Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Sex differences in central cholinergic and angiotensinergic control of vasopressin release

1992 ◽  
Vol 263 (5) ◽  
pp. R1030-R1034 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Estrous Cycle ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Female Rats ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin

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.

Bradykinin in reflex cardiovascular responses to static muscular contraction

1986 ◽  
Vol 61 (1) ◽  
pp. 271-279 ◽  
Author(s):  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Response ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Carboxypeptidase B ◽  
Arterial Blood ◽  
Static Contraction ◽  
Stimulation Of

We examined the contribution of bradykinin to the reflex hemodynamic response evoked by static contraction of the hindlimb of anesthetized cats. During electrical stimulation of ventral roots L7 and S1, we compared the cardiovascular responses to hindlimb contraction before and after the following interventions: inhibition of converting enzyme (kininase II) with captopril (3–4 mg/kg, n = 6); inhibition of kallikrein activity with aprotinin (Trasylol, 20,000–30,000 KIU/kg, n = 8); and injection of carboxypeptidase B (500–750 U/kg, n = 7). Treatment with captopril augmented the rise in mean arterial blood pressure and maximal time derivative of pressure (dP/dt) caused by static contraction from 21 +/- 3 to 39 +/- 7 mmHg and 1,405 +/- 362 to 2,285 +/- 564 mmHg/s, respectively. Aprotinin attenuated the contraction-induced rise in mean arterial blood pressure (28 +/- 4 to 9 +/- 2 mmHg) and maximal dP/dt (1,284 +/- 261 to 469 +/- 158 mmHg/s). Carboxypeptidase B reduced the cardiovascular response to static contraction. Thus the mean arterial blood pressure response was decreased from 36 +/- 12 to 24 +/- 11 mmHg, maximal dP/dt from 1,618 +/- 652 to 957 +/- 392 mmHg/s, and heart rate from 12 +/- 2 to 7 +/- 1 beats/min. These data suggest that stimulation of muscle afferents by bradykinin contributes to a portion of the reflex cardiovascular response to static contraction.

scholarly journals Alterations in the Baroreceptor-Heart Rate Reflex in Conscious Inbred Polydipsic (STR/N) Mice

2015 ◽  
pp. 173-182
Author(s):  
C. P. CHU ◽  
B. R. CUI ◽  
H. KANNAN ◽  
D. L. QIU
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Baroreceptor Reflex ◽  
Central Administration ◽  
Icr Mice ◽  
Arterial Blood ◽  
And Control

STR/N is an inbred strain of mice which is known to exhibit extreme polydipsia and polyuria. We previously found central administration of angiotensin II enhanced cardiovascular responses in STR/N mice than normal mice, suggesting that STR/N mice might exhibit different cardiovascular responses. Therefore, in this study, we investigated daily mean arterial blood pressure and heart rate, and changes in the baroreceptor-heart rate reflex in conscious STR/N mice and control (ICR) mice. We found that variability in daily mean arterial blood pressure and heart rate was significantly larger in STR/N mice than in ICR mice (p<0.05). There was a stronger response to phenylephrine (PE) in STR/N mice than in ICR mice. For baroreceptor reflex sensitivity, in the rapid response period, the slopes of PE and sodium nitroprusside (SNP) were more negative in STR/N mice than in ICR mice. In the later period, the slopes of PE and SNP were negatively correlated between heart rate and blood pressure in ICR mice, but their slopes were positively correlated in STR/N mice. These results indicated that STR/N mice exhibited the different cardiovascular responses than ICR mice, suggesting that the dysfunction of baroreceptor reflex happened in conscious STR/N mice.

Muscle mechanosensitive receptors close to the myotendinous junction of the Achilles tendon elicit a pressor reflex

2007 ◽  
Vol 102 (6) ◽  
pp. 2112-2120 ◽  
Author(s):  
Tomoko Nakamoto ◽  
Kanji Matsukawa
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Achilles Tendon ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Myotendinous Junction ◽  
Arterial Blood ◽  
Pressor Reflex ◽  
Passive Stretch

