scholarly journals Osmotic Pressure and Angiotensin II Stimulation of Arginine Vasopressin Release from a Guinea Pig Hypothalamo-Neurohypophyseal Complex in Organ Culture

1980 ◽  
Vol 56 (3) ◽  
pp. 262-273 ◽  
Author(s):  
San-e ISHIKAWA ◽  
Toshikazu SAITO ◽  
Sho YOSHIDA
Keyword(s):  
Angiotensin Ii ◽  
Guinea Pig ◽  
Organ Culture ◽  
Osmotic Pressure ◽  
Arginine Vasopressin ◽  
Vasopressin Release ◽  
Stimulation Of

Role of calcium in osmotic and nonosmotic release of vasopressin from rat organ culture

1983 ◽  
Vol 244 (5) ◽  
pp. R703-R708
Author(s):  
S. Ishikawa ◽  
R. W. Schrier
Keyword(s):  
Angiotensin Ii ◽  
Organ Culture ◽  
Arginine Vasopressin ◽  
Ionophore A23187 ◽  
Ang Ii ◽  
Ca Uptake ◽  
High Concentrations ◽  
Cellular Ca ◽  
Stimulation Of

In the present study the role of calcium (Ca) in the stimulation of arginine vasopressin (AVP) release from the cultured rat hypothalamoneurohypophyseal complex (HNC) was examined in response to three different stimuli, 56 mM potassium chloride, an increase in medium osmolality from 290 to 310 mosmol/kg H2O, or 1 X 10(-6) M angiotensin II (ANG II). With all three stimuli AVP release from rat HNC explants was enhanced by increasing Ca concentration in the medium from 0 to 1.8 mM Ca. However, high concentrations of Ca (8 mM) inhibited the response of AVP release to either hyperosmolality or angiotensin II. Chemically dissimilar blockers of cellular Ca uptake, verapamil (5.2 X 10(-6) or 5.2 X 10(-5) M) or nifedipine (5.8 X 10(-6) or 5.8 X 10(-5) M), completely abolished AVP release from rat HNC explants in response to the three different stimuli in 1.8 mM Ca. In a normal concentration of medium Ca (1.8 mM) a Ca ionophore, A23187 (3.8 X 10(-5) M), significantly enhanced the osmotic and nonosmotic (ANG II-stimulated) release of AVP from rat HNC explants compared with controls without Ca ionophore. This effect of Ca ionophore to enhance AVP release was more evident in a lower Ca medium (0.9 mM Ca in the hyperosmolality study and 0.3 mM Ca in the ANG II study). These results therefore indicate that cellular Ca uptake is an important modulator of osmotic and nonosmotic AVP release from the intact rat hypothalamoneurohypophyseal system. The influence of extracellular Ca on the osmotic and nonosmotic release of AVP is also demonstrated.

Central angiotensin II stimulation of ovine fetal swallowing

1994 ◽  
Vol 76 (3) ◽  
pp. 1340-1345 ◽  
Author(s):  
M. G. Ross ◽  
L. K. Kullama ◽  
A. Ogundipe ◽  
K. Chan ◽  
M. G. Ervin
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Low Voltage ◽  
Control Period ◽  
Late Gestation ◽  
Ang Ii ◽  
Fetal Plasma ◽  
Plasma Arginine ◽  
Ovine Fetal ◽  
Stimulation Of

In the late-gestation ovine fetus, spontaneous swallowing occurs primarily during fetal low-voltage electrocortical (ECoG) activity in association with fetal breathing movements. Fetal swallowing activity may be stimulated in response to systemic or carotid plasma hyperosmolality, although not to increased plasma angiotensin II (ANG II) levels. In view of the potent dipsogenic effects of central, but not peripheral, ANG II in adult sheep, the present study investigated the effect of intracerebroventricular (ICV) ANG II on fetal swallowing activity. Six ovine fetuses (127 +/- 1 days) were chronically prepared with electromyogram and cortical electrodes and with vascular and lateral ventricle catheters. After a 2-h control period, fetuses received ICV injections of artificial cerebrospinal fluid and increasing concentrations of ANG II (0.1, 1.0, 10, 100, and 500 ng/kg). Fetal ECoG activity did not change, although fetal swallowing activity significantly increased in response to the 100- and 500- ng/kg ANG II doses (1.20 +/- 0.14 to 3.34 +/- 0.59 and 3.46 +/- 0.81 swallows/min of low-voltage ECoG, respectively). In response to the highest ANG II dose, fetal plasma arginine vasopressin levels significantly increased (5.7 +/- 1.2 to 17.2 +/- 4.6 pg/ml). ICV ANG II stimulation of fetal swallowing and arginine vasopressin secretion demonstrates that central ANG II dipsogenic mechanisms are intact by 0.9 of ovine gestation.

