonic shortening (i.e., greater isotonic shortening for comparable degrees of force generation) was elicited with ACh and NE for all levels of force generation between 15 and 85% of maximum and for all concentrations of ACh from 3 X 10(-8) to 3 X 10(-5) M (P less than 0.05 for all points). Facilitated isotonic shortening also was elicited for all concentrations of NE from 10(-8) to 10(-6) M (P less than 0.05 for all points). Removal of Ca2+ from the perfusate substantially reduced the potency of ACh (P less than 0.001) and abolished differences between ECS50 (2.23 +/- 0.28 X 10(-5) M) and ECT50 (2.50 +/- 0.46 X 10(-5) M, P = NS). We demonstrate that for comparable degrees of force generation, muscarinic and alpha-adrenergic receptor activation cause greater isotonic shortening than KCl or 5-HT and that this facilitated shortening is associated with the concentration of external Ca2+.

β-blockade abolishes the augmented cardiac tPA release induced by transactivation of heterodimerised bradykinin receptor-2 and β2-adrenergic receptor in vivo

2014 ◽  
Vol 112 (11) ◽  
pp. 951-959 ◽  
Author(s):  
Morten Eriksen ◽  
Arnfinn Ilebekk ◽  
Alessandro Cataliotti ◽  
Cathrine Rein Carlson ◽  
Torstein Lyberg ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Sympathetic Nerves ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Adrenergic Stimulation ◽  
Β2 Adrenergic Receptor ◽  
Β Blocker

SummaryBradykinin (BK) receptor-2 (B2R) and β2-adrenergic receptor (β2AR) have been shown to form heterodimers in vitro. However, in vivo proofs of the functional effects of B2R-β2AR heterodimerisation are missing. Both BK and adrenergic stimulation are known inducers of tPA release. Our goal was to demonstrate the existence of B2R-β2AR heterodimerisation in myocardium and to define its functional effect on cardiac release of tPA in vivo. We further investigated the effects of a non-selective β-blocker on this receptor interplay. To investigate functional effects of B2R-β2AR heterodimerisation (i. e. BK transactivation of β2AR) in vivo, we induced serial electrical stimulation of cardiac sympathetic nerves (SS) in normal pigs that underwent concomitant BK infusion. Both SS and BK alone induced increases in cardiac tPA release. Importantly, despite B2R desensitisation, simultaneous BK infusion and SS (BK+SS) was characterised by 2.3 ± 0.3-fold enhanced tPA release compared to SS alone. When β-blockade (propranolol) was introduced prior to BK+SS, tPA release was inhibited. A persistent B2R-β2AR heterodimer was confirmed in BK-stimulated and nonstimulated left ventricular myocardium by immunoprecipitation studies and under non-reducing gel conditions. All together, these results strongly suggest BK transactivation of β2AR leading to enhanced β2AR-mediated release of tPA. Importantly, non-selective β-blockade inhibits both SS-induced release of tPA and the functional effects of B2R-β2AR heterodimerisation in vivo, which may have important clinical implications.

Adrenergic activation of glycogen phosphorylase in primary culture diabetic cardiomyocytes

1992 ◽  
Vol 262 (3) ◽  
pp. H649-H653 ◽  
Author(s):  
J. A. Buczek-Thomas ◽  
S. R. Jaspers ◽  
T. B. Miller
Keyword(s):  
Hypersensitive Response ◽  
Adrenergic Receptor ◽  
Glycogen Phosphorylase ◽  
Receptor Activation ◽  
Receptor Stimulation ◽  
Beta Adrenergic ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Adrenergic Activation

The basis of catecholamine-induced activation of glycogen phosphorylase was investigated in adult rat cardiomyocytes isolated from normal and alloxan-diabetic animals. Cells derived from diabetic animals exhibited a hypersensitive response to epinephrine stimulation that was apparent 3 h after cell isolation and was further enhanced on maintenance of the myocytes in culture for 24 h. Normal cells initially lacked the hypersensitive response to epinephrine stimulation, although on maintenance of these cells in culture for 24 h, the hypersensitive response was acquired in vitro. To assess alpha- and beta-adrenergic mediation of the response, normal and diabetic cardiomyocytes were incubated with propranolol, a beta-blocker, before direct alpha 1-receptor stimulation with phenylephrine. Both normal and diabetic myocytes failed to undergo activation of phosphorylase in 3- or 24-h cell cultures. In addition, the effects of epinephrine on phosphorylase activation were completely inhibited by propranolol, whereas prazosin, an alpha-blocker, was unsuccessful. The present data suggest that the hypersensitive response of glycogen phosphorylase in normal and diabetic cardiomyocytes is solely mediated through beta-adrenergic receptor activation.