Feedback regulation by activation of mechanosensitive afferents in the exercising muscle causes the cardiovascular and sympathetic nerve responses, which follow tension development and are almost identical between static contraction and passive stretch. The precise location of the mechanoreceptors contributing to the exercise pressor reflex, however, remained unknown. To test the hypothesis that the mechanoreceptors will be located around the myotendinous junction to monitor a change in muscle tension than a change in muscle length, we examined the reflex cardiovascular responses to passive stretch of the triceps surae muscle in anesthetized rats with three interventions; systemic injection of gadolinium, cutting the Achilles tendon, and local injection of lidocaine into the myotendinous junction. Gadolinium (42 μmol/kg iv) blunted the increases in heart rate and mean arterial blood pressure during passive stretch by 36 and 22–26%, respectively, suggesting that the reflex cardiovascular responses were evoked by stimulation of muscle mechanosensitive receptors. The cardiovascular responses to passive stretch were not different between the cut Achilles tendon and the intact tendon in the same rats, suggesting that any mechanoreceptors, terminated in the more distal part of the tendon, did not contribute to the reflex cardiovascular responses. Lidocaine (volume, 0.04–0.1 ml) injected into the myotendinous junction blunted the stretch-induced increases in heart rate and mean arterial blood pressure by 37–49 and 27–34%, respectively. We conclude that the muscle mechanosensitive receptors evoking the reflex cardiovascular responses at least partly locate at or close to the myotendinous junction of the Achilles tendon.

Central indomethacin enhances volume-dependent vasopressin release

1984 ◽  
Vol 247 (6) ◽  
pp. R1017-R1021
Author(s):  
D. P. Brooks ◽  
L. Share ◽  
J. T. Crofton ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E2 ◽  
Mean Arterial Blood Pressure ◽  
Inhibitory Effect ◽  
Volume Depletion ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Severe Hemorrhage ◽  
Vasopressin Secretion

The effect of centrally administered indomethacin on hemorrhage-induced vasopressin release was studied in the morphine-sedated, urethan/chloralose-anesthetized dog. Ventriculocisternal perfusion of indomethacin 1) significantly reduced the amount of prostaglandin E2 in the effluent from the cisterna magna, 2) significantly enhanced the vasopressin response to volume depletion, and led to a greater fall in mean arterial blood pressure during severe hemorrhage. The results suggest that central prostaglandins may have an inhibitory effect on vasopressin secretion during volume depletion.

Effects of l-arginine on systemic and renal haemodynamics in conscious dogs

1991 ◽  
Vol 81 (6) ◽  
pp. 727-732 ◽  
Author(s):  
Marohito Murakami ◽  
Hiromichi Suzuki ◽  
Atsuhiro Ichihara ◽  
Mareo Naitoh ◽  
Hidetomo Nakamoto ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Renal Haemodynamics ◽  
Conscious Dogs ◽  
Arginine Infusion ◽  
Arterial Blood

1. The effects of l-arginine on systemic and renal haemodynamics were investigated in conscious dogs. l-Arginine was administered intravenously at doses of 15 and 75 μmol min−1 kg−1 for 20 min. 2. Mean arterial blood pressure, heart rate and cardiac output were not changed significantly by l-arginine infusion. However, l-arginine infusion induced a significant elevation of renal blood flow from 50 ± 3 to 94 ± 12 ml/min (means ± sem, P < 0.01). 3. Simultaneous infusion of NG-monomethyl-l-arginine (0.5 μmol min−1 kg−1) significantly inhibited the increase in renal blood flow produced by l-arginine (15 μmol min−1 kg−1) without significant changes in mean arterial blood pressure or heart rate. 4. Pretreatment with atropine completely inhibited the l-arginine-induced increase in renal blood flow, whereas pretreatment with indomethacin attenuated it (63 ± 4 versus 82 ± 10 ml/min, P < 0.05). 5. A continuous infusion of l-arginine increased renal blood flow in the intact kidney (55 ± 3 versus 85 ± 9 ml/min, P < 0.05), but not in the contralateral denervated kidney (58 ± 3 versus 56 ± 4 ml/min, P > 0.05). 6. These results suggest that intravenously administered l-arginine produces an elevation of renal blood flow, which may be mediated by facilitation of endogenous acetylcholine-induced release of endothelium-derived relaxing factor and vasodilatory prostaglandins.

