Alpha Adrenergic Receptor Agents☆

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.

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Dogfish pressor response to potassium blocked by magnesium and phentolamine

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1982.242.3.r185 ◽

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.

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A5 noradrenergic neurons and the carotid sympathetic chemoreflex

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.267.2.r519 ◽

1994 ◽

Vol 267 (2) ◽

pp. R519-R526 ◽

Cited By ~ 15

Author(s):

N. Koshiya ◽

P. G. Guyenet

Keyword(s):

Spinal Cord ◽

Neural Activity ◽

Adrenergic Receptor ◽

Intrathecal Injection ◽

Noradrenergic Neurons ◽

Alpha Adrenergic Receptor ◽

Adrenergic Antagonist ◽

A5 Area ◽

6 Hydroxydopamine ◽

Nerve Discharge

Inhibition of neural activity in the caudal ventrolateral pons (A5 area) by microinjection of muscimol (Mus) attenuates (-65%) the carotid sympathetic chemoreflex (SChR) without altering the concomitant activation of the phrenic nerve (PND). The present study, performed in urethan-anesthetized rats, explores the possibility that activation of the noradrenergic (NE) neurons of the A5 area is involved in the SChR. The NE neuron-selective toxin 6-hydroxydopamine (6-OHDA) was microinjected bilaterally into the spinal cord at T2 level (4 micrograms). This dose reduced the SChR by 55% (n = 5) 90 min after injection, while 0.4 microgram of 6-OHDA produced no effect (n = 5). In seven rats that had received 250 micrograms 6-OHDA intracisternally 2 wk before, Mus injections into the A5 area failed to attenuate the SChR. These rats also had a lower resting mean arterial pressure than controls (97 vs. 112 mmHg). Spinal intrathecal injection of alpha-adrenergic receptor antagonists (prazosin, 10 and 20 micrograms) or phentolamine (20 and 40 micrograms) attenuated resting sympathetic nerve discharge (SND) and SChR in a roughly proportional manner (25-40%); the beta-adrenergic antagonist nadolol (10 and 20 microgram(s) intrathecally) attenuated the SChR selectively but modestly (-10%). The results are generally compatible with the hypothesis that A5 NE neurons and particularly their spinal cord projection could play a facilitating role in the SChR. However, clear evidence that A5 cells contribute selectively to sympathoactivation during chemoreceptor stimulation by releasing NE in the spinal cord could not be obtained.

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