Medial septal area ANG II receptor subtypes in the regulation of urine and sodium excretion induced by vasopressin

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Role of serotonergic 5-HT1A and oxytocinergic receptors of the lateral septal area in sodium intake regulation

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Vasopressin and angiotensin receptors of the medial septal area in the control of mean arterial pressure induced by vasopressin

Introduction. Brain arginine(8)-vasopressin (AVP), through the V-1a- and V-2-receptors, is essential for the maintenance of mean arterial pressure (MAP). Central AVP interacts with the components of the renin-angiotensin system, which participate in MAP regulation. This study all to determine the effects of V-1a-, V-2- and V-1a/V-2-AVP selective antagonists and AT(1)- and AT(2)-angiotensin II (Ang II) selective antagonists on the MAP induced by AVP injected into the medial septal area (MSA) of the brain.Materials and methods. Male Holtzman rats with stainless steel cannulae implanted into the MSA were used in experiments. Direct MAP was recorded in Conscious rats.Results. AVP administration into the MSA caused a prompt and potent pressor response in a dose-dependent fashion. Pretreatment with the V-1a- and V-2-antagonists reduced, whereas prior injection of the V-1a/V-2-antagonist induced a decrease in the MAP that remained below the baseline. Both AT(1)- and AT(2)-antagonists elicited a decrease, While simultaneous injections of two antagonists were more effective in decreasing the MAP induced AVP.Conclusion. These results indicate there is a synergism bell the V-1a- and V-2-AVP, and AT(1)- AT, and AT(2)-Ang II receptors in the MSA in the regulation of MAP.

On a possible dual role for the lateral septal area 5-HT1A receptor system in the regulation of water intake and urinary excretion

The 5-hydroxytryptamine (5-HT)(1A) receptor system plays a prominent role in a variety of physiological functions and behavior and regulation of this responsiveness of the receptor system has been implicated in the central regulation of water intake and urinary excretion. The lateral septal area (LSA) exhibits a high density of 5-HT1A receptors, as well as a subpopulation of oxytocin (OT) receptors. Here we report the effects of pMPPF (a selective 5-HT1A antagonist), d(CH2)(5)[Tyr(Me)(2)Thr(4), Orn(5), Tyr(NH2)(9)]-vasotocin (an OT antagonist), and that 5-HT1A receptor system is regulated as a consequence of activation of the Na+ channel by veratridine. Cannulae were implanted into the LSA of rats to enable the introduction of the drugs. Injections of 8-OH-DPAT (a 5-HT1A agonist) blocked water intake and increased urinary excretion, while pMPPF or the OT antagonist injected bilaterally before 8-OH-DPAT blocked its inhibitory effect on water intake and its diuretic effect. In contrast, increases in extracellular sodium levels induced by the sodium channel modulator, veratridine, enhanced 5-HT1A responsiveness for water intake and reduced the diuretic effects induced by 8-OH-DPAT. These trials demonstrated that the responsiveness of the 5-HT1A receptor system in the LSA can be enhanced or depressed as a consequence of an induced rise in extracellular sodium. (C) 2010 Elsevier B.V. All rights reserved.

Involvement of the intermediate nucleus of the lateral septal area on angiotensin II-induced dipsogenic and pressor responses

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Role of the medial septal area on pilocarpine-induced salivary secretion and water intake

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influence of arginine vasopressin receptors and angiotensin receptor subtypes on the water intake and arterial blood pressure induced by vasopressin injected into the lateral septal area of the rat

