Cholinergic activation of neurons in the medulla oblongata changes urinary bladder activity by plasma vasopressin release in female rats

2016 ◽  
Vol 776 ◽  
pp. 116-123 ◽  
Author(s):  
Eduardo M. Cafarchio ◽  
Luiz A. da Silva ◽  
Luciana C. Auresco ◽  
Cristiana A. Ogihara ◽  
Roberto L. Almeida ◽  
...  
1994 ◽  
Vol 267 (4) ◽  
pp. R923-R928 ◽  
Author(s):  
M. Ota ◽  
J. T. Crofton ◽  
H. Liu ◽  
G. Festavan ◽  
L. Share

It has been demonstrated that the neurohypophysial hormones can be released intrahypothalamically by the paraventricular (PVN) and supraoptic nuclei. The present experiments were undertaken to determine whether a physiological stimulus for vasopressin release, increased plasma osmolality, will stimulate the release of vasopressin by the PVN into the surrounding interstitial fluid, and whether the responses are affected by gender. Intravenous infusion of 2.5 M NaCl for 60 min (0.1 ml.kg-1.min-1) in conscious rats resulted in an increased vasopressin concentration in the dialysate from a microdialysis probe adjacent to the PVN. This response was greater in nonestrous females than in males. On the other hand, the rise in the plasma vasopressin concentration was greater in males than in nonestrous females. Mean arterial blood pressure increased and heart rate decreased, but these responses were not affected by gender. The role of centrally released vasopressin in the control of the peripheral release of vasopressin is conjectural, but both responses may be modulated by the gonadal steroid hormones.


2015 ◽  
Vol 192 ◽  
pp. 57
Author(s):  
E.M. Cafarchio ◽  
R.L. Almeida ◽  
C.A. Ogihara ◽  
L.C. Valdo ◽  
M.C.B. Luz ◽  
...  

1993 ◽  
Vol 265 (1) ◽  
pp. R132-R138 ◽  
Author(s):  
C. L. Cheng ◽  
C. P. Ma ◽  
W. C. de Groat

The effect of capsaicin on micturition and associated reflexes was studied in urethan-anesthetized female rats. Capsaicin or vehicle solution were administered 4 days before the experiment in a dose of 125 mg/kg sc or during the experiment in a dose of 50-100 mg/kg sc. Activity of the urinary bladder was recorded by measuring intravesical pressure via a urethral catheter while slowly filling (0.052 ml/min) the bladder or when the bladder was distended beyond the micturition threshold and maintained at a constant volume. Pretreatment with capsaicin did not significantly change various parameters of urinary bladder function including micturition volume threshold or the amplitude, duration, and interval between reflex bladder contractions. However, capsaicin pretreatment significantly reduced (80% decrease) the arterial pressor responses accompanying reflex bladder contractions and reduced by approximately one-half the percentage of animals in which bladder activity was inhibited by stimulation of the uterine cervix. A large dose of capsaicin (50 mg/kg sc) elicited an acute block of bladder activity that persisted for 8-15 h. This effect is attributable to an action on myelinated afferent or efferent components of the micturition reflex pathway. It is concluded that capsaicin-sensitive afferents are not essential for the performance of micturition in the rat. However, these afferents are involved in cervicovesical reflex mechanisms that modulate bladder activity and in vascular reflexes triggered by isometric bladder contractions.


1992 ◽  
Vol 263 (5) ◽  
pp. R1030-R1034 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share

In conscious, unrestrained rats, the intracerebroventricular injection of the cholinergic agonist, carbachol, or angiotensin II resulted in the transient stimulation of vasopressin secretion, elevation of mean arterial blood pressure, and reduction of heart rate. After the injection of carbachol (25 ng) into a lateral cerebral ventricle, the plasma vasopressin concentration in male rats was increased to twice that of female rats in each phase of the estrous cycle; mean arterial blood pressure was elevated more in males than females, whereas heart rate fell to the same extent in both sexes. In contrast, the increase in the plasma vasopressin concentration of males after the injection of angiotensin II (20 ng) was one-half that of females, and the hypertensive and bradycardic responses were similar in both sexes. Phase of the female estrous cycle had no effect on the responses to either agent. These findings indicate that central cholinergic and angiotensinergic mechanisms controlling vasopressin release are influenced differently by gender. The role of the gonadal steroid hormones in these mechanisms remains to be determined.


1988 ◽  
Vol 254 (4) ◽  
pp. R641-R647 ◽  
Author(s):  
T. J. Vokes ◽  
N. M. Weiss ◽  
J. Schreiber ◽  
M. B. Gaskill ◽  
G. L. Robertson

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.


2010 ◽  
Vol 634 (1-3) ◽  
pp. 142-148 ◽  
Author(s):  
Yulia Shakirova ◽  
Michiko Mori ◽  
Mari Ekman ◽  
Jonas Erjefält ◽  
Bengt Uvelius ◽  
...  

2019 ◽  
Vol 33 (5) ◽  
pp. 640-646 ◽  
Author(s):  
Brian H Harvey ◽  
Wilmie Regenass ◽  
Walter Dreyer ◽  
Marisa Möller

Background: The chronobiotic antidepressant, agomelatine, acts via re-entrainment of circadian rhythms. Earlier work has demonstrated late-life anxiety and reduced corticosterone in post-weaning social isolation reared (SIR) rats. Agomelatine was anxiolytic in this model but did not reverse hypocortisolemia. Reduced corticosterone or cortisol (in humans) is well-described in anxiety states, although the anxiolytic-like actions of agomelatine may involve targeting another mechanism. Central oxytocin and vasopressin exert anxiolytic and anxiogenic effects, respectively, and are subject to circadian fluctuation, while also showing sex-dependent differences in response to various challenges. Aims and methods: If corticosterone is less involved in the anxiolytic-like actions of agomelatine in SIR rats, we wondered whether effects on vasopressin and oxytocin may mediate these actions, and whether sex-dependent effects are evident. Anxiety as assessed in the elevated plus maze, as well as plasma vasopressin, oxytocin, and corticosterone were analyzed in social vs SIR animals receiving sub-chronic treatment with vehicle or agomelatine (40 mg/kg/day intraperitoneally at 16:00) for 16 days. Results: Social isolation rearing induced significant anxiety together with increased plasma vasopressin levels, but decreased corticosterone and oxytocin. While corticosterone displayed sex-dependent changes, vasopressin, and oxytocin changes were independent of sex. Agomelatine suppressed anxiety as well as reversed elevated vasopressin in both male and female rats and partially reversed reduced oxytocin in female but not male rats. Conclusion: SIR-associated anxiety later in life involves reduced corticosterone and oxytocin, and elevated vasopressin. The anxiolytic-like effects of agomelatine in SIR rats predominantly involve targeting of elevated vasopressin.


Sign in / Sign up

Export Citation Format

Share Document