Beta-Adrenergic Receptors and Renin Release: Studies with Beta-Adrenoreceptor-Blocking Agents in the Conscious Rabbit

1974 ◽  
Vol 48 (s2) ◽  
pp. 89s-91s
Author(s):  
M. A. Weber ◽  
Helen F. Oates ◽  
G. S. Stokes
Keyword(s):  
Blood Pressure ◽  
Adrenergic Receptors ◽  
Plasma Renin ◽  
Renin Release ◽  
Beta Adrenergic Receptors ◽  
Blood Pressure Lowering Effect ◽  
Beta Adrenergic ◽  
Blocking Agents ◽  
Pressure Lowering ◽  
Beta 2

1. Plasma renin activity (PRA) and mean blood pressure were studied in conscious rabbits infused with beta-adrenoreceptor antagonists. 2. Oxprenolol and dl-propranolol each significantly reduced PRA and blood pressure, but prindolol, which had a strong blood pressure-lowering effect, increased PRA. 3. When prindolol was given to animals in which PRA and blood pressure had been reduced by dl-propranolol, PRA returned to control values but blood pressure remained low. Thus the increase in PRA caused by prindolol is not mediated by hypotension. These findings, together with the observation that compound H35/25 reduced PRA without altering blood pressure, suggest that the effects of the beta-adrenoreceptor-blocking drugs on blood pressure are unrelated to their effects on renin release. 4. Studies with d-propranolol and with blocking agents with either beta-1 or beta-2 specificity indicated that the effects of beta-adrenoreceptor blockade on renin are directly dependent upon their action on beta-adrenergic receptors, probably of the beta-2 type.

Analysis of beta-adrenoceptors mediating renin release produced by isoproterenol in conscious dogs

1980 ◽  
Vol 238 (5) ◽  
pp. F387-F393
Author(s):  
N. Himori ◽  
A. Izumi ◽  
T. Ishimori
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oral Dose ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Renin Release ◽  
Blocking Drug ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Beta 2

Types of beta-adrenoceptors mediating renin release induced by isoproterenol were investigated in conscious dogs. The nonselective beta-adrenoceptor blocking drugs propranolol, D-32, and pindolol significantly inhibited increases in heart rate and plasma renin activity and a fall of blood pressure produced by intravenous infusion of isoproterenol (10 microgram . kg-1 . 20 min-1). d-Propranolol and d-D-32 did not inhibit these three responses to isoproterenol. The selective beta 1-adrenoceptor blocking drug atenolol, at the oral dose of 6 mg/kg, which selectively suppressed isoproterenol-induced tachycardia, significantly inhibited the renin release caused by isoproterenol. By contrast, the renin release induced by isoproterenol was not modified by the selective beta 2-adrenoceptor blocking drug IPS-339 at an oral dose of 3 mg/kg, which fully and selectively antagonized the fall of blood pressure in response to isoproterenol. There was good correlation between suppression of isoproterenol-induced renin release and that of isoproterenol-induced tachycardia after various beta-adrenoceptor blocking drugs. These results lead to the conclusion that in conscious dogs the beta-adrenoceptors mediating release are mainly of the beta 1 type.

Regulation of atrial autonomic receptors in experimental cyanotic heart disease

1991 ◽  
Vol 261 (4) ◽  
pp. H1135-H1140 ◽  
Author(s):  
R. Doshi ◽  
E. Strandness ◽  
D. Bernstein
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Receptor Subtypes ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Beta 2 ◽  
The Right ◽  
Chronic Hypoxemia ◽  
Inotropic Responses