In this study we investigated the influence of d(CH2)(5)-Tyr(Me)-[Arg(8)]vasopressin (AAVP) and [adamanteanacetyl(1),0-ET-DTyr(2), Val(4), aminobutyryl(6), Arg(8,9)]-[Arg(8)]vasopressin (ATAVP), which are antagonists of vasopressin V-1 and V-2 receptors, and the effects of losartan, a selective angiotensin AT(1) receptor antagonist, and CGP42112A, a selective AT(2) receptor antagonist, injected into the lateral septal area (LSA) on thirst and hypertension induced by [Arg(8)]vasopressin (AVP). AAVP and ATAVP injected into the LSA reduced the drinking responses elicited by injecting AVP into the LSA. Both the AT(1) and AT(2) ligands administered into the LSA elicited a concentration-dependent decrease in the water intake induced by AVP injected into the LSA, but losartan was more effective than CGP42112A. The increase in MAP, due to injection of AVP into the LSA, was reduced by prior injection of AAVP from 18 +/- 1 to 6 +/- 1 mm Hg. Losartan injected into the LSA prior to AVP reduced the increase in MAP to 7 +/- 0.8 mm Hg. ATAVP and CGP42112A produced no changes in the pressor effect of AVP. These results suggest that the dipsogenic effects induced by injecting AVP into the LSA were mediated primarily by AT(1) receptors. However, doses of losartan were more effective when combined with CGP42112A than when given alone, suggesting that the thirst induced by AVP injections into LSA may involve activation of multiple AVP and angiotensin II receptor subtypes. The pressor response of AVP was reduced by losartan and by AAVP. CGP42112A and ATAVP did not change the AVP pressor response. These results suggest that facilitator effects of AVP on water intake are mediated through the activation of V-1 receptors and that the inhibitory effect requires V-2 receptors. The involvement of AT(1) and AT(2) receptors can be postulated. Based on the present findings, we suggest that the AVP in the LSA may play a role in the control of water and arterial blood pressure balance. (C) 2004 Elsevier B.V. All rights reserved.

Floral anatomy of Bromeliaceae, with particular reference to the evolution of epigyny and septal nectaries in commelinid monocots

Floral anatomy is described in ten genera of Bromeliaceae, including three members of subfamily Bromelioideae, three Tillandsioideae, and four genera of the polyphyletic subfamily Pitcairnioideae (including Brocchinia, the putatively basal genus of Bromeliaceae). Bromeliaceae are probably unique in the order Poales in possessing septal nectaries and epigynous or semi-epigynous flowers. Evidence presented here from floral ontogeny, vasculature, and the relative positions of nectary and ovules indicates that there could have been one or more reversals to apparent hypogyny in Bromeliaceae, although this hypothesis requires a better-resolved phylogeny. Such evolutionary reversals probably evolved in response to specialist pollinators, and in conjunction with other aspects of floral morphology of Bromeliaceae, such as the petal appendages of some species. The ovary is initiated in an inferior position even in semi-epigynous or hypogynous species. The ovary of all so-called hypogynous Bromeliaceae is actually semi-inferior, because the septal nectary is infralocular; in these species the nectaries have a labyrinthine surface and many vascular bundles. Brocchinia differs from most other fully epigynous species in that each carpel is secretory at the apex and reproductive, rather than secretory, at the base.

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

We investigated the role of alpha-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na+, K+ and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/µl) increased water intake (12.5 ± 1.7 ml/120 min). Clonidine (20 nmol/µl) injected into the MSA reduced the ANGII-induced water intake (2.9 ± 0.5 ml/120 min). Pretreatment with 80 nmol/µl yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 ± 0.4 and 3.1 ± 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGII-induced water intake (0.2 ± 0.1 and 0.2 ± 0.1 ml/120 min, respectively). ANGII reduced Na+ (23 ± 7 µEq/120 min), K+ (27 ± 3 µEq/120 min) and urine volume (4.3 ± 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of alpha1- and alpha2-antagonists decreased ANGII-induced water intake, and abolished the Na+, K+ and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal alpha1- and alpha2-adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII.

