NM  Vol.3 No.1 , March 2012
Interaction between Dopaminergic and Angiotensinergic Systems on Thirst in Adult Male Rats
Abstract: Thirst, which provides the motivation to drink, is an important component of the coordinated sequence of physiological responses that maintain the volume and composition of body fluids. Special structures in the central nervous system like periventricular organs detect changes in these parameters continuously. The present study investigated the interaction between dopaminergic and angiotensinergic systems on water intake in adult male rats. Intracerebroventricular (ICV) injections were carried out in all experiments after 24 h deprivation of water intake. After the deprivation interval, the volume of consumed water was measured for 1h. Administration the angiotensinergic (AT1) receptor antagonist Losartan (45 μg/rat), and the dopaminergic antagonist Chlorpromazine (40 μg/rat) significantly decreased water intake when compared to saline-treated controls. In contrast, ICV microinjection of the dopaminergic agonist Bromocriptine (10 μg/rat) significantly increased water intake when compared to saline-treated controls. ICV injection of Bromocriptine 15min after Losartan administration was able to attenuate the inhibitory effect of Losartan on water intake, whereas administration of Chlorpromazine 15 min after Losartan was unable to change the Losartan effect. These results suggest that the dopaminergic system interactions with the angiotensinergic system to regulate water intake through circumventricular organs. Dopaminergic and angiotensinergic neurons can monitor and regulate water intake via the stimulatory and inhibitory effects on each other, respectively.
Cite this paper: Z. Sharifkhodaei, N. Naghdi and S. Oryan, "Interaction between Dopaminergic and Angiotensinergic Systems on Thirst in Adult Male Rats," Neuroscience and Medicine, Vol. 3 No. 1, 2012, pp. 75-82. doi: 10.4236/nm.2012.31012.

[1]   A. K. Johnson and R. L. Thunhorst, “The Neuroendocrinology of Thirst and Salt Appetite: Visceral Sensory Signals and Mechanisms of Central Integration,” Journal of Frontiers in neuroendocrinology, Vol. 18, No. 3, 1997, pp. 292-353.

[2]   J. Magrani, E. Silva, A. C. Ramos, R. Athanazio, M. Barbetta and J. B. Fregoneze, “Central H1 and H2 Receptor Participation in the Control of Water and Salt Intake in Rats,” Physiology & Behavior, Vol. 84, No. 2, 2004, pp. 233-243. doi:10.1016/j.physbeh.2004.11.010

[3]   M. J. McKinley and A. K. Johnson, “The Physiological Regulation of Thirst and Fluid Intake,” News in Physiological Sciences, Vol. 19, No. 1, 2004, pp. 1-6. doi:10.1152/nips.01470.2003

[4]   A. K. Johnson, J. T. Cunningham and R. L. Thunhorst, “Integrative Role of the Lamina Terminalis in the Regulation of Cardiovascular and Body Fluid Homeostasis,” Clinical and Experimental Pharmacology and Physiology, Vol. 23, No. 2, 1996, pp. 183-191. doi:10.1111/j.1440-1681.1996.tb02594.x

[5]   E. Bagi, E. Fekete, D. Banyai and L. Lenard, “Effects of Angiotensin II and AIII Microinjections into the Zona Incerta after Intra- and Extracellular Fluid Loss,” Brain Research, Vol. 1002, No. 1-2, 2004, pp. 110-119. doi:10.1016/j.brainres.2004.01.002

[6]   S. M. McCann, Ka. J. Gutkows, C. R. Franci, A. L. Favaretto and R. J. Antunes, “Hypothalamic Central of Water and Salt Intake and Excretion,” Brazilian Journal of Medical and Biological Research, Vol. 27, 1994, pp. 865-884.

[7]   E. Gland and R. C. Ritter, “Area postrema Lesions Increase drinking to Angiotensin and Extra Cellular Dehydration,” Physiology & Behavior, Vol. 29, No. 5, 1982, pp. 943-947. doi:10.1016/0031-9384(82)90348-1

[8]   P. C. Wong, W. A. Price, A. T. Chiu, J. V. Duncia, D. J. Carin, R. R. Wexler and A. L. Johnson, “Timmermans P. B.; Nonpeptide Angiotensin II Receptor Antagonosts,” Journal of Pharmacology and Experimental Therapeutics, Vol. 252, 1990, pp. 719-725.

