scholarly journals Effects of guanethidine on the blood pressure response to splanchnic nerve stimulation in the rat: role of the adrenal medulla

1968 ◽  
Vol 34 (2) ◽  
pp. 259-266 ◽  
Author(s):  
A. CARPI ◽  
CARLA CARTONI
Keyword(s):  
Blood Pressure ◽  
Adrenal Medulla ◽  
Nerve Stimulation ◽  
Blood Pressure Response ◽  
Splanchnic Nerve ◽  
Pressure Response ◽  
Splanchnic Nerve Stimulation

Brain angiotensin receptors and sympathoadrenal regulation during insulin-induced hypoglycemia

2001 ◽  
Vol 280 (4) ◽  
pp. R1162-R1168 ◽  
Author(s):  
René H. Worck ◽  
Dennis Staahltoft ◽  
Thomas E. N. Jonassen ◽  
Erik Frandsen ◽  
Hans Ibsen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibition ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Angiotensin Receptors ◽  
Converting Enzyme ◽  
Reflex Regulation ◽  
Conscious Rats ◽  
Converting Enzyme Inhibition

Simultaneous blockade of systemic AT1 and AT2 receptors or converting enzyme inhibition (CEI) attenuates the hypoglycemia-induced reflex increase of epinephrine (Epi). To examine the role of brain AT1 and AT2 receptors in the reflex regulation of Epi release, we measured catecholamines, hemodynamics, and renin during insulin-induced hypoglycemia in conscious rats pretreated intracerebroventricularly with losartan, PD-123319, losartan and PD-123319, or vehicle. Epi and norepinephrine (NE) increased 60-and 3-fold, respectively. However, the gain of the reflex increase in plasma Epi (Δplasma Epi/Δplasma glucose) and the overall Epi and NE responses were similar in all groups. The ensuing blood pressure response was similar between groups, but the corresponding bradycardia was augmented after PD-123319 ( P < 0.05 vs. vehicle) or combined losartan and PD-123319 ( P < 0.01 vs. vehicle). The findings indicate 1) brain angiotensin receptors are not essential for the reflex regulation of Epi release during hypoglycemia and 2) the gain of baroreceptor-mediated bradycardia is increased by blockade of brain AT2 receptors in this model.

Study on clinical and endocrine characteristics of dexamethasone-suppressible hyperaldosteronism compared with those in primary aldosteronism owing to aldosterone-producing adenoma

1989 ◽  
Vol 121 (3) ◽  
pp. 334-344 ◽  
Author(s):  
Noriyoshi Yamakita ◽  
Keigo Yasuda ◽  
Nobuyasu Noritake ◽  
Leilani B. Mercado-Asis ◽  
Hiroshi Murase ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Primary Aldosteronism ◽  
Blood Pressure Response ◽  
Laboratory Data ◽  
Japanese Patients ◽  
Pressure Response ◽  
Plasma Aldosterone ◽  
Vascular Damage ◽  
Aldosterone Producing Adenoma

Abstract. The clinical and endocrine characteristics of 12 Japanese patients with dexamethasone-suppressible hyperaldosteronism were compared with those in 49 Japanese patients with primary aldosteronism due to aldosteronoma. The results were as follows: 1. Most of the laboratory data in the two groups were almost the same. 2. The grade of vascular damage in both uncontrolled (3) and well-controlled (9) patients with dexamethasonesuppressible hyperaldosteronism did not correlate with blood pressure response. 3. The responsiveness of plasma aldosterone to exogenous ACTH in 6 patients with dexamethasone-suppressible hyperaldosteronism was not different from that in 9 patients with aldosteronoma. Even in 3 well-controlled patients in the former group, the plasma aldosterone response was as low as in all the 3 patients with small aldosteronomas. 4. In 4 patients with small aldosteronomas, plasma aldosterone was continuously suppressed with daily dexamethasone to the same degree as in dexamethasone-suppressible hyperaldosteronism. 5. The blood pressure, however, did not improve even in the patients with small aldosteronomas. The possible indistinguishable mechanism in dexamethasone-suppressible hyperaldosteronism and primary aldosteronism with small adenomas and the role of unknown hypertensinogenic steroid(s) other than aldosterone in inducing hypertension in dexamethasone-suppressible hyperaldosteronism are discussed.

