[Efficacy of acupuncture combined with auricular point sticking on the content of serum prostaglandin F2α, and plasma arginine vasopressin in patients with menstrual headache].
2
Citation
0
Reference
10
Related Paper
Citation Trend
Abstract:
To observe the clinical efficacy of acupuncture combined with auricular point sticking for menstrual headache and to discuss its mechanism.Eighty-five patients with menstrual headache were randomly divided into an observation group (43 cases) and a control group (42 cases). The observation group was treated with body acupuncture combined with auricular point sticking and the control group was treated with flunarizine hydrochloride capsules orally. The treatments of 3 menstrual cycles were required. The clinical efficacy was observed in the two groups. The content of serum prostaglandin F2α, (PGF2α) and plasma arginine vasopressin (AVP) in the menstrual periods of some patients randomly selected in the two groups was tested before and after treatment and was compared with that of 20 cases in a normal group. Results The total effective rate was 95.4% (41/43) in the observation group which was obviously superior to 81.0% (34/42) in the control group (P<0.01). Before treatment, the content of serum PGF2α and plasma AVP of patients in the two groups was higher than that in the normal group (all P<0.01). After treatment,the content of serum PGF2α and plasma AVP was lower than that before treatment in the two groups (P<0.01, P<0.05). The content of serum PGF2α in the observation group was decreased significantly compared with that in the control group (P<0.05) and returned to the level of the normal group.Body acupuncture combined with auricular point sticking achieves positive efficacy for menstrual headache and its mechanism could be related to regulating the abnormal levels of serum PGF2α and plasma AVP.Keywords:
Menstruation
Cite
Arginine vasopressin (AVP) is regarded as facilitatory to adenohypophysial ACTH secretion at the level of the corticotropic cell. A central facilitatory action of AVP on hypothalamic corticotropin-releasing factor (CRF) has also been postulated, although conclusive evidence on this point is lacking. We directly tested this hypothesis and have found that intracerebroventricular administration of AVP attenuates secretion of immunoreactive CRF (irCRF) into the hypophysial portal circulation in urethane-anesthetized rats. This suppression occurred in a dose-dependent fashion. Conversely, immunoneutralization of AVP or treatment with an AVP antagonist increased portal concentrations of irCRF by 53% and 30%, respectively. These unexpected observations provide evidence for a tonic inhibitory role of central AVP in regulation of irCRF and thus ACTH secretion.
Tonic (physiology)
Corticotropin-releasing hormone
Cite
Citations (59)
It has been suggested that PTH-related protein (PTHrP) is an endogenous modulator of cardiovascular systems. We have reported that PTHrP(1–34), but not PTH(1–34), causes the release of arginine-vasopressin (AVP) from the supraoptic nucleus (SON) of the hypothalamus in vitro through a novel receptor distinct from the PTH/PTHrP receptors (type I or type II) described previously. In this study, we have investigated the in vivo effects of PTHrP(1–34) on AVP secretion and its messenger RNA (mRNA) expression in the SON in conscious rats. Intracerebroventricular (icv) administration of PTHrP(1–34) resulted in an increase in plasma AVP concentration in a dose-dependent manner (0–400 pmol/rat). The maximal effect was obtained at 15 min after icv administration of PTHrP(1–34). Neither PTHrP(7–34) nor PTH(1–34) had any effect on plasma AVP levels. PTHrP(1–34)-induced AVP secretion was antagonized by pretreatment with PTHrP(7–34) but not by that with PTH(1–34). In addition, in situ hybridization study revealed that AVP mRNA expression in the SON and paraventricular nucleus was significantly increased 30 min after icv administration of PTHrP(1–34) and reached a maximum at 180 min. Furthermore, in Northern blot analyses, AVP mRNA expression in the SON was increased to approximately a 2-fold of basal level by PTHrP(1–34). On the other hand, neither PTHrP(7–34) or PTH(1–34) had any effect on the mRNA expression. The PTHrP(1–34)-stimulated AVP mRNA expression was eliminated by pretreatment with PTHrP(7–34) but not with PTH(1–34). These results suggest that, in the central nervous system, PTHrP(1–34) is involved in AVP secretion through a novel receptor distinct from the PTH/PTHrP receptors reported previously, playing a role in the body water and electrolyte homeostasis.
