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.

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 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.

scholarly journals Effects of glucagon-like peptide-1(7-36) amide on neurohypophysial and cardiovascular functions under hypo- or normotensive hypovolaemia in the rat

2002 ◽  
Vol 172 (2) ◽  
pp. 303-310 ◽  
Author(s):  
E Bojanowska ◽  
B Stempniak
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Mean Arterial Blood Pressure ◽  
Volume Depletion ◽  
Arterial Blood ◽  
The Mean ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Cardiovascular Functions

To date, glucagon-like peptide 1(7-36) amide (tGLP-1) has been found to affect the neurohypophysial and cardiovascular functions in normotensive and normovolaemic rats. The aim of the present study was to investigate possible effects of tGLP-1 on the mean arterial blood pressure and the release of vasopressin and oxytocin under conditions of blood volume depletion in the rat. In the first series of experiments, the animals were injected i.p. with either 0.15 M saline or 30% polyethylene glycol (PEG). PEG caused an 18% reduction of blood volume 1 h after injection. No significant changes in the mean arterial blood pressure were found in either normo- or hypovolaemic rats during the experiment. tGLP-1 injected i.c.v. at a dose of 1 microg/5 microl 1 h after the i.p. injection increased similarly the arterial blood pressure in normo- and hypovolaemic rats. The plasma vasopressin/oxytocin concentrations were markedly elevated in hypovolaemic animals and tGLP-1 further augmented the release of both hormones. In the second study, hypovolaemia was induced by double blood withdrawal. The haemorrhage resulted in a marked decrease of the mean arterial blood pressure and in the elevated plasma vasopressin/oxytocin concentrations. tGLP-1 injected immediately after the second blood withdrawal increased the arterial blood pressure. In parallel, tGLP-1 enhanced significantly vasopressin and oxytocin secretion when compared with haemorrhaged, saline-injected rats. The results of this study indicate that tGLP-1 may affect the arterial blood pressure and the secretion of neurohypophysial hormones under pathological conditions brought about by blood volume depletion.

Effect of systemic arterial hypotension on the rate of cerebrospinal fluid formation in dogs

1974 ◽  
Vol 41 (3) ◽  
pp. 350-355 ◽  
Author(s):  
Michael E. Carey ◽  
A. Richard Vela
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Mean Arterial Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Fluid Formation ◽  
The Mean ◽  
Csf Production ◽  
Fine Print

✓The rate of cerebrospinal fluid (CSF) production in dogs was measured by ventriculocisternal perfusion with artificial CSF containing inulin. In normotensive animals, the average CSF production was 36 ± 6 µl/min. When the mean arterial blood pressure was reduced to 62 ± 1 mm Hg, the CSF production fell to 22 ± 5 µl/min, a 39% reduction in fluid formation. The authors briefly discuss various hypotheses to explain this reduction.

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.

Control of ACTH and vasopressin in neurohypophysectomized conscious dogs

1985 ◽  
Vol 249 (2) ◽  
pp. R281-R284
Author(s):  
H. Raff ◽  
D. Merrill ◽  
M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Sodium Nitroprusside ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Corticotropin Releasing Factor ◽  
Conscious Dogs ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Cortisol Responses

Adrenocorticotropin (ACTH), cortisol, and vasopressin responses to clamped decreases in blood pressure (MAP) and to ovine corticotropin-releasing factor (CRF) infusion (20 ng X kg-1 X min-1) in intact and neurohypophysectomized (NHX) conscious dogs were examined. Mean arterial blood pressure was decreased 28 mmHg by a controlled infusion of sodium nitroprusside. Hypotension induced large increases in ACTH (peak 164 +/- 25 pg/ml), cortisol (peak 12.5 +/- 2.5 micrograms/dl), and vasopressin (peak 221 +/- 64 pg/ml) in intact (n = 7) dogs. NHX (n = 7) significantly attenuated these responses to hypotension. CRF infusion induced increases in ACTH similar in intact (n = 4) and NHX (n = 4) dogs. However, cortisol responses were significantly attenuated by NHX. Interestingly, CRF infusion induced small but significant increases in vasopressin from 3.0 +/- 1.1 to 8.1 +/- 2.0 pg/ml. We conclude that NHX attenuates ACTH and vasopressin responses to hypotension and cortisol responses to CRF-induced increases in ACTH. CRF seems to stimulate vasopressin release.

Paraventricular nucleus histamine increases blood pressure by adrenoreceptor stimulation of vasopressin release

1995 ◽  
Vol 269 (1) ◽  
pp. H80-H85 ◽  
Author(s):  
S. L. Bealer ◽  
S. O. Abell
Keyword(s):  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Peripheral Mechanism ◽  
Adrenergic Antagonist ◽  
Vasopressin Secretion ◽  
Local Release ◽  
Stimulation Of

The role of adrenoreceptor stimulation and the peripheral mechanism mediating the increase in mean arterial blood pressure (MAP) and heart rate (HR) during administration of histamine (HA) in the paraventricular nucleus/anterior hypothalamus (PVN/AH) was evaluated in conscious rats. HA administered through microdialysis probes in the PVN/AH region increased MAP (18 +/- 1 mmHg) and HR (81 +/- 10 beats/min). The pressor response was abolished by simultaneous administration of phentolamine (alpha 1- and alpha 2-antagonist) or prazosin (alpha 1-antagonist) but not altered by yohimbine (alpha 2-antagonist). The tachycardia was not effected by any adrenergic antagonist. Furthermore, ganglionic blockade did not reduce the increase in MAP (21 +/- 2 mmHg) during PVN/AH perfusion with HA, while V1-vasopressin receptor blockade abolished the pressor response (4 +/- 2 mmHg). These data suggest that HA administered to the PVN/AH increases blood pressure by local release of norepinephrine and alpha 1-adrenoreceptor stimulation of vasopressin secretion, while the tachycardia is not mediated by alpha-adrenoreceptors.

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.

scholarly journals On the Pathology of the dropsy produced by obstruction of the superior and inferior venœ and the portal vein.— Preliminary communication

1907 ◽  
Vol 79 (532) ◽  
pp. 267-283 ◽  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Mean Arterial Blood Pressure ◽  
Normal Limit ◽  
The Body ◽  
Diastolic Filling ◽  
Arterial Blood ◽  
Preliminary Communication ◽  
The Mean

In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.

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