Interactions between the brain renin-angiotensin system and brain prostanoids in the control of vasopressin secretion
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.Experimental Brain Research (Impact Factor: 2.04). 02/1990; 83(1):131-6. DOI: 10.1007/BF00232201
Experiments were carried out in conscious, unrestrained, male rats to evaluate possible interactions between brain prostanoids and the brain renin-angiotensin system in the control of vasopressin release and in cardiovascular regulation. The intracerebroventricular (icv) administration of prostaglandin D2 (PGD2) resulted in transient increases in the plasma vasopressin concentration (PAVP) and heart rate and a gradual increase in mean arterial blood pressure (MABP). Pretreatment icv with saralasin, an angiotensin II-receptor antagonist, moderately attenuated the vasopressin response to PGD2, but had no effect on the heart rate and blood pressure responses. Angiotensin II icv increased both PAVP and MABP. This vasopressin response was almost completely prevented by prior icv meclofenamate, a cyclooxygenase inhibitor, and the blood pressure response was attenuated. These observations, combined with previous studies of the role of central angiotensin II and central prostanoids in the physiological control of vasopressin release, suggest that there may be important interactions between brain prostanoids and the brain renin-angiotensin system in this control.
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ABSTRACT: To evaluate roles of prostaglandins (PGs) in vasopressin (AVP) secretion elicited by stimulating alpha-adrenergic and dopaminergic receptors in the periventricular region, we examined in conscious rats the effects of intracerebroventricular (i.c.v.) injections of a cyclooxygenase inhibitor meclofenamate on the plasma AVP responses to i.c.v. applications of angiotensin II (ANG II), phenylephrine and dopamine. I.c.v. injections of 58 pmol ANG II produced, 5 and 15 min later, augmentations of plasma AVP accompanied by elevations of arterial pressure and tendencies of reduction in heart rate. Similarly, the administrations of 0.53 mumol phenylephrine or dopamine enhanced plasma AVP 5 min later, without altering arterial pressure and heart rate significantly. Meclofenamate (0.31 mumol) applied i.c.v. 30 min prior to the administrations of ANG II remarkably inhibited the AVP and pressor responses to this peptide. However, the responses of plasma AVP, arterial pressure and heart rate to phenylephrine or dopamine were not affected by the i.c.v. administrations of 0.31 mumol meclofenamate. The injections of meclofenamate followed by the administrations of a vehicle for ANG II and the catecholamines were without effect on plasma AVP and the cardiovascular parameters. Plasma osmolality, sodium, potassium and chloride in all the groups mentioned above were not significantly changed during experiments. These results suggest that PGs generated in the periventricular region, despite their probable stimulatory roles in the ANG II-evoked AVP secretion, may not participate in the AVP-releasing mechanisms activated by dopaminergic and alpha-adrenergic receptors, supporting the view that PGs and the catecholamines may facilitate AVP release via separate pathways.Brain Research 05/1993; 607(1-2):149-53. DOI:10.1016/0006-8993(93)91500-R · 2.84 Impact Factor
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ABSTRACT: Prostaglandin D2 (PGD2) is the major prostanoid formed among other prostanoids in cultured microvascular endothelium derived from human brain (HBEC). Angiotensin II, arginine vasopressin and endothelium-1 stimulated the production of PGD2 and PGF2 alpha in a concentration-dependent manner, and this effect was inhibited by their specific receptor antagonists or dexamethasone (inhibitor of phospholipase A2/cyclooxygenase II). Both the peptidergic-induced PGD2 and the exogenously added PGD2 were converted in HBEC to 9 alpha, 11 beta-PGF2, a potent vasoconstrictor. Exogenous PGD2 also dose-dependently enhanced the production of vasoconstrictive PGF2 alpha, thromboxane B2, vasodilatory prostaglandin PGE2, and cAMP in these cells. The PGD2 stimulated formation of the prostanoids was inhibited by acetylsalicylic acid or indomethacin (inhibitors of cyclooxygenase I) but not dexamethasone, demonstrating for the first time that PGD2 may contribute to the production of prostanoids in HBEC. These findings strongly suggest that PGD2 may play a pivotal role in the regulation of cerebromicrovascular function.Journal of the Autonomic Nervous System 10/1994; 49. DOI:10.1016/0165-1838(94)90099-X
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ABSTRACT: This study explored the roles of prostaglandins in the anteroventral third ventricular region, a cerebral osmoreceptor site, in the osmoregulation mechanism of vasopressin release. We injected (1 microliter) prostaglandin E2 (12.8 nmol) or meclofenamate (78.3 nmol), an inhibitor of prostaglandin biosynthesis, into the brain region or the lateral cerebral ventricle of conscious rats, examining their effects on plasma vasopressin and its controlling factors in the presence or absence of an osmotic stimulus. The injection of prostaglandin E2 into the anteroventral third ventricular region augmented plasma vasopressin and arterial pressure after 5 min and 15 min, without influencing plasma osmolality, sodium, potassium, or chloride. In contrast, intraventricular injection of prostaglandin E2 did not cause any significant effect on those variables. The i.v. infusion (0.1 ml.kg-1.min-1) of hypertonic saline (2.5 mol/l) enhanced plasma vasopressin after 15 min and 30 min; this was accompanied by increased plasma osmolality, sodium, and chloride, and by unaltered or elevated arterial pressure. Meclofenamate given into the anteroventral third ventricular region 30 min before starting the hypertonic saline infusion abolished the osmotic vasopressin response without significantly changing the responses of the other variables. Histological analysis showed that the injection sites of meclofenamate in these rats were close to those of prostaglandin E2 in the anteroventral third ventricular region and included the organum vasculosum of the lamina terminalis and the surrounding area, the medial preoptic area, and periventricular and median preoptic nuclei. When injection cannulae for meclofenamate deviated from those areas incidentally or when the drug was expressly administered into the cerebral ventricle, the osmotic vasopressin response was not inhibited. Plasma vasopressin and the other variables observed during the i.v. infusion of isotonic saline (0.15 mol/l) were not affected significantly by meclofenamate administration into the anteroventral third ventricular region or the cerebral ventricle. On the basis of these results, we concluded that prostaglandins synthesized in and/or near the anteroventral third ventricular region might contribute to the facilitation of vasopressin release in the hyperosmotic state.Experimental Brain Research 03/1997; 113(2):265-72. DOI:10.1007/BF02450324 · 2.04 Impact Factor
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