Supraoptic nucleus
Northern blot
Parathyroid hormone-related protein
Cite
Citations (10)
Arginine vasopressin (AVP) regulates ACTH release under certain conditions, and exogenously administered AVP is used clinically to stimulate ACTH secretion. We attempted to determine at what plasma concentration AVP can stimulate ACTH release. Six normal men were given infusions of AVP (Ferring) or vehicle between 1600 and 1700 h on five occasions: 1) saline (30 mL/h); 2) 10 ng AVP/min; 3) 30 ng AVP/min; 4) 100 ng AVP/min; and 5) 300 ng AVP/min. Plasma AVP, ACTH, and cortisol concentrations were measured every 10 min during the infusions. Basal plasma AVP levels were less than 1 ng/L (<0.92 pmol/ L). The lowest AVP dose raised plasma AVP into the range found in fluid-deprived subjects (7–8 ng/L; 6.5–7.3 pmol/L), but had no effect on plasma ACTH concentrations. AVP in a dose of 30 ng/min also had no effect. The 100 ng AVP/min dose raised plasma AVP concentrations to 51.4–65.5 ng/L (46–60pmol/L). This increase led to a transient insignificant increase in plasma ACTH from 13.9 ± 1.2 (±SEM) ng/L (3.1 ± 0.3 pmol/ L) to 20.0 ± 1.4 ng/L (4.4 ± 0.3 pmol/L), while plasma cortisol rose significantly from 146 ± 10 to 209 ± 19nmol/L (P < 0.01) after 60 min of infusion. The 300 ng AVP/min dose raised plasma AVP levels to about 260 ng/L (239 pmol/L); the maximal plasma ACTH andcortisol levels were 39.5 ± 5.0 ngpmol/L). This increase led to a transient insignificant increase in plasma ACTH from 13.9 ± 1.2 (±SEM) ng/L (3.1 ± 0.3 pmol/ L) to 20.0 ± 1.4 ng/L (4.4 ± 0.3 pmol/L), whileplasma cortisol rose significantly from 146 ± 10 to 209 ± 19 nmol/L(P < 0.01) after 60 min of infusion. The 300 ng AVP/min dose raisedplasma AVP levels to about 260 ng/L (239 pmol/L); the maximal plasma ACTH andcortisol levels were 39.5 ± 5.0 ng/L (8.7 ± 1.1 pmol/L; P < 0.01) and 348 nmol/L (P < 0.01), respectively. Thus, peripheral plasma AVP levels have to be raised high above the physiological range before ACTH release is stimulated. We conclude that any AVP reaching the adenohypophysis through the peripheral circulation is of much less importance for the regulation of ACTH secretion than is AVP derived from the pituitary portal circulation.
Basal (medicine)
ACTH secretion
Cite
Citations (33)
Effect of thyrotropic releasing hormone (TRH) on plasma arginine vasopressin (AVP) was studied in human subjects. All 7 normal controls and 2 hypothyrotropic hypothyroid subjects failed to show any rise of AVP on TRH administration. The 4 primary hypothyroid subjects had elevated basal AVP level and showed further elevation on TRH administration. Our data suggests that elevated TRH in primary hypothyroid subjects may act directly as a nonosmotic stimulus or modulate the osmoreceptor and hypothalamic neurohypophyseal system for AVP release.
Osmoreceptor
Basal (medicine)
Cite
Citations (11)
Abstract While the effects of cytokines on the hypothalamo-pituitary-adrenal axis have received a great deal of attention in recent years the effects of cytokines on posterior pituitary hormone release has been less well characterized. In the present study we have investigated the effects of a single i.p. injection of interleukin (IL)-1β on circulating levels of vasopressin (AVP) in the rat. We have found that the ability of IL-1β to increase plasma AVP is strongly influenced by circulating levels of glucocorticoid steroids. IL-1β did not affect plasma AVP in sham-operated control animals over the 4 h period of study. In contrast, following adrenalectomy we were able to stimulate AVP substantially with increases over the 4 h period. This effect was reduced by treatment of adrenalectomized rats with a low dose of dexamethasone and abolished with a high dose. These data suggest an inverse relationship between circulating levels of glucocorticoids and the ability of IL-1β to stimulate plasma AVP. Journal of Endocrinology (1994) 142, 361–366
Posterior pituitary
Cite
Citations (13)
Cite
Citations (12)
Cite
Citations (3)
Increased Vasopressin Secretion and Release in Mice Transgenic for the Rat Arginine Vasopressin Gene
The rat arginine vasopressin (AVP) genomic sequence has been utilized to develop a line of transgenic mice homozygous and heterozygous for the transgene. Expression of the rat AVP gene was demonstrated by Southern blotting and resulted in increased amounts of AVP in hypothalamus and frontotemporal brain cortex. Secretion of AVP from the neurohypophysial system results in an increased concentration of the hormone in the plasma and in an increased excretion in the urine in amounts three to five times those of normal mice. Extraneural ectopic hormone production was found only in the pancreas. Despite chronic hypersecretion of AVP, 24-hour urine volume and osmolality did not show evidence of increased antidiuretic hormone action on the kidney, so that, under basal conditions, the water balance in the animals is unaffected.
Urine osmolality
Cite
Citations (11)
Pancreatic Islets
Basal (medicine)
Cite
Citations (29)
Arginine vasopressin stimulates the secretion of adrenocorticotropin. A direct stimulatory effect of AVP on cortisol as well as aldosterone secretion has been postulated by several investigators. To study the possible role of a direct stimulatory action of AVP on the adrenal cortex, normal volunteers were treated with incremental injections of ACTH or with incremental infusions of AVP which raised plasma AVP levels to a maximum of 256 +/- 16 pmol/l. In both situations, a significant (p less than 0.001) linear correlation between plasma ACTH and plasma cortisol was observed. The regression coefficients were not different (p greater than 0.5). Plasma aldosterone was stimulated by both treatments, but the weakly positive correlation between plasma ACTH and plasma aldosterone was not significant for either stimulus. Thus, in man, a direct stimulatory effect of AVP on cortisol secretion cannot be demonstrated. A direct effect of AVP on aldosterone cannot be definitely excluded, but is certainly of minor importance.
Cite
Citations (9)