Receptor-Mediated Effects of Clonidine on Need-Induced 3% NaCl and Water Intake

Non-adrenergic ligands that bind to imidazoline receptors (I-R), a selective ligand that binds to = 2 -adrenoceptors (= 2 -AR) and mixed ligands that bind to both receptors were tested for their action on water intake behavior of 24-h water-deprived rats. All drugs were injected into the third cerebral ventricle. Except for agmatine (80 nmol), mixed ligands binding to I-R/= 2 -AR such as guanabenz (40 nmol) and UK 14304 (20 nmol) inhibited water intake by 65% and up to 95%, respectively. The selective non-imidazoline = 2 -AR agonist, = -methylnoradrenaline, produced inhibition of water intake similar to that obtained with guanabenz, but at higher doses (80 nmol). The nonadrenergic I-R ligands histamine (160 nmol, mixed histaminergic and imidazoline ligand) and imidazole-4-acetic acid (80 nmol, imidazoline ligand) did not alter water intake. The results show that selective, nonimidazoline = 2 -AR activation suppresses water intake, and suggest that the action on imidazoline sites by non-adrenergic ligands is not sufficient to inhibit water intake.

Section: Introductionmentioning

confidence: 99%

Effects of central imidazolinergic and alpha2-adrenergic activation on water intake

Sugawara

Miguel

Pereira

et al. 2001

“…Furosemide (Sigma) was administered subcutaneously (sc) at 20 mg/kg body weight and was dissolved in alkaline saline (pH adjusted to 9.0 with NaOH), as described previously (29).…”

Section: Drugsmentioning

confidence: 99%

Antidipsogenic effects of central adenosine-5'-triphosphate

Faria

Sant'Ana

Menani

et al. 2009

Besides other physiological functions, adenosine-5'-triphosphate (ATP) is also a neurotransmitter that acts on purinergic receptors. In spite of the presence of purinergic receptors in forebrain areas involved with fluid-electrolyte balance, the effect of ATP on water intake has not been investigated. Therefore, we studied the effects of intracerebroventricular (icv ) injections of ATP (100, 200 and 300 nmol/μL) alone or combined with DPCPX or PPADS (P1 and P2 purinergic antagonists, respectively, 25 nmol/μL) on water intake induced by water deprivation. In addition, the effect of icv ATP was also tested on water intake induced by intragastric load of 12% NaCl (2 mL/rat), acute treatment with the diuretic/natriuretic furosemide (20 mg/kg), icv angiotensin II (50 ng/μL) or icv carbachol (a cholinergic agonist, 4 nmol/μL), on sodium depletion-induced 1.8% NaCl intake, and on food intake induced by food deprivation. Male Holtzman rats (280-320 g, N = 7-11) had cannulas implanted into the lateral ventricle. Icv ATP (300 nmol/μL) reduced water intake induced by water deprivation (13.1 ± 1.9 vs saline: 19.0 ± 1.4 mL/2 h; P < 0.05), an effect blocked by pre-treatment with PPADS, but not DPCPX. Icv ATP also reduced water intake induced by NaCl intragastric load (5.6 ± 0.9 vs saline: 10.3 ± 1.4 mL/2 h; P < 0.05), acute furosemide treatment (0.5 ± 0.2 vs saline: 2.3 ± 0.6 mL/15 min; P < 0.05), and icv angiotensin II (2.2 ± 0.8 vs saline: 10.4 ± 2.0 mL/2 h; P < 0.05), without changing icv carbachol-induced water intake, sodium depletion-induced 1.8% NaCl intake and food deprivation-induced food intake. These data suggest that central ATP, acting on purinergic P2 receptors, reduces water intake induced by intracellular and extracellular dehydration.

“…Water deprivation (5,6,10,12,13) Sodium depletion (10,13,22) Cholinergic activation (6,7) Water deprivation (22) Angiotensin II (4,6,11,42) Angiotensin II (21) Cell dehydration (6) Mineralocorticoid (21) Meal associated (10) Non-regulatory (need-free) (22) A multifactorial model for dehydration-induced hydrosaline intake…”

Section: Water Intakementioning

confidence: 99%

“…Thus, clonidine is a ubiquitous inhibitor of thirst-inducing mechanisms. This inhibition is mediated by central α 2 -adrenergic receptors since it is antagonized by the α 2 -adrenergic antagonists yo-himbine and idazoxan injected into the brain (5, [11][12][13]. Prazosin, an α 1 -adrenergic antagonist, also inhibits the effect of clonidine (5,12,13), but it can also bind to α 2 -adrenergic receptors (14).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Multifactorial control of water and saline intake: role of <FONT FACE=Symbol>a</font>2-adrenoceptors

Deluca¹,

Menani²

1997

Water and saline intake is controlled by several mechanisms activated during dehydration. Some mechanisms, such as the production of angiotensin II and unloading of cardiovascular receptors, activate both behaviors, while others, such as the increase in blood osmolality or sodium concentration, activate water, but inhibit saline intake. Aldosterone probably activates only saline intake. Clonidine, an α 2 -adrenergic agonist, inhibits water and saline intake induced by these mechanisms. One model to describe the interactions between these multiple mechanisms is a wire-block diagram, where the brain circuit that controls each intake is represented by a summing point of its respective inhibiting and activating factors. The α 2 -adrenoceptors constitute an inhibitory factor common to both summing points.