Mediation of isoproterenol-induced thirst in rats by β2-adrenergic receptors

1978 ◽  
Vol 56 (3) ◽  
pp. 465-470 ◽  
Author(s):  
M. J. Katovich ◽  
M. J. Fregly
Keyword(s):  
Water Intake ◽  
Adrenergic Receptors ◽  
Subcutaneous Administration ◽  
Female Rats ◽  
Acute Administration ◽  
Drinking Response ◽  
Adrenergic Antagonist ◽  
Blocking Activity ◽  
Β Adrenergic Receptors ◽  
Adrenergic Blocking

Isoproterenol-induced thirst in rats has been attributed to the activation of β-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into β1 and β2 types, experiments were performed using several β-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The β1- and β2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 μg/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little β-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 μg/kg). Practolol (125 mg/kg), a β1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective β2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 μg/kg), a β2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that β2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

α-Adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blocking Agent ◽  
Sympathetic Ganglia ◽  
Canine Heart ◽  
Receptor Modulation ◽  
Adrenergic Antagonist ◽  
Cervical Ganglia ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administraiton of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the α-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the β-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by α-adrenergic receptors and that these effects are dependent upon β-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.Key words: α-adrenergic inotropism, sympathetic ganglia, hexamethonium, phentolamine.

OESTRADIOL-INDUCED SYNTHESIS OF A SPECIFIC UTERINE PROTEIN IN PROPRANOLOL-TREATED RATS

1975 ◽  
Vol 65 (2) ◽  
pp. 215-218 ◽  
Author(s):  
N. DUPONT-MAIRESSE ◽  
P. GALAND
Keyword(s):  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Blocking Agent ◽  
Conflicting Evidence ◽  
Early Increase ◽  
Β Adrenergic Receptors ◽  
Adrenergic Blocking

SUMMARY While there is conflicting evidence concerning an effect of oestradiol on uterine cyclic AMP concentration, results from different laboratories (including ours) are in agreement that even when observed, the early increase in uterine cyclic AMP after oestradiol injection fails to occur when propranolol, a β-adrenergic blocking agent, is given (50 μg, i.p.) 20 min before the oestradiol. The present work shows that pretreatment with propranolol failed to inhibit an early uterine response to oestradiol, namely the synthesis after 1 h of uterine protein, or class of proteins, IP. It is concluded that the induction of IP by oestradiol does not depend on an increase in uterine cyclic AMP concentration and that β-adrenergic receptors do not have a role in this oestrogenic response.

Hypothalamic α-adrenergic blockade modifies drinking and blood pressure responses to central angiotensin II in conscious rats

1988 ◽  
Vol 66 (10) ◽  
pp. 1270-1277 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptors ◽  
Adrenergic Blockade ◽  
Drinking Response ◽  
Pressor Responses ◽  
Awake Rat ◽  
Rostral Hypothalamus ◽  
Blood Pressure Responses ◽  
Β Adrenergic Receptors ◽  
Dose Dependent

These experiments investigated in the awake rat the involvement of noradrenergic projections to the rostral hypothalamus in the drinking and pressor responses elicited by intracerebroventricular (i.c.v.) injections of 25 ng of angiotensin II. Phentolamine mesylate in doses of 2.5–125 μg injected into the rostral hypothalamus produced a dose-dependent depression of both the drinking and pressor responses elicited by i.c.v. administration of angiotensin II. A paradoxical increase in heart rate was associated with a decrease in pressor responses with increasing doses of phentolamine. This response was due to tissue injections, since pretreatment by injecting 12.5 μg of phentolamine into the ventricle did not block either the cardiovascular or drinking responses to i.c.v. injections of angiotensin II. Yohimbine (0.33–3.3 μg), DL-propranolol (25 μg), and atenolol (25 μg) did not, but prazosin (0.7 μg) did significantly alter the pressor responses. Although yohimbine also was without effect on drinking, prazosin reduced the drinking responses. These results suggest that α1-adrenergic receptors in the rostral hypothalamus are involved in the control of both the drinking and pressor responses elicited by i.c.v. injections of angiotensin II. In the case of propranolol and atenolol, β-adrenergic receptors altered only the drinking response in a nonspecific manner by eliciting competing behaviors. Whether they are involved in modifying the drinking response only remains to be demonstrated.