[9]   L. J. Waldecy and R. F. Celso, “Angiotensinergi Pathway through the Media Preoptic Nucleus in the Control Ofoytocine Secretion and Water and Sodium Intake,” Brain Research, Vol. 1014, No. 1-2, 2004, pp. 236-243. doi:10.1016/j.brainres.2004.03.077

[10]   A. Jucaite, “Dopami-nergic Modulation of Cerebral Activity and Cognitive Func-tions,” Medicina Kaunas Lithuania, Vol. 38, No. 4, 2002, pp. 357-362.

[11]   M. Puigde, X. Paez, M. A. Parada, L. Hernandez, G. Molina, E. Murzi and Q. Contreras, “Changes in Dopamine and Acetylcholine Release in the Rat Lateral Hypothalamus during Deprivation-Induced Drinking,” Neuroscience Letters, Vol. 227, No. 3, 1997, pp. 153-156. doi:10.1016/S0304-3940(97)00326-1

[12]   M. Le Moal and H. Simon, “Mesocorticolimbic Dopaminergic Network: Functional and Regulatory Roles,” Physiological Reviews, Vol. 71, No. 1, 1991, pp. 155- 234.

[13]   G. K. Pal, P. Pal and M. Rajss Moham, “Modulation of Feeding and Drinking Behavior by Catecholamines Injected into Nucleus Caudatus in Rats,” Indian Journal of Physiology and Pharmacology, Vol. 45, No. 2, 2001, pp. 172-180.

[14]   F. J. Gordon, M. J. Brody, G. D. Fink, J. Buggy and A. Johnson, “Role of Central Catecholamine in the Control of Blood Pressure and Drinking Behavior,” Brain Re-search, Vol. 178, No. 1, 1979, pp. 161-173. doi:10.1016/0006-8993(79)90095-7

[15]   H. Kobayashi and Y. Takei, “Mechanisms for Induction of Drinking with Special Reference to Angiotensin II,” Comparative Biochemistry and Physiology Part A: Physiology, Vol. 71, No. 4, 1982, pp. 485-494. doi:10.1016/0300-9629(82)90197-9

[16]   J. T. Fitzsimons and P. E. Setter, “The Relative Importance of Central nervous Ca-techolaminergic and Cholinergic Mechanisms in Drinking in Response to Angiotensin and Other Thirst Stimuli,” Journal of Physiology, Vol. 250, 1975, pp. 613-631.

[17]   M. A. Parada, L. Hernandez and B. G. Hoebel, “Sulpiride Injections in the Lateral Hypothalamus Induce Feeding and Drinking in Rats,” Journal of Behavioral and Neuroscience Research, Vol. 30, 1988, pp. 917-923.

[18]   S. Hohle, H. Spitznagel, W. Rascher, J. Culman and T. Unger, “Angiotensin AT1 Receptor-Mediated Vasopressin Release and Drinking Are Potentiated by an AT2 Receptor Antagonist,” European Journal of Pharmacology, Vol. 275, No. 3, 1995, pp. 277-282. doi:10.1016/0014-2999(95)00005-6

[19]   M. J. McKinley, L. Walker Lesley, T. Alexiou, A. M. Allen, D. J. Campbell, R. D. Nicolantonio, B. J. Oldfield and A. D. Denton, “Osmoregulatory Fluid Intake but Not Hypovolemic Thirst Is Intact in Mice Lacking Angiotensin,” American Journal of Physiolo-gy—Regulatory, Integrative and Comparative Physiology, Vol. 294, No. 5, 2008, pp. R1533-R1543. doi:10.1152/ajpregu.00848.2007

[20]   F. Qadri, T. Waldmann, A. Wolf, S. H?hle, R. Wolfgang and T. Unger, “Differential Contribution of Angiotensinergic and Cholinergic Receptors in the Hypothalamic Paraventricular Nucleus to Osmotically Induced AVP Release,” Journal of Pharmacology and Experi-mental Therapeutics, Vol. 285, No. 3, 1998, pp. 1012-1018.