Adrenergic stimulation of inositol phosphate accumulation in tracheal epithelium

1989 ◽  
Vol 66 (1) ◽  
pp. 504-508 ◽  
Author(s):  
T. Bainbridge ◽  
R. D. Feldman ◽  
M. J. Welsh
Keyword(s):  
Adrenergic Receptor ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Second Messengers ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Cl Secretion ◽  
Phosphate Accumulation ◽  
Inositol Phosphate Accumulation ◽  
Stimulation Of

To determine whether inositol phosphates are important second messengers in the regulation of Cl- secretion by airway epithelia, we examined the relationship between inositol phosphate accumulation and Cl- secretion in response to adrenergic agonists. We found that epinephrine stimulated Cl- secretion and inositol phosphate accumulation with similar concentration dependence. Although isoproterenol stimulated Cl- secretion, there was no effect of beta-adrenergic receptor activation on inositol phosphate accumulation. In contrast, alpha 1-adrenergic receptor activation stimulated inositol phosphate accumulation but failed to induce Cl- secretion. Another Cl- secretagogue, prostaglandin E1, also failed to stimulate inositol phosphate accumulation. These data suggest that inositol phosphate accumulation is neither sufficient nor required for stimulation of Cl- secretion in cultured canine tracheal epithelial cells.

Dogfish pressor response to potassium blocked by magnesium and phentolamine

1982 ◽  
Vol 242 (3) ◽  
pp. R185-R188
Author(s):  
R. G. Carroll ◽  
D. F. Opdyke ◽  
N. E. Keller
Keyword(s):  
Adrenergic Receptor ◽  
Pressor Response ◽  
In Vitro Experiments ◽  
Spontaneous Release ◽  
Alpha Adrenergic Receptor ◽  
Receptor Sites ◽  
Catecholamine Levels ◽  
Chromaffin Tissue

In vivo infusion of MgCl2 blocks the dogfish pressor response to K+. This action of Mg2+ was contrasted to phentolamine in in vivo and in vitro experiments. Mg2+ blocks the spontaneous release of catecholamines from dogfish chromaffin tissue but does not alter the norepinephrine-induced contraction of the isolated dogfish artery. In vivo infusion of Mg2+ causes a significant decrease in resting catecholamine levels and diminishes the catecholamine release caused by K+ challenge. Both Mg2+ and phentolamine block the pressor action of K+, Mg2+ by preventing the K+-induced release of catecholamines and phentolamine by preventing the circulating catecholamines from interacting with alpha-adrenergic receptor sites.

Secretory response of dispersed rat submandibular cells. II. Mucin secretion

1980 ◽  
Vol 238 (3) ◽  
pp. C99-C106 ◽  
Author(s):  
D. O. Quissell ◽  
K. A. Barzen
Keyword(s):  
Adrenergic Receptor ◽  
Partial Agonist ◽  
Receptor Activation ◽  
Secretory Response ◽  
Mucin Secretion ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptor ◽  
Median Effective Concentration ◽  
Higher Doses

The secretory response of dispersed rat submandibular cells as it relates to the secretion of D-[1-14C]glucosamine hydrochloride-labeled mucin following sympathomimetic and parasympathomimetic stimulation was evaluated. The adrenergic agonists (-)-norepinephrine and (-)-epinephrine were found to have equal efficacy and potency with a median effective concentration (EC50) of 7.1 x 10(-7) M. (-)-Isoproterenol was found to be acting as a "partial" agonist and had an EC50 of 3.9 x 10(-7) M. (-)-Phenylephrine addition resulted in a small, but significant, secretion of mucin at higher doses tested (10(-4) M--10(-3) M). Neither cholinergic nor alpha-adrenergic receptor stimulation was able to elicit a net increase in the secretion of mucin. However alpha-adrenergic receptor activation in conjunction with beta-adrenergic receptor activation facilitated the rate of secretion. Extracellular Ca2+ and Mg2+ were not required for the secretion of mucin, but extracellular Ca2+ enhanced the rate of secretion following alpha- and beta-adrenergic receptor activation. However extracellular Ca2+ did not enhance mucin secretion following beta-adrenergic receptor activation. Both cellular Ca2+ and beta-adrenergic receptor activation were required to elicit a secretory response following sympathomimetic stimulation.

scholarly journals Phenylephrine induces relaxation of longitudinal strips from small arteries of goat legs

2019 ◽  
Author(s):  
Kawin Padmaja Marconi ◽  
Bhavithra Megan ◽  
Alen Major Venis ◽  
Renu Raj ◽  
Sathya Subramani
Keyword(s):  
Smooth Muscle ◽  
Adrenergic Receptor ◽  
Contractile Response ◽  
Receptor Subtype ◽  
Adrenergic Stimulation ◽  
Small Artery ◽  
Small Arteries ◽  
Alpha Adrenergic Receptor ◽  
Longitudinal Smooth Muscle ◽  
Relaxant Response

AbstractAlpha adrenergic stimulation is known to produce vasoconstriction. We have earlier shown that, in spiral strips of small arteries Phenylephrine (PE) caused vasorelaxation under high nitric oxide (NO) environment. However on further experimentation it was realized that the PE-induced vasorelaxant response occurred only with longitudinal strips of small arteries even under normal NO environment while circular strips showed contraction with PE even under high NO environment. Such PE-induced vasorelaxation of longitudinal strips was blocked by Phentolamine, an alpha-adrenergic receptor blocker. On delineation of specific receptor subtype, PE-induced relaxation was found to be mediated through alpha 1D receptor. However, this phenomenon is specific to small artery, as longitudinal smooth muscle of aorta showed only contractile response to adrenergic stimulation. There is no prior report of longitudinal smooth muscle in small artery up to our knowledge. The results of this study and histological examination of vessel sections suggest the presence of longitudinal smooth muscle in small artery and their relaxant response to alpha adrenergic stimulation is a novel phenomenon.

Sign in / Sign up

Export Citation Format

Share Document