Effects of ACTH and ACTH fragments on DNA synthesis in guinea-pig adrenal segments kept in organ culture

1987 ◽  
Vol 115 (3) ◽  
pp. 505-510 ◽  
Author(s):  
N. M. Wulffraat ◽  
H. A. Drexhage ◽  
P. Jeucken ◽  
R. D. van der Gaag ◽  
W. M. Wiersinga
Keyword(s):  
Guinea Pig ◽  
Organ Culture ◽  
Dna Synthesis ◽  
Intermediate Lobe ◽  
Terminal Part ◽  
Terminal Fragment ◽  
Acth Fragments ◽  
Epidermal Growth ◽  
Stimulation Of

ABSTRACT Stimulation of adrenal DNA synthesis by ACTH(1–39) and its fragments ACTH(1–24) (Synacthen) and ACTH(18–39) was investigated. Synthesis of DNA was measured as the increase in the percentage of cells in S-phase (Feulgen densitometry) in guinea-pig adrenal explants kept in organ culture and exposed to the peptides for 5 h at 37 °C. ACTH(1–39) and its C-terminal fragment ACTH(18–39) (corticotrophin-like intermediate lobe peptide) were found to be potent stimulators of in-vitro adrenal DNA synthesis. The dose–response kinetics were biphasic and optimal responsiveness was reached in both instances at 1 fmol/1–10 pmol/l (this biological effect of ACTH(18–39) has hitherto not been described). The N-terminal fragment ACTH(1–24) gave only minimal responses. Thyrotrophin and LH, tested as controls, did not induce adrenal DNA synthesis. Epidermal growth factor was a potent stimulator of adrenal DNA synthesis in vitro. Our data suggest a trophic action of the C-terminal part (ACTH(18–39)) of the corticotrophic molecule. Clear trophic effects were also found for the N-terminal part of the pro-opiomelanocortin molecule N-POC(1–76) (optimum 0·1 nmol/l) and N-POC(51– 62) (optimum 0·1 pmol/l). The latter observations support earlier concepts that this part of the proopiomelanocortin molecule has a stimulatory effect on adrenal DNA synthesis. J. Endocr. (1987) 115, 505–510

scholarly journals Neuropeptide S Stimulates the Hypothalamo-Pituitary-Adrenal Axis and Inhibits Food Intake

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3510-3518 ◽  
Author(s):  
Kirsty L. Smith ◽  
Michael Patterson ◽  
Waljit S. Dhillo ◽  
Sejal R. Patel ◽  
Nina M. Semjonous ◽  
...  
Keyword(s):  
Food Intake ◽  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Arginine Vasopressin ◽  
Lateral Ventricle ◽  
Neuropeptide S ◽  
Plasma Acth ◽  
Vasopressin Release ◽  
Pituitary Adrenal Axis ◽  
Stimulation Of

Neuropeptide S (NPS) is a recently discovered peptide shown to be involved in the modulation of arousal and fear responses. It has also been shown that lateral ventricle administration of NPS causes a significant decrease in food intake. Neuropeptides involved in the modulation of arousal have been shown to be involved in the regulation of the hypothalamo-pituitary adrenal (HPA) axis and food intake. In this study, we have examined the effect of intracerebroventricular (ICV) administration of NPS on behavior, regulation of the HPA axis, and food intake. ICV NPS significantly increased plasma ACTH and corticosterone 10 and 40 min after injection, respectively. A single ICV injection of NPS caused a significant increase in rearing activity as well as ambulatory movement for up to 45 min after injection. We then studied the effect of paraventricular nucleus (PVN) administration of NPS on the regulation of the HPA axis, behavior, and food intake. There was a significant increase in plasma ACTH and corticosterone after a single NPS PVN injection. Incubation of hypothalamic explants with increasing concentrations of NPS caused a significant increase in CRH and arginine vasopressin release. In addition, PVN administration of NPS dose-dependently inhibited food intake in the first hour after injection, although no effect on food intake was seen after this time. PVN administration of NPS caused a significant increase in rearing activity. These data demonstrate a novel role for NPS in the stimulation of the HPA axis.

EFFECTS OF ANGIOTENSIN II ON ARGININE-VASOPRESSIN IN PHYSIOLOGICAL AND PATHOLOGICAL SITUATIONS IN MAN

1977 ◽  
Vol 74 (2) ◽  
pp. 251-259 ◽  
Author(s):  
P. L. PADFIELD ◽  
J. J. MORTON
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
High Plasma ◽  
Physiological Control ◽  
Vasopressin Release ◽  
Normal Volunteers ◽  
Plasma Angiotensin ◽  
Plasma Arginine ◽  
Acute Changes

Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions. Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5·4 ± 0·3 (s.e.m.) to 6·4 ± 0·2 pg/ml) only when plasma angiotensin II levels were supraphysiological. Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.

Role of dopamine in the angiotensin II-induced vasopressin release in the conscious dehydrated dog

1982 ◽  
Vol 94 (2) ◽  
pp. 243-249 ◽  
Author(s):  
D. P. Brooks ◽  
J. R. Claybaugh
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Mean Arterial Blood Pressure ◽  
Arginine Vasopressin ◽  
Plasma Renin ◽  
Dopamine Antagonist ◽  
Vasopressin Release ◽  
Arterial Blood

The effect of the dopamine antagonist, haloperidol, on arginine-vasopressin (AVP) release induced by angiotensin II was studied in six dehydrated conscious dogs. Angiotensin II (10 ng/kg per min) alone caused a twofold increase (P<0·05) in plasma AVP concentration, a 25 mmHg increase (P<0·01) in mean arterial blood pressure (ABP) and a 70% decrease (P<0·01) in plasma renin activity (PRA). In the presence of haloperidol (3 μg/kg per min), angiotensin II caused similar changes in mean ABP (+25 mmHg; P<0·01) and PRA (−65%, P<0·01), but a small insignificant decrease in plasma AVP (−22%). The AVP response to angiotensin II in the presence of haloperidol was significantly (P<0·05) different from its response to angiotensin II alone. Neither haloperidol alone nor the two vehicles had any effect on plasma AVP or mean ABP but PRA dropped slightly. The results suggest that a dopaminergic mechanism may be involved in angiotensin II-induced AVP release.

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