[21]   M. Tham, M. K. Sim and F. R. Tang, “Location of Rennin-Angiotansin System Components in the Hypog-lossal Nucleus of the Rat,” Regulatory Peptides, Vol. 101, No. 1-3, 2001, pp. 51-57. doi:10.1016/S0167-0115(01)00260-9

[22]   L. Grobe Justin, X. Di and D. Sigmund Curt, “An Intra- cellular Rennin-Angiotensin System in Neurons: Fact, Hypothesis, or Fantasy,” Physiology, Vol. 23, No. 4, 2008, pp. 187-193. doi:10.1152/physiol.00002.2008

[23]   Z. Pirnik, D. Jezova, J D. Mikkelsen and A. Kiss, “Xylazine Activates Oxytocinergic but Not Vasopressinergic Hypothalamic Neurons under Normal and Hyperosmotic Conditions in Rats,” Neurochemistry Inter-national, Vol. 47, No. 7, 2005, pp. 458-465. doi:10.1016/j.neuint.2005.07.001

[24]   J. Culman, C. Vontleyer, B. P. Penburg, W. Rascher and T. Unger, “Effects of Systemic Treatment with Irbesartan and Losartan on Central Responses to Angiotensin II conscious Normotensive Rats,” European Journal of Pharmacology, Vol. 367, No. 2-3, 1999, pp. 255-265. doi:10.1016/S0014-2999(98)00983-2

[25]   P. Gohlke and S. Weiss, A. Janson, W. Wienen, J. Stangier, W. Rascher, J. Culman, T. Unger, “AT1 Receptor Antagonist Telmisartan Administered Peripherally Inhibits Central Responses to Angiotensin II in Conscious rats,” Pharmacology, Vol. 298, No. 1, 2001, pp. 62-70.

[26]   M. J. McKinley, A. M. Allen, M. L. Mathal, C. May, R. M. McAllen, B. J. Old field and R. S. Wei-singer, “Brain Angiotensin and Body Fluid Homeostasis,” The Japanese Journal of Physiology, Vol. 51, No. 3, 2001, pp. 281-289. doi:10.2170/jjphysiol.51.281

[27]   K. A. Al-Barazanji and R. J. Balment, “The Renal and Vascular Effects of Central Angiotensin II and Atrial Natriuretic Factor in the Anaesthetized Rat,” Journal of Physiology, Vol. 423, 1990, pp. 485-493.

[28]   J. A. Saydoff, P. A. Rittenhouse, M. Carnes, J. Armstrong, L. D. Van De Kar and M. S. Brownfield, “Neuroendocrine and Cardiovascular Effects of Serotonin: Selective Role of Brain Angiotensin on Vasopressin,” American Journal of Physiology—Endocrinology, Vol. 270, 1996, pp. E513-E521.

[29]   J. L. Lavoie, X. Liu, R. A. Bianco, T. G. Beltz, A. K. Johnson and C. D. Sigmund, “Evidence Supporting a Functional Role for Intracellular Rennin in the Brain,” Hypertension, Vol. 47, 2006, pp. 461-466. doi:10.1161/01.HYP.0000203308.52919.dc

[30]   E. Lazartigues, S. M. Dunlay, A. K. Loihl, P. Sinnayah, J. A. Lang, J. J. Espelund, C. D. Sibmund and R. L. Davisson, “Brain-Selective Overexpression of Angiotensin (AT1) Receptors Causes Enhanced Cardiovascular Sensitivity in Transgenic Mice,” Circu-lation Research, Vol. 90, 2002, pp. 617-624. doi:10.1161/01.RES.0000012460.85923.F0

[31]   Y. Sagara, Y. Hirooka, M. Nozoe, K. Ito, Y. Kimura and K. Sunagawa, “Pressor Response Induced by Central Angiotensin II Is Mediated by Activation of Rho/Rho-Kinase Pathway via AT1 Receptors,” Journal of Hypertension, Vol. 25, No. 2, 2007, pp. 399-406. doi:10.1097/HJH.0b013e328010b87f

[32]   Q. H. Chen, M. Glenn and G. M. Toney, “AT1-Receptor Blockade in the Hy-pothalamic PVN Reduces Central Hyperosmolality-Induced Renal Sympathoexcitation,” American Journal of Physiology, Vol. 281: No. 6, 2001, pp. R1844-R1853.