Interaction between paraventricular nucleus and septal area in the control of physiological responses induced by angiotensin II

We determined the effects of losartan (40 nmol) and PD 123319 (40 nmol) (both non-peptides and selective antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar¹, Ala8] angiotensin II (ANG II) (40 nmol) (a non-selective peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on the water and salt appetite, diuresis and natriuresis and mean arterial pressure (MAP) induced by administration of 10 nmol of ANG II into the medial septal area (MSA) of male Holtzman rats weighing 250-300 g. The volume of drug solution injected was 0.5 µl over a period of 10-15 s. The responses were measured over a period of 120 min. ANG II alone injected into the MSA induced an increase in all the above parameters (8.1 ± 1.2, 1.8 ± 0.3, and 17.1 ± 1.0 ml, 217 ± 25 µEq/120 min, and 24 ± 4 mmHg, respectively, N = 10-12) compared with vehicle-treated rats (1.4 ± 0.2, 0.6 ± 0.1, and 9.3 ± 0.5 ml, 47 ± 5 µEq/120 min, and 4.1 ± 0.8 mmHg, respectively, N = 10-14). Pretreatment with losartan and [Sar¹, Ala8] ANG II completely abolished the water and sodium intake, and the pressor increase (0.5 ± 0.2, 1.1 ± 0.2, 0.5 ± 0.2, and 0.8 ± 0.2 ml, and 1.2 ± 3.9, 31 ± 4.6 mmHg, respectively, N = 9-12), whereas losartan blunted the urinary and sodium excretion induced by ANG II (13.9 ± 1.0 ml and 187 ± 10 µEq/120 min, respectively, N = 9). Pretreatment with PD 123319 and [Sar¹, Ala8] ANG II blocked the urinary and sodium excretion (10.7 ± 0.8, 9.8 ± 0.7 ml, and 67 ± 13 and 57 ± 17 µEq/120 min, respectively, N = 9), whereas pretreatment with PD 123319 partially blocked the water and sodium intake, and the MAP induced by ANG II administration (2.3 ± 0.3, 1.1 ± 0.1 ml, and 12 ± 3 mmHg, respectively, N = 9-10). These results suggest the angiotensinergic effect of the MSA on the AT1 and AT2 receptors of the PVN in terms of water and sodium homeostasis and MAP modulation.

QUANTIFICATION OF IMMUNOGLOBULIN-A IN CHORIOAMNIOTIC MEMBRANE OF PATIENTS WITH PREMATURE RUPTURE OF MEMBRANES

Objective: the proposal was to study the presence of immunoglobulin A (IgA) in the chorioamniotic membrane of healthy postpartum women with premature rupture of the chorioamniotic membrane (FROM). Method: A single radial immunodiffusion technique was used to quantify the IgA in the chorioamniotic membrane tissues. Results: the level of IgA was approximately 10 times higher in patients whose membranes had been ruptured for > 10 h (24.58 mg/dl). These results were compared with those of a previously published study where the mean of amount of IgA was 2.52 mg/dl in membranes of patients with rupture < 10 h. Our results show that IgA began to rise after 10-15 h following rupture. Conclusion: Although more studies need to be performed our data indicate that the increasing IgA in our patients after 10 h of latency probably represents the beginning of an ascending colonization of bacteria which could be the source of future infection.

ROLE OF CHOLINERGIC AND ADRENERGIC PATHWAYS OF THE MEDIAL SEPTAL AREA IN THE WATER-INTAKE AND PRESSOR-RESPONSE TO CENTRAL ANGIOTENSIN-II AND CARBACHOL IN RATS

In the present study, we investigated the effect of previous injection of either prazosin (alpha 1-adrenergic antagonist) or atropine (muscarinic cholinergic antagonist) into the medial septal area (MSA) on the presser and dipsogenic responses induced by intracerebroventricular (ICV) injection of carbachol (cholinergic agonist) and angiotensin II (ANGII) in rats. The presser and dipsogenic responses to ICV carbachol (7 nmol) were reduced after previous treatment of the MSA with atropine (0.5 to 5 nmol), but not prazosin (20 and 40 nmol). The dipsogenic response to ICV ANGII (25 ng) was reduced after prazosin (40 nmol) into the MSA. The presser response to ICV ANGII was not changed either by previous treatment of the MSA with prazosin or atropine. The present results suggest a dissociation among the pathways subserving the control of dipsogenic and presser responses to central cholinergic or angiotensinergic activation.