Effect of α- and β-Adrenergic Blocking Agents on the Increase in Renin Secretion Produced by Stimulation of the Medulla Oblongata in Dogs

1971 ◽  
Vol 7 (2) ◽  
pp. 97-104 ◽  
Author(s):  
S.S. Passo ◽  
T.A. Assaykeen ◽  
A. Goldfien ◽  
W.F. Ganong
Keyword(s):  
Medulla Oblongata ◽  
Renin Secretion ◽  
Blocking Agents ◽  
Adrenergic Blocking ◽  
Stimulation Of ◽  
Adrenergic Blocking Agents

Stimulation of calcium pump activity in heart sarcolemma by timolol

1983 ◽  
Vol 61 (3) ◽  
pp. 240-244 ◽  
Author(s):  
Andre Dzurba ◽  
Pallab K. Ganguly ◽  
Robert E. Beamish ◽  
Naranjan S. Dhalla
Keyword(s):  
Membrane Fluidity ◽  
Concanavalin A ◽  
Rat Heart ◽  
Calcium Pump ◽  
Blocking Agents ◽  
Heart Sarcolemma ◽  
Pump Activity ◽  
Adrenergic Blocking ◽  
Stimulation Of ◽  
Adrenergic Blocking Agents

The effects of β-adrenergic blocking agents, timolol and atenolol (1–1000 μM), were studied on rat heart sarcolemmal ATPase and Ca2+ binding activities. Timolol, unlike atenolol, increased both Ca2+-stimulated ATPase and ATP-dependent Ca2+ binding; the maximal effects were seen at 1 μM concentration of timolol. Both timolol and atenolol did not alter the sarcolemmal Mg2+ ATPase and nonspecific Ca2+ binding activities. Sarcolemmal Ca2+ -stimulated ATPase was also activated by concanavalin A (6–66 μg/mL) which is known to alter membrane fluidity; however, Mg2+ ATPase was unaffected by this agent. These results indicate that timolol may stimulate Ca2+ pump activity in heart sarcolemma by changing membrane fluidity in a manner similar to that of concanavalin A.

Liberation of antidiuretic hormone: pharmacologic blockade of ascending pathways

1964 ◽  
Vol 207 (6) ◽  
pp. 1405-1410 ◽  
Author(s):  
Elliott Mills ◽  
S. C. Wang
Keyword(s):  
Brain Stem ◽  
Ulnar Nerve ◽  
Nociceptive Response ◽  
Water Diuresis ◽  
Blocking Agents ◽  
Ascending Pathways ◽  
Adrenergic Blocking ◽  
The Brain ◽  
Stimulation Of ◽  
Adrenergic Blocking Agents

Water diuresis was established and maintained in dogs anesthetized with chloralose. Both ureters were cannulated and a continuous recording of urine flow obtained. ADH release was obtained from stimulation of the central end of a vagus nerve (the vagus-pituitary reflex), and ulnar nerve (nociceptive response) as well as from stimulation of reactive areas in the brain stem. Meperidine (10–15 mg/kg) and morphine (1–4 mg/kg) blocked the response to ulnar nerve stimulation and some brain-stem responses, but not the vagus-pituitary reflex. Similarly, the adrenergic blocking agents, Hydergine (0.3–0.6 mg/kg), phenoxybenzamine (2.0 mg/kg) and phentolamine (0.25 mg/ kg) markedly reduced the ulnar response and some brain-stem responses but not the vagus-pituitary reflex. However, larger doses of phenoxybenzamine (5 mg/kg) and Hydergine (1 mg/ kg) did inhibit the vagus-pituitary reflex. The anticholinergic agents, atropine (1–10 mg/kg) and ethybenztropine (0.5–2.0 mg/kg), were not effective blocking agents themselves but did render the inhibitory action of the adrenergic blocking agents more effective. These results suggest the existence of at least two different ascending pathways for ADH liberation. In addition, the evidence is compatible with the participation of adrenergic as well as cholinergic mechanisms in ADH liberation.

Nervous Control of the Motility of the Alimentary Canal of the Silver Carp

1971 ◽  
Vol 55 (2) ◽  
pp. 469-487
Author(s):  
Y. ITO ◽  
H. KURIYAMA
Keyword(s):  
Alimentary Canal ◽  
Silver Carp ◽  
Circular Muscle ◽  
Field Stimulation ◽  
Blocking Agents ◽  
Muscle Receptors ◽  
Adrenergic Blocking ◽  
Rapid Contraction ◽  
Stimulation Of ◽  
Adrenergic Blocking Agents

1. The electrical and mechanical activities of the alimentary canal of the silver carp, Carassius auratus, were investigated using the strain-gauge tension-recording method and also the double sucrose-gap method. 2. In responses to field stimulation of the alimentary canal four different responses from the stomach and three different responses from the intestine could be evoked. (i) An initial rapid contraction was produced by stimulation of high-frequency or long pulses. The onset of the contraction appeared 0.5 sec after the stimulation. The initial rapid contraction was blocked by tetrodotoxin and D-tubocurarine. This response is thought to be from the striated muscles distributed in the stomach muscle layers. (ii) With or without the initial rapid contraction, field stimulation of low frequency (1-5 c/s) evoked relaxation of the tissue. The latency for the onset of the relaxation was 2 sec. This response was blocked by tetrodotoxin, but α- and β-adrenergic blocking agents had no effect on it. This response is thought to be from thesmooth muscle and to be due to the release of an unknown inhibitory chemical transmitter from the nerve fibres. (iii) The slow phasic contraction appeared with a latency of 8.2 sec, and the amplitude of the contraction was reduced by treatment with atropine and tetrodotoxin but not D-tubocurarine. This response is thought to result from release from the nerve terminals of acetylcholine, which acts on the muscarinic receptors of the smooth muscle. (iv) The delayed contraction appeared with a latency of 11 sec after the onset of field stimulation. The contractions often continued for several minutes. The amplitude and duration of the contraction were reduced or abolished by atropine and tetrodotoxin and were slightly reduced by D-tubocurarine. This response is thought to result from release from the enteric plexus of acetylcholine, which diffuses on to the muscarinic receptors of the muscle. 3. It was difficult to demonstrate a response of the muscle to the excitation of the adrenergic nerve by field stimulation, since α- and β-adrenergic blocking agents had no marked effects on the responses evoked by field stimulation. However, treatment with adrenaline and noradrenaline hyperpolarized the circular muscle membrane and blocked the spike generation. 4. The spontaneous slow potential changes and contractions originated from the myogenic and the neurogenic components. The former was blocked by Mn2+ but not by tetrodotoxin and atropine. The latter was blocked by atropine and tetrodotoxin. 5. Spontaneous hyperpolarizations of the membrane could be recorded. The adrenergic blocking agents had no effect on them. 6. Tetraethyl-ammonium enhanced the tone of the muscle and the amplitude and frequency of the slow depolarizations and contractions recorded from the longitudinal as well as from the circular muscle, in the presence or absence of tetrodotoxin. 7. From the above results it was concluded that there are two kinds of slow depolarization of the muscle, i.e. neurogenic and myogenic. There are three kinds of nerve distributed in the muscle, i.e. excitatory vagal nerve, inhibitory vagal nerve and inhibitory sympathetic nerve. Excitatory nerves innervated two different receptors, i.e. nicotinic striated muscle receptors and muscarinic smooth-muscle receptors.

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