During chronic hypoxemia, left ventricular beta-adrenergic receptor density is decreased and a dissociation occurs between increased chronotropic and decreased inotropic responses to chronically elevated sympathetic tone. To determine whether this dissociation was related to alterations in autonomic receptor populations in the right atrium, we studied right atrial cholinergic and beta-adrenergic receptors in chronically hypoxemic newborn lambs and in normoxemic controls. Heart rate response was determined by infusing isoproterenol at 0.1 or 0.5 microgram.kg-1.min-1. Muscarinic receptors were quantified with [3H]quinuclidinyl benzilate and beta-adrenergic receptors with [125I]iodocyanopindolol. Competition with ICI 118,551 was used to determine beta 1- vs. beta 2-receptor subtypes. In the hypoxemic lambs, isoproterenol resulted in a lesser percentage increase in heart rate (hypoxemic, 46 +/- 6% vs. control, 89 +/- 17%, P less than 0.05); however, because baseline heart rate was higher in the hypoxemic lambs (213 +/- 7 vs. 177 +/- 12 beats/min, P less than 0.05), maximal heart rate responses were similar (310 +/- 7 vs. 326 +/- 6 beats/min, NS). There was no change in receptor density or affinity of either muscarinic or beta-adrenergic receptors and no change in the proportion of beta 1- vs. beta 2-receptor subtypes. Thus the dissociation between the chronotropic and inotropic responses to chronic hypoxemia may be in part secondary to a differential regulation of beta-adrenergic receptors between the left ventricle and the right atrium.

Characterization of beta-adrenergic receptors in cultured bovine tracheal gland cells

1989 ◽  
Vol 256 (2) ◽  
pp. C310-C314 ◽  
Author(s):  
J. M. Madison ◽  
C. B. Basbaum ◽  
J. K. Brown ◽  
W. E. Finkbeiner
Keyword(s):  
Binding Sites ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Rank Order ◽  
Beta Adrenergic Receptors ◽  
Binding Studies ◽  
Beta Adrenergic ◽  
High Affinity ◽  
Gland Cells ◽  
Beta 2

We characterized the beta-adrenergic receptors that mediate secretory responses to isoproterenol in cultured bovine tracheal submucosal gland cells. Previous studies have shown that these cells have morphological and biochemical features characteristic of serous cells. Isoproterenol, epinephrine, and norepinephrine each stimulated the secretion of 35SO4-labeled macromolecules from these cultured serous cells with a rank order of potency (isoproterenol greater than epinephrine greater than norepinephrine) consistent with the presence of beta 2-adrenergic receptors. These functional studies were supported by radioligand-binding studies using [I125]-iodocyanopindolol (125I-CYP) to identify beta-adrenergic receptors. 125I-CYP binding to membrane particulates prepared from cultured serous cells was saturable and of high affinity (equilibrium dissociation constant 20 +/- 3 pM; mean +/- SE, n = 6) and was antagonized stereoselectively by propranolol. Adrenergic agonists competed for 125I-CYP-binding sites with a rank order of potency characteristic of the beta 2-adrenergic receptor subtype. A specific beta 2-adrenergic receptor antagonist, ICI 118.551, competed for a single class of 125I-CYP-binding sites with high affinity (inhibition constant 1.8 +/- 0.3 nM, n = 3). We concluded that the secretory response of cultured tracheal gland cells to isoproterenol is a response mediated by beta-adrenergic receptors of the beta 2 subtype.

Evidence that beta 2-receptors mediate action of catecholamines on endolymphatic sac DC potential

1991 ◽  
Vol 260 (5) ◽  
pp. R911-R915 ◽  
Author(s):  
N. Mori ◽  
N. Uozumi
Keyword(s):  
Direct Current ◽  
Adrenergic Receptors ◽  
Endolymphatic Sac ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Selective Antagonist ◽  
Dc Potential ◽  
Beta 2 ◽  
Current Potential

Our recent study has revealed that catecholamines depress the endolymphatic sac direct current potential (ESP) by the beta-adrenergic action [Mori et al., Am. J. Physiol. 259 (regulatory Integrative Comp. Physiol. 28): R921-R924, 1990]. Beta-Adrenergic receptors have been subclassified into beta 1- and beta 2-receptors. Using beta 1-selective (dobutamine) and beta 2-selective (salbutamol) agonists and a beta 1-selective antagonist (atenolol), we determined the subtype of beta-adrenergic receptors that mediate the action of catecholamines on the ESP. Salbutamol depressed the ESP to a larger degree than dobutamine [34.0 +/- 2.6 (n = 7) vs. 13.0 +/- 2.0% (n = 8)] with a much lower dose (100 vs. 1,000 micrograms/kg). Atenolol failed to block the action of salbutamol on the ESP at a dose of 1 mg/kg, whereas propranolol inhibited it at the same dose. The results indicate that beta 2-receptors mediate the action of catecholamines on the ESP.