Life Events, Cardiovascular Reactivity, and Risk Behavior in Adolescent Boys

PEDIATRICS ◽  
1995 ◽  
Vol 96 (6) ◽  
pp. 1101-1105
Author(s):  
Sai-Woon Liang ◽  
John M. Jemerin ◽  
Jeanne M. Tschann ◽  
Charles E. Irwin ◽  
Diane W. Wara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Risk Behavior ◽  
Arterial Blood Pressure ◽  
Life Events ◽  
Cardiovascular Reactivity ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Adolescent Boys ◽  
Positive Life Events ◽  
Arterial Blood

Background. Risk behavior contributes to injuries, one of the most important sources of morbidity and mortality in adolescents. Although research has shown that environmental stress makes adolescents more likely to engage in risk behavior and to sustain injuries, the magnitude of these associations has been small. Little is known about the role of individual differences in psychobiologic reactivity to stress in moderating the impact of stressful events. In this study, we examined associations among environmental stressors, cardiovascular reactivity to stress, and the level of risk behavior in adolescent boys. Methods. Twenty-four 14- to 16-year-old boys underwent a laboratory protocol designed to measure responses to psychologically and physically stressful tasks. Changes in heart rate and mean arterial blood pressure were measured serially at standard points in the protocol, and levels of positive and negative life events and recent risk behavior were measured using self-report questionnaires. Results. Neither life events nor cardiovascular reactivity were independently associated with risk behavior. Positive life events and mean arterial blood pressure reactivity significantly interacted, however, in predicting risk behavior (R2 increment = .25). Boys with high reactivity who reported numerous positive life events engaged in markedly less risk behavior than their peers. Conclusion. We conclude that adolescents with exaggerated cardiovascular responses to laboratory stressors are associated with less risk behavior in a setting of positive life circumstances. This result suggests that reactivity may exert protective, rather than harmful, influences in some environments.

Sex differences in central adrenoreceptor-mediated vasopressin response to hemorrhage

1991 ◽  
Vol 260 (5) ◽  
pp. E780-E786 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Sex Differences ◽  
Mean Arterial Blood Pressure ◽  
Intracerebroventricular Injection ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses ◽  
Induced Changes

Hemorrhage-induced changes in the plasma vasopressin concentration and mean arterial blood pressure (MABP) were studied in conscious rats of both sexes with and without central alpha 1-adrenoreceptor blockade. Rats were subjected to two sequential hemorrhages (H1 and H2), each 0.8% of body weight after an intracerebroventricular injection of the alpha 1-adrenoreceptor antagonist corynanthine or of vehicle. H1 stimulated vasopressin secretion more in proestrous females than in males; there were no significant sex-related differences in responses to H2. Corynanthine pretreatment attenuated the vasopressin response to H2 in males, potentiated this response in proestrous females, but had no effect in estrous females. MABP decreased after H1 in all female groups and in corynanthine-pretreated males. After H2, all groups were hypotensive to the same extent. These data indicate that central alpha 1-adrenoreceptor-mediated pathways participate in vasopressin and blood pressure responses to hemorrhage, but their role is complex and is dependent on gender and on the phase of the estrous cycle.

Rhythmicity of urinary sodium excretion, mean arterial blood pressure, and heart rate in conscious dogs

1992 ◽  
Vol 262 (1) ◽  
pp. H149-H156 ◽  
Author(s):  
U. Palm ◽  
W. Boemke ◽  
H. W. Reinhardt
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
Infusion Regimen

The existence of urinary excretion rhythms in dogs, which is a matter of controversy, was investigated under strictly controlled intake and environmental conditions. In seven conscious dogs, 14.5 mmol Na, 3.55 mmol K, and 91 ml H2O.kg body wt-1.24 h-1 were either administered with food at 8:30 A.M. or were continuously infused at 2 consecutive days. During these 3 days, automatized 20-min urine collections, mean arterial blood pressure (MABP), and heart rate (HR) recordings were performed without disturbing the dogs. Fundamental and partial periodicities, the noise component of urinary sodium excretion (UNaV), MABP, and HR were analyzed using a method derived from Fourier and Cosinor analysis. Oral intake (OI) leads to powerful 24-h periodicities in all dogs and seems to synchronize UNaV. UNaV on OI peaked between 1 and 3 P.M. Under the infusion regimen, signs of nonstationary rhythms and desynchronization predominated. UNaV under the infusion regimen could be separated into two components: a rather constant component continuously excreted and superimposed to this an oscillating component. No direct coupling between UNaV and MABP periodicities could be demonstrated. On OI, an increase in HR seems to advance the peak UNaV in the postprandial period. HR and MABP signals were both superimposed with noise. We conclude that UNaV rhythms are present in dogs. They are considerably more pronounced on OI.

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