Adrenergic receptors of adrenal medullary vasculature

1989 ◽  
Vol 256 (1) ◽  
pp. H233-H239
Author(s):  
D. A. Jordan ◽  
M. J. Breslow ◽  
K. L. Kubos ◽  
R. J. Traystman
Keyword(s):  
Nerve Stimulation ◽  
Adrenergic Receptors ◽  
High Performance ◽  
Vascular Tone ◽  
Splanchnic Nerve ◽  
Saline Control ◽  
Control Group ◽  
Medullary Blood Flow ◽  
Splanchnic Nerve Stimulation ◽  
Catecholamine Concentration

The present study evaluates possible effects of adrenal catecholamines, released by splanchnic nerve stimulation, on adrenal medullary blood flow (MQ) and adrenal catecholamine secretion (CS). Twelve pentobarbital-anesthetized mongrel dogs were subjected to three identical splanchnic nerve stimulations (5 V, 20 Hz, for 3 min) at 30-min intervals, and MQ (radiolabeled microsphere technique) and CS (high-performance liquid chromatography) were measured before and during each nerve stimulation. Animals were assigned to one of three groups and administered either saline, pindolol (1 and 4 mg/kg), or prazosin (1 and 4 mg/kg) before the second and third nerve stimulation, respectively. In the saline control group, each nerve stimulation resulted in similar increases in MQ and CS. Pindolol attenuated nerve stimulation-induced increases in MQ and CS by 50%, but had no effect on medullary catecholamine concentration. Prazosin augmented nerve stimulation-induced MQ, CS, and medullary catecholamine concentration by 35%. These data suggest that adrenal adrenergic receptors modulate elicited CS and mediate changes in adrenal medullary vascular tone.

Effects of adrenomedullin and PAMP on adrenal catecholamine release in dogs

1999 ◽  
Vol 276 (4) ◽  
pp. R1118-R1124
Author(s):  
Kimiya Masada ◽  
Takahiro Nagayama ◽  
Akio Hosokawa ◽  
Makoto Yoshida ◽  
Mizue Suzuki-Kusaba ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Induced Response ◽  
Dependent Manner ◽  
Pentobarbital Sodium ◽  
Anesthetized Dogs ◽  
Dose Dependent ◽  
Splanchnic Nerve Stimulation

We examined the effects of proadrenomedullin-derived peptides on the release of adrenal catecholamines in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered into the adrenal gland through the phrenicoabdominal artery. Splanchnic nerve stimulation (1, 2, and 3 Hz) and ACh injection (0.75, 1.5, and 3 μg) produced frequency- or dose-dependent increases in adrenal catecholamine output. These responses were unaffected by infusion of adrenomedullin (1, 3, and 10 ng ⋅ kg−1 ⋅ min−1) or its selective antagonist adrenomedullin-(22—52) (5, 15, and 50 ng ⋅ kg−1 ⋅ min−1). Proadrenomedullin NH2-terminal 20 peptide (PAMP; 5, 15, and 50 ng ⋅ kg−1 ⋅ min−1) suppressed both the splanchnic nerve stimulation- and ACh-induced increases in catecholamine output in a dose-dependent manner. PAMP also suppressed the catecholamine release responses to the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (0.5, 1, and 2 μg) and to muscarine (0.5, 1, and 2 μg), although the muscarine-induced response was relatively resistant to PAMP. These results suggest that PAMP, but not adrenomedullin, can act as an inhibitory regulator of adrenal catecholamine release in vivo.

The effects of adrenergic antagonists on the serotonin levels of feline enterochromaffin cells after splanchnic nerve stimulation

1980 ◽  
Vol 47 (2) ◽  
pp. 89-98 ◽  
Author(s):  
I. Larsson ◽  
A. Dahlström ◽  
G. Pettersson ◽  
P. -A. Larsson ◽  
J. Kewenter ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Enterochromaffin Cells ◽  
Adrenergic Antagonists ◽  
Splanchnic Nerve Stimulation

Neural control of adrenal medullary and cortical blood flow during hemorrhage

1987 ◽  
Vol 252 (3) ◽  
pp. H521-H528 ◽  
Author(s):  
M. J. Breslow ◽  
D. A. Jordan ◽  
S. T. Thellman ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Nerve Stimulation ◽  
Neural Control ◽  
Splanchnic Nerve ◽  
Nerve Section ◽  
Cortical Blood Flow ◽  
Hemorrhagic Hypotension ◽  
Medullary Blood Flow ◽  
Greater Splanchnic Nerve

Hemorrhagic hypotension produces an increase in adrenal medullary blood flow and a decrease in adrenal cortical blood flow. To determine whether changes in adrenal blood flow during hemorrhage are neurally mediated, we compared blood flow responses following adrenal denervation (splanchnic nerve section) with changes in the contralateral, neurally intact adrenal. Blood pressure was reduced and maintained at 60 mmHg for 25 min by hemorrhage into a pressurized bottle system. Adrenal cortical blood flow decreased to 50% of control with hemorrhage in both the intact and denervated adrenal. Adrenal medullary blood flow increased to four times control levels at 15 and 25 min posthemorrhage in the intact adrenal, but was reduced to 50% of control at 3, 5, and 10 min posthemorrhage in the denervated adrenal. In a separate group of dogs, the greater splanchnic nerve on one side was electrically stimulated at 2, 5, or 15 Hz (n = 4 each group) for 40 min. Adrenal medullary blood flow increased 5- to 10-fold in the stimulated adrenal but was unchanged in the contralateral, nonstimulated adrenal. Adrenal cortical blood flow was not affected by nerve stimulation. We conclude that activity of the splanchnic nerve profoundly affects adrenal medullary vessels but not adrenal cortical vessels and mediates the observed increase in adrenal medullary blood flow during hemorrhagic hypotension.

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