beta-Adrenergic receptors in the developing rabbit lung

1981 ◽  
Vol 240 (4) ◽  
pp. E351-E357 ◽  
Author(s):  
J. A. Whitsett ◽  
M. A. Manton ◽  
C. Darovec-Beckerman ◽  
K. G. Adams ◽  
J. J. Moore
Keyword(s):  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptors ◽  
Rabbit Lung ◽  
Beta Adrenergic ◽  
Beta 2

beta-Adrenergic receptors and catecholamine-sensitive adenylate cyclase were identified and partially characterized in membrane fractions of rabbit lungs from day 25 of gestation to adulthood with the beta-adrenergic antagonists (--)-[3H]dihydroalprenolol [(--)-[3H]DHA] and (--)-[125I]iodohydroxybenzylpindolol [(--)-[125I]HYP]. beta-Adrenergic receptor number (Bmax) increased 11.5-fold during this time period, increasing progressively during the latter days of gestation and the early neonatal period, from 37 +/- 10 fmol/mg protein at 25 days gestation to 425 +/- 51 fmol/mg in the adult rabbit lung (mean +/- SD). Receptor affinity for (--)-[3H]DHA (KD = 1.8 nM) or (--)-[125I]HYP (KD - 0.104 nM) and the proportion of beta 1- and beta 2-adrenergic receptor subtypes (60% beta 1 and 40% beta 2) did not change with advancing age. Basal adenylate cyclase activity in lung homogenates decreased significantly with increasing age, whereas the activity in the presence of catecholamine or NaF remained nearly constant. Catecholamines stimulated adenylate cyclase activity at all ages studied supporting a role of the maturation of beta-adrenergic receptors in the regulation of pulmonary function.

Molecular and functional identification of beta-adrenergic receptors in distal convoluted tubule cells

1997 ◽  
Vol 272 (6) ◽  
pp. F712-F720 ◽  
Author(s):  
F. A. Gesek ◽  
K. E. White
Keyword(s):  
Adrenergic Receptors ◽  
Receptor Activation ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptors ◽  
Functional Responses ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Beta 2 ◽  
Camp Formation

Renal nerve stimulation or circulating catecholamines activate the beta-adrenergic receptors that mediate direct effects on tubular transport. Three subtypes of beta-adrenergic receptors have been characterized: beta 1, beta 2, and beta 3. beta-Adrenergic-receptor effects on Na+ and Ca2+ transport in distal convoluted tubules (DCT) have not been established. The focus of this study was to 1) identify the subtypes of beta-adrenergic receptors in DCT cells and 2) examine functional responses to beta-receptor activation on adenosine 3',5'-cyclic monophosphate (cAMP) formation and Na+ and Ca2+ entry. To determine the subtypes of beta-receptors present, RNA isolated from immortalized mouse DCT cells was reverse transcribed, and the cDNA was amplified using primers designed to reported sequences for beta 1-, beta 2-, and beta 3-receptor subtypes. Products of the appropriate sizes were obtained with beta 1- and beta 2-primers. No product was observed with primers to the beta 3 sequence. Receptor products were confirmed by sequencing and are identical to reported mouse beta 1- and beta 2-receptor sequence. Receptor binding of[3H]dihydroalprenolol was 123 +/- 13 fmol/mg protein, and a 3:1 ratio of beta 1- to beta 2-receptors was observed with DCT cell membranes. Isoproterenol, a beta-receptor agonist, increased cAMP formation 8.5-fold. Pretreatment with the antagonist propranolol abolished agonist-induced cAMP accumulation. Isoproterenol significantly increased 22Na+ uptake to 345 +/- 23 compared with a basal rate of 256 +/- 12 nmol.min-1.mg protein-1 and was blocked with propranolol and beta 1- and beta 2-selective antagonists. Isoproterenol had no effect on 45Ca2+ entry into DCT cells. In summary, DCT cells express three times more beta 1- than beta 2-receptors and express no detectable beta 3-adrenergic receptors. beta-Receptors couple to adenylyl cyclase, and activation of beta-adrenergic receptors increases Na+ but not Ca2+ entry in DCT cells.

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