β-Adrenergic receptors are involved in histamine-induced secretion of proopiomelanocortin-derived peptides and prolactin in rats

1995 ◽  
Vol 132 (2) ◽  
pp. 223-228 ◽  
Author(s):  
Andreas Kjær ◽  
Ulrich Knigge ◽  
Steen Matzen ◽  
Jørgen Warberg
Keyword(s):  
Adrenergic Receptors ◽  
Receptor Agonist ◽  
Receptor Activation ◽  
Anterior Lobe ◽  
Intermediate Lobe ◽  
Central Administration ◽  
Melanocyte Stimulating Hormone ◽  
Adrenergic Antagonist ◽  
Β Receptor ◽  
Β Adrenergic Receptors

Kjær A, Knigge U, Matzen S, Warberg J. β-Adrenergic receptors are involved in histamine-induced secretion of proopiomelanocortin-derived peptides and prolactin in rats. Eur J Endocrinol 1995;132: 223–8. ISSN 0804–4643 The neurotransmitter histamine (HA) is involved in central regulation of secretion of prolactin (PRL) and the proopiomelanocortin (POMC)-derived peptides adrenocorticotropin (ACTH), β-endorphin (β-END) and α-melanocyte-stimulating hormone (α-MSH). The effect of HA on POMC-derived peptides and PRL release is, at least in part, indirect and may involve activation of catecholaminergic systems. Therefore, we investigated the effect of β-adrenergic receptor blockade on HA or HA agonist-induced release of ACTH, β-END, α-MSH and PRL. Central administration of HA, the H1-receptor agonist 2-thiazolylethylamine (2-TEA) or the H2-receptor agonist 4-methylhistamine (4-MeHA) stimulated the secretion of ACTH, β-END, α-MSH and PRL. Pretreatment with the β-adrenergic antagonist propranolol inhibited secretion of the POMC peptides in response to HA, 2-TEA or 4-MeHA. Propranonol only inhibited the PRL response to HA or 2-TEA, but had no effect on the PRL response to 4-MeHA. Administration of the β-receptor agonist isoproterenol stimulated ACTH, β-END, α-MSH and PRL two to five-fold. This effect was totally blocked by pretreatment with propranolol. We conclude that HA-induced secretion of POMC-derived peptides from the anterior and intermediate lobe of the pituitary gland and of PRL from the anterior lobe is, at least in part, mediated via catecholamines. β-Adrenergic receptors are involved in the mediation of the POMC response to H1- as well as H2-receptor activation, whereas β-receptors are involved only in the mediation of the PRL response to H1-receptor activation. Andreas Kjær, Department of Medical Physiology, Division of Endocrinology and Metabolism, The Panum Institute (Building 12.3), University of Copenhagen, Blegdamsvej 3c, DK-2200 Copenhagen N, Denmark

DEPENDENCE OF SPONTANEOUS AND ANGIOTENSIN-INDUCED DRINKING IN THE RAT UPON THE OESTROUS CYCLE AND OVARIAN HORMONES

1979 ◽  
Vol 82 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. L. R. FINDLAY ◽  
J. T. FITZSIMONS ◽  
J. KUCHARCZYK
Keyword(s):  
Water Intake ◽  
Renin Angiotensin System ◽  
Ovarian Hormones ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Angiotensin System ◽  
Cellular Dehydration ◽  
Drinking Response ◽  
Oestradiol Benzoate ◽  
Reduced Drinking

SUMMARY The influence of the oestrous cycle on spontaneous and dipsogen-induced drinking was studied in female rats. Spontaneous fluid intake was lowest on the day of oestrus. Drinking induced by subcutaneous isoprenaline, and by angiotensin II (injected into the preoptic area), also showed marked cyclical variation, being lower at pro-oestrus and oestrus than at other stages of the cycle. Drinking induced by subcutaneous hypertonic NaCl or by intracranial carbachol did not vary with the oestrous cycle. Cyclicity of spontaneous and of angiotensin-induced water intake was not apparent in rats before puberty or after ovariectomy. Ovariectomy reduced drinking in response to isoprenaline. Treatment with oestradiol benzoate (20 μg) caused a reduction in spontaneous water intake, but a marked increase in the drinking response to isoprenaline. Treatment with oestradiol benzoate and progesterone (2·5 mg) caused a larger decrease in spontaneous water intake and an insignificant increase in isoprenaline-induced drinking. Water intake induced by subcutaneous hypertonic saline was unaffected by gonadal steroids. The results provide further evidence for the view that the thirst of extracellular origin, in which the renin–angiotensin system is involved, is brought about by mechanisms different from those that respond to cellular dehydration. Only drinking caused by activation of extracellular mechanisms appeared to be sensitive to the ovarian cycle and to ovarian hormones.