scholarly journals Oscillatory blood pressure response to the onset of cycling exercise in men: role of group III/IV muscle afferents

2015 ◽  
Vol 100 (3) ◽  
pp. 302-311 ◽  
Author(s):  
Thales C. Barbosa ◽  
Igor A. Fernandes ◽  
Nisval Magalhães-Jr ◽  
Ismar L. Cavalcanti ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Muscle Afferents ◽  
Pressure Response ◽  
Cycling Exercise ◽  
Group Iii

Release of galanin from isolated perfused porcine adrenal glands: role of splanchnic nerves

1991 ◽  
Vol 261 (1) ◽  
pp. E31-E40 ◽  
Author(s):  
J. J. Holst ◽  
M. Ehrhart-Bornstein ◽  
T. Messell ◽  
S. S. Poulsen ◽  
H. Harling
Keyword(s):  
Nerve Stimulation ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
High Concentration ◽  
Vitro Model ◽  
Arterial Plasma ◽  
Regulatory Functions ◽  
Splanchnic Nerve Stimulation

We found a high concentration of galanin in extracts of porcine adrenal glands (114 pmol/g). By immunohistochemistry, galanin was localized to groups of medullary cells previously shown to produce norepinephrine. To study mechanisms for the release of galanin, we developed the following in vitro model: isolated perfused porcine adrenals with intact splanchnic nerve supply. When the nerves were electrically stimulated, epinephrine and norepinephrine secretion increased 276- and 291-fold, respectively, and galanin release increased up to 1,300-fold. Acetylcholine at 10(-6) M stimulated galanin release, and hexamethonium almost abolished the response to nerve stimulation. Galanin infusions had no effect on epinephrine and norepinephrine secretion in concentrations of 10(-8) and 10(-7) M, but increased both cortisol and aldosterone secretion (P less than 0.05). Splanchnic nerve stimulation in anesthetized pigs increased the concentration of galanin in the caval vein but not in arterial plasma. It is concluded that galanin, coreleased with catecholamines from the adrenal glands, may have endocrine functions but that galanin may also have local regulatory functions in the adrenals.

PACAP release from the canine adrenal gland in vivo: its functional role in severe hypotension

2003 ◽  
Vol 284 (2) ◽  
pp. R588-R597 ◽  
Author(s):  
Stéphane Lamouche ◽  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Gland ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Dependent Manner ◽  
Severe Hypotension ◽  
Pituitary Adenylate Cyclase ◽  
Catecholamine Response ◽  
Splanchnic Nerve Stimulation

This study was to investigate if endogenous pituitary adenylate cyclase-activating polypeptide (PACAP) can be released during direct splanchnic nerve stimulation in vivo and to determine whether PACAP in the adrenal gland can modulate the medullary response to sympathoadrenal reflex. The output of adrenal catecholamine and PACAP-38-like immunoreactivity (PACAP-38-ir) increased in a frequency-dependent manner after direct splanchnic nerve stimulation (0.2–20 Hz). Both responses were highly reproducible, and PACAP-38-ir output closely correlated with catecholamine output. Sodium nitroprusside (SNP; 0.1 mg/kg iv bolus) caused a severe hypotension resulting in marked increases in catecholamine secretion. In the presence of local PACAP-27 (125 ng), the maximum catecholamine response to SNP was significantly potentiated in a synergistic manner compared with that obtained in the group receiving SNP or PACAP-27 alone. The study indicates that endogenous PACAP-38 can be released particularly when the sympathoadrenal system is highly activated and that the local exogenous PACAP-27 enhanced the reflex-induced catecholamine release, suggesting collectively a facilitating role of PACAP as neuromodulator in the sympathoadrenal function in vivo.

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