[33]   T. Hussain and M. F. Lokhandwala, “Society for Experimental Biology and Medicine Renal Dopamine Receptors and Hypertension,” Experimental Biology and Medicine, Vol. 228, No. 2, 2003, pp. 134-142.

[34]   M. L. Forsling and H. Williams, “Central Effects of Dopamine on Vasopressin in the Normally Hydrated and Water-Loaded Rat,” Journal of Physiology, Vol. 346, 1984, pp. 49-59.

[35]   J. L. Cornish, D. P. Wilks and M. Van, “A Functional Interaction between the Mesolimbic Dopamine System and Vasopressin Release in the Regulation of Blood Pressure in Conscious Rats,” Neuroscience, Vol. 81, No. 1, 1997, pp. 69-78. doi:10.1016/S0306-4522(97)00157-7

[36]   M. Sakata, H. Sei, K. Toida, H. Fujihara, R. Urushihara and Y. Morita, “Mesolimbic Dopaminergic System Is Involved in Diurnal blood Pressure Regulation,” Brain Research, Vol. 22, No. 2, 2002, pp. 194-201. doi:10.1016/S0006-8993(01)03402-3

[37]   M. Velasco and A. Luchsinger, “Dopamine: Pharmacologic and Therapeutic As-pects,” American Journal of Therapeutics, Vol. 5, No. 1, 1998, pp. 37-43. doi:10.1097/00045391-199801000-00007

[38]   M. V. Buuse, “Role of the mesolimbic dopamine System in Cardiovascular Homeostasis: Stimulation of the Ventral Tegmental Area Modulates the Effect of Vasopressin on Blood Pressure in Conscious Rat,” Clinical and Experimental Pharmacology and Physiology, Vol. 25, No. 9, 2007, pp. 661-668. doi:10.1111/j.1440-1681.1998.tb02273.x

[39]   E. Diaz, M. Silva and A. Israel, “Role of Brain Dopaminergic System in the Adrenomedullin-Induced Diuresis and Natriuresis,” Pharma-cological Research, Vol. 48, No. 5, 2003, pp. 489-496. doi:10.1016/S1043-6618(03)00186-5

[40]   S. J. Hill, C. R. Ganellin, H. Timnerman, J. C. Schwartz, N. P. Shankley, J. M. Young, W. Schunack, R. Levi and H. L. Haas, “International Union of Pharmacology XIII. Classification of Histamine Receptors,” Pharmacological Reviews, Vol. 49: 1997, pp. 253-278.

[41]   T. A. Jenkins, A. M. Allen, S. Y. Chai, D. P. MacGregor, G. Poxinos and F. A. Mendelsohn, “Interaction of Angiotensin II with Central Dopamine,” Advances in Experimental Medicine and Biology, Vol. 396, 1996, pp. 93-103.

[42]   B. Maul, W. Krause, K. Pankow, M. Becker, F. Gembardt and N. Alenina, T. Walther, M. Bader, W. Siems, “Central angiotensin II Controls Alcohol Consumption via Its AT1 Receptor,” FASEB Journal, Vol. 19, No. 11, 2005, pp. 1474-1481. doi:10.1096/fj.05-3742com

[43]   D. P. Brooks and J. R. Claybaugh, “Role of Dopmine in the Angiotensin II-Induced Vasopressin Release in the Conscious Dehydrated Dog,” Journal of Endocrinology, Vol. 94, 1982, pp. 243-249. doi:10.1677/joe.0.0940243

[44]   R. S. Weisinger, J. R. Blair-West, P. Burns, A. Denton and B. Purcell, “Central Na concentration, Na Appetite and Thirst of Sheep: Influence of Somatostatin and Losartan,” American Journal of Physiology, Vol. 280, No. 3, 2001, pp. 686-694.