Binding of the hydrophilic β-adrenergic antagonist [3H]CGP-12177 to cardiac tissue slices: characterization and ontogenetic studies in dogs

1987 ◽  
Vol 65 (9) ◽  
pp. 1928-1933 ◽  
Author(s):  
C. Haddad ◽  
M. Wilkinson ◽  
L. M. Roeder ◽  
J. T. Tildon ◽  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Cardiac Tissue ◽  
Tissue Slices ◽  
Tissue Handling ◽  
Neonatal Life ◽  
Adrenergic Antagonist ◽  
Cgp 12177 ◽  
A New Technique ◽  
The Right ◽  
Β Adrenergic Receptors

A new technique was developed to characterize the binding of a hydrophilic β-adrenergic antagonist, [3H]CGP-12177, to 1-mm thick slices of canine cardiac tissue. This technique was used to quantify the density (Bmax) and the affinity (Kd) of these receptors in the right ventricular conus (RVC) and the left ventricle (LV) at day 1 to 6 weeks of age, and in the adult. Binding was found to be reversible, saturable, stereospecific, of high affinity, and thermolabile. There was an increase in the density of β-adrenergic receptors between day 1 (Bmax = 2.2 ± 0.3 fmol/mg tissue in RVC and 2.9 ± 0.8 fmol/mg tissue in the LV) and 2 weeks of age postnatally, after which it remained constant until 6 weeks of age (Bmax = 7.5 ± 0.4 and 6.8 ± 0.9 fmol/mg tissue in RVC and LV, respectively); however, by 6 weeks of age it had not reached adult levels (10.3 ± 1.0 fmol/mg tissue). The affinity of these receptors did not change between early neonatal life (Kd = 1.3 ± 0.4 nM) and adulthood (Kd = 1.4 ± 0.2 nM). The density of β-adrenergic receptors in the RVC was similar to that in the LV. This new method of quantifying β-adrenergic receptors in cardiac tissue is simple and fast, and requires minimal tissue handling. It proved to be useful in studying the development of cardiac β-adrenergic receptors with age.

The effect of atenolol on the growth hormone response to growth hormone-releasing hormone in obese children

1992 ◽  
Vol 126 (2) ◽  
pp. 124-127 ◽  
Author(s):  
Sandro Loche ◽  
Stefano Pintus ◽  
Daniela Carta ◽  
Anna Carla Muntoni ◽  
Gabriella Congiu ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Acute Administration ◽  
Adrenergic Blockade ◽  
Obese Children ◽  
Gh Secretion ◽  
Adrenergic Antagonist ◽  
Significant Augmentation ◽  
Obese Subjects ◽  
Β Adrenergic Receptors

We have evaluated the effect of acute administration of atenolol, a selective β-adrenergic antagonist, on the GH response to GHRH in nine obese children and in eight age-matched controls. The GH response to GHRH (1–29, 1 μg/kg iv), evaluated both as the GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with atenolol (50 or 100mg orally in subjects with body weight <or >40 kg, respectively, administered 120 min before the GHRH injection) significantly increased the GH response to GHRH in the obese subjects, such that their mean peak GH levels and mean integrated area under the curve after atenolol plus GHRH were similar to those of the control children after GHRH. Also in control children, atenolol caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after atenolol plus GHRH were significantly higher in the controls than in the obese children given the same treatment. These data show that inhibition of central β-adrenergic receptors counteracts the blunted GH response to GHRH present in the obese children. In view of the alleged mechanism of action of β-adrenergic blockade (inhibition of endogenous SRIH release), our data suggest that the somatostatinergic system is intact in obesity, and that the suppressed GH secretion is